Hamid Ali.pdf

Clinical Evaluation of Safoof Ziabetus

In

Management of Ziabetus Shakri

By

HAMID ALI

Dissertation Submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore.

In Partial fulfilment of the requirements for the degree of

MAHIRE TIB ( M. D. Unani)

In

MOALEJAT

(Medicine)

Department of Moalejat

National Institute of Unani Medicine

Bangalore

2007

Clinical Evaluation of Safoof Ziabetus In


By

HAMID ALI

Dissertation Submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore. In Partial fulfilment of the requirements for the degree of

MAHIRE TIB ( M. D. Unani) In

MOALEJAT (Medicine)

Under the Guidance of

DR. MOHD ANWAR

Department of Moalejat National Institute of Unani Medicine

Bangalore

2007

Rajiv Gandhi University of Health Sciences, Karnataka

DECLARATION BY THE CANDIDATE

I hereby declare that the Dissertation entitled “Clinical Evaluation Of Safoof

Ziabetus In Management Of Ziabetus Shakri” is a bonafide and genuine

research work carried out by me under the guidance of Dr. Mohd Anwar,

Reader, Dept. of Moalejat, National Institute of Unani Medicine, Bangalore.

Date: HAMID ALI

Place: Bangalore

National Institute of Unani Medicine (Dept. of AYUSH, Ministry of Health & Family Welfare, Govt. of India)

Kottigepalya, Magadi Main Road, Bangalore‐91: 0‐580725

CERTIFICATE BY THE GUIDE

This is to certify that the Dissertation entitled “Clinical Evaluation Of Safoof

Ziabetus In Management Of Ziabetus Shakri” is a bonafide research work

done by HAMID ALI in partial fulfilment of the requirement for the degree of

“Mahire Tib (M.D. Unani) in Moalejat (Medicine)”.

Date : Dr. Mohd Anwar Place : Bangalore Reader

Department Of Moalejat

National Institute of Unani Medicine

Bangalore

National Institute of Unani Medicine (Dept. of AYUSH, Ministry of Health & Family Welfare, Govt. of India)

Kottigepalya, Magadi Main Road, Bangalore‐91: 083580725

ENDORSEMENT BY THE HOD, HEAD OF THE INSTITUTION

This is to certify that the Dissertation entitled “Clinical Evaluation of Safoof

Ziabetus in Management of Ziabetus Shakri” is a bonafide research work

done by HAMID ALI under the guidance of Dr. Mohd Anwar, Reader, Dept. of

Moalejat, National Institute of Unani Medicine, Bangalore.

Prof. Mansoor Ahmad Siddiqui Prof. M. A. Jafri

HOD, Department of Moalejat Director

National Institute of Unani Medicine National Institute of Unani Medicine

Date: Date:

Place: Bangalore Place: Bangalore

COPYRIGHT

Declaration by the Candidate

Thereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka

shall have the rights to preserve, use and disseminate this Dissertation in print or

electronic format for academic / research purpose.

Date : HAMID ALI

Place: Bangalore

© Rajiv Gandhi University Of Health Sciences, Karnataka.

ACKNOWLEDGEMENT

“All praises to Almighty ALLAH the most beneficent the most merciful, the

omnipresent and creator of all living and non-living being, by thanking him

for best owing upon me to courage, mindset, patience strength and zeal that

enabled me to complete this work successfully."

‘After the praise of almighty ALLAH, Salam and Darood on our Prophet

Huzoor Mohammad Mustafa (SAW).’

I exceed my bliss height in expressing my deep sense of gratitude to

Prof. M. A. Jafri, Director, National Institute of Unani Medicine, Bangalore, for

his moral encouragement and providing me the necessary facilities that I needed

for my research work.

My sincere thanks are to Prof. M. A. Siddiqui, HOD, Department of

Moalejat, National Institute of Unani Medicine, Bangalore, for his valuable advice

and moral encouragement.

It is with a deep and abiding sense of gratitude that I acknowledge my debt

to my guide Dr. Mohd. Anwar, the fountainhead of the work enclosed in the

following pages. His sense of responsibility towards this work, constructive

criticism and wise counsel smoothed the rough patches and his able guidance

throughout, are the pillars upon which this dissertation stands. It was a pleasure to

have been under his supervision and his dynamism inspired me to efforts that I

would have otherwise been incapable of, my respect and admiration for him is

unbounded.

I deem it a sacred privilege to express my deep sense of gratitude and

obligation to my co- guide Dr. Tanzeel Ahmad, whose constructive guidance,

constant inspiration, valuable advice and moral encouragement has accelerated me

to reach my destination. His critical suggestions have added more dimension to the

study.

i

I pray that the soul of our beloved ‘Late Hakeem Ajmal Khan Sahab’

may rest in peace, who established A & U Tibbia College and Hospital and

stressed the need for research and the use of modern sciences indigenous

medicine, instead of blindly followed old prescriptions.

I exceed my bliss height in expressing my deep sense of gratitude to my

teacher ‘Dr. Rais-ur-Rahman Sahab, H.O.D. and Reader of Department of

Moalejat, A&U Tibbia College Karol Bagh, for his perpetual guidance and

constant encouragement. He has been my source of inspiration throughout the

course of my study, not only at post-graduate level but also during graduation

level. His guidance is a gift that I would cherish for the rest of my life.

I am indebted to all my esteemed teachers of the Deptt. Of Moalejat,

namely Prof. Syed Abrar, Dr. A. N. Ansari, Dr. M. A. Quamri, who have enlighten

me with their knowledge and experiences and provided academic support during

the course of my research work.

I wish great fully to acknowledge to my other teachers specially

Prof.Ghufran Ahmad, Dr.G. D. Sofi, Dr. Nasreen Jahan, and Dr. A. H. Ansari for

their constant sympathetic attitude and special blessing to me.

I am deeply thankful to Dr. Mohd. Nafees Khan, Dr. Mohd. Azam for their

help and co-operation.

I am also thankful to my colleagues Dr. Mohd. Zubair and Dr. Abdul

Hakeem for their kind co-operation and help during my research work.

I am deeply thankful to Mr.Ehtesham and Mr.Danish Ghani (NIUM library)

who never expressed signs of exhaustion in providing me literature.

I want to offer my gratitude with great honour and respect to my parents

whose love and prayers have always been a great source of strength to me and

have proved icon for the ship of my carrier. My heart goes out in reverence to

them for their tremendous patience, endurance and affections.

ii

I do not find adequate words to express my deep sense of respect and

sincere thanks to my elder brothers Er. Athar Mustafa and Er. Kausar Murtaza,

who left no stone unturned in enabling and whetting me to obtain and achieve the

aims and objectives in life, whose perennial patronization enabled me to beat the

impossible. Their inspirations and prayers have always been a driving force behind

my efforts.

My acknowledgement would remain incomplete without making a special

mention for the sustained help, encouragement moral boost up and kind co-

operation which I received from my Sisters Zehra Anjum, Dr.Wajida Tabassum,

Dr.Nigar Tabassum.

I am highly obliged and deeply touched by the pains taken by ‘Dr.Naghma

Chand (M.D.)’ who never expressed sign of exhaustion in providing me literature

and to the thesis to correct shape, her moral support and wishes are invaluable and

valuable advice to my life.

At this moment how can I forget to express my deep affection and thanks

for my beloved son Mohd. Hamd, who missed me during my academic period.

Lastly, and by no means least, I would specially like to mention the name

of my beloved wife Samreen Fatma, there is no way I could have completed this

work without her moral support, constant encouragement, persistent co-operation,

endless forbearance and inexhaustible store of affections that sustains me at each

and every step and helped me to bring this work to end.

Date : HAMID ALI

Place : Bangalore

iii

ABBREVIATIONS

Acetyl CoA : Acetyl Coenzyme A

Acyl CoA : Acyl-coenzyme A

AD : Anno Domain (after the death of Christ)

ALT : Alanine amino transferase

aq. : Aqua ( Water)

AST : Aspartate amino transferase

AT : After Treatment

ATP : Adenosine triphosphate

BC : Before Christ

BMI : Body mass index

BP : Blood Pressure

BT : Before Treatment

Cap : Capsule

cm : Centimetre

CRF : Case report form

cu.mm : Cubic millimetre

dl : Decilitre

DLC : Differential Leucocytes Count

DNA : Deoxyribonucleic acid

Dr : Doctor

E.coli : Escherichia coli

ECG : Electrocardiogram

ed. : Edition

iv

e.g. : example gratv (for example)

ESR : Erythrocyte sedimentation rate

et.al. : et alii or et alia (and other)

etc. : etcetera (and the rest)

FDA : Food and Drug Administration

FFA : Free fatty acid

GDM : Gestational Diabetes Mellitus

GLUTS : Glucose transporters

gm : Gram

GOD/ POD : Glucose Oxidase / Peroxidase

G.Sylvestre : Gymnema Sylvestre

Hb : Haemoglobin

HDL : High density lipoprotein

Hg : Mercury

HGP : Hepatic glucose production

HNF : Hepatocyte Nuclear Factor

hr : Hour

IBW : Ideal Body Weight

ICMR : Indian council of Medical research

IDDM : Insulin Dependent Diabetes Mellitus

IDF : International Diabetes federation

i.e. : “idest” (that is)

IFCC : International Federation of Clinical Chemistry

IPF : Insulin promoter factor

v

IU/L : International Units per Liter

JVP : Jugular Venous Pressure

Kcal : Kilo Calorie

KFT : Kidney Function Test

Kg : Kilogram

Lb : Pound

LFT : Liver Function Test

m2 : Square metre

m3 : Cubic millimetre

mg : Milligram

mg/dl : Milligram per decilitre

min : Minutes

mm : Millimetre

mmol/L : Millimol per litre

MODY : Maturity onset diabetes of the young

MUFA : Monounsaturated fatty acids

n : Total number

NAD : Nicotinamide adenine dinucleotide

NIDDM : Non Insulin Dependent Diabetes Mellitus

NIUM : National Institute of Unani Medicine

No. : Number

p : Probability of error

PNPP : p-Nitrophenyl Phosphate

PP cells : Polypeptide cells

vi

pts. : Points

PUFA : Polyunsaturated fatty acids

R. Br. : Roxburgh

RIA : Radio immunological assay

R.R. : Respiratory Rate

S.Cholesterol : Serum Cholesterol

SGOT : Serum glutamic oxaloacetic transaminase

SGPT : Serum glutamic pyruvic transaminase

Sol. : Solution

T.Cordifolia : Tinospora Cordifolia

Temp : Temperature

TLC : Total Leucocytes Count

UV : Ultra Violet

Vol. : Volume

WHO : World Health Organisation

Β : Beta

2nd : Second

% : Percentage

> : Greater than

> : Greater than or equal to

+ : Positive

_ : Negative

vii

Clinical evaluation of Safoof Ziabetus

In


ABSTRACT

_____________________________________________________________

Nowadays, Ziabetus Shakri (Diabetes Mellitus) has become a global problem in spite of

advances in modern science, and prevails all over the world. Globally it affects about 246

million peoples. It causes Disability through its complications like blindness, kidney

failure, coronary artery disease, gangrene of lower extremities. Owing to these

complications, the researchers of different system of medicine are concentrating

themselves for the development of the new antidiabetic drugs. The different antidiabetic

drugs have been already evaluated by main stream of medicine and have very much

potent and effective hypoglycaemic action, but the long term use of these drugs resulted

in development of various side effects. Hence, there is a dire need to develop safe and

effective drug for the management of Ziabetus Shakri. Unani physicians have been

treating Ziabetus Shakri since ancient times; they have described a number of Unani

drugs both single and compound for the management of Ziabetus Shakri. Recently

several single herbal drugs has been experimentally and clinically evaluated and reported

as hypoglycaemic agents. However, the scientific study of compound formulation is

largely ignored by the scientists and physicians despite the fact that a good number of

compound drugs have been described in Unani literature to be effective in Ziabetus

viii

condition as large number of physicians of Unani medicine are using them successfully

since long. Keeping this fact in mind a randomized single blind placebo diet control trial

was conducted on the “Clinical evaluation of Safoof Ziabetus in management of

Ziabetus Shakri”.

The trial was conducted on 50 newly diagnosed patients of Ziabetus Shakri, at National

Institute of Unani Medicine Hospital, Bangalore. They were divided into two Groups;

Group A (Test Group-30 Patients) was given test drug and Group B (Placebo-20

Patients) placebo in a dose of 6 gm thrice a day in capsule form orally with water,15

minutes before meal along with planned diet and exercise for the period of 45 days. This

study shows good response on blood sugar level of the cases treated with Unani

formulation i.e. Average reduction of 56.83 mg/dl (32.80 %) in fasting and 67.23 mg/dl

(26.94 %) in post prandial blood sugar was recorded. On comparing before treatment

observations of Blood sugar fasting and post prandial with their corresponding after

treatment observations, with the help of Student’s ‘t’ test, it was found significant

statistically (p < 0.05) [ Calculated value of ‘t’= 9.31 (Fasting) and 7.42 (Post prandial) ] .

Study also reveals that the Ziabetus Shakri is relatively more common in person having

age 40 years and above with har mizaj. The advantage of this treatment is that, it is very

much cost effective and offer maximum success without any adverse effect.

Keywords: Ziabetus Shakri; Antidiabetic drugs; Safoof Ziabetus; Clinical evaluation.

ix

TABLE OF CONTENTS

S.No. Contents Page No.

1. Introduction Page No. 1-6

2. Objectives Page No. 7-8

3. Review of Literature Page No. 9-71

4. Methodology Page No. 72-86

5. Results Page No. 87-118

6. Discussion Page No. 119-135

7. Conclusion Page No. 136-138

8. Summary Page No. 139-143

9. Bibliography Page No. 144-170

10. Annexures Page No. 171-192

x

LIST OF TABLES

S.No. Table No. Page No.

1. Table No.1 85

2. Table No.2 85

3. Table No.3 87

4. Table No.4A 89

5. Table No.4B 89

6. Table No.5A 91

7. Table No.5B 92

8. Table No.6A 94

9. Table No.6B 94

10. Table No.7A 96

11. Table No.7B 97

12. Table No.8A 99

13. Table No.8B 99

14. Table No.9A 102

15. Table No.9B 103

16. Table No.10A 107

17. Table No.10B 107







xi

LIST OF FIGURES

Figures Page No.

Photograph of Gurmar Booti 55

Photograph of Gilo Khushk 62

Photograph of Safoof Ziabetus and Placebo 82

Graph No.1 89

Graph No.2 89

Graph No.3 91

Graph No.4A 93

Graph No.4B 93

Graph No.5A 96

Graph No.5B 96

Graph No.6A 98

Graph No.6B 98

Graph No.7A 101

Graph No.7B 101

Graph No.8A 103

Graph No.8B 103

Graph No.9A 107

Graph No.9B 107

Graph No.10A 111

Graph No.10B 111

Graph No.11A 114

Graph No.11B 114

Graph No.12A 118

Graph No.12B 118

xii

DEDICATED TO

MY PARENTS

xiii

Introduction

INTRODUCTION

1

Introduction

INTRODUCTION

The term Ziabetus is a Greek word which means “to run through” or “Siphon”, is

characterized by hyperglycaemia, glycosuria, increased appetite, excessive thirst and

gradual loss of body weight. The concept of Ziabetus also exists in ancient world; it is

proved by the discovery of Ebers papyrus, written about 1550 BC. Ebers papyrus

contains descriptions of various diseases including a polyuric state resembling Ziabetus

Shakri. Although Buqrat “ The father of medicine” did not specifically mention

Ziabetus in his writings, but there are accounts in the Buqrat’s writings that are consistent

with the sign and symptoms of Ziabetus, like excessive urinary flow with wasting of the

body. After Buqrat, Arsyatoos (Aretaeus) was the first to use the term “Ziabetus” in

connection with this ailment, which means “to run through” or “Siphon” and provided the

accurate description of the symptoms of Ziabetus for the first time. After Arsyatoos,

Jalinoos described Ziabetus as a rare disease, and referred to the ailment as “Diarrhoea

Urinosa (Diarrhoea of Urine)”, and “Dipsakos (the thirsty disease)”. However, the

association of polyuria with a sweet tasting substance in the urine was first reported in

Sanskrit literature by Susruta, Charaka and Vaghbata (5th Century AD). They also

classified Ziabetus like condition into two: congenital and late onset, and described its

relationship with heredity, obesity, sedentary life and diet. During the same era, Chinese

and Japanese physicians also described the sweetness of urine and observed that people

with Ziabetus were prone to develop boils and an affliction which clinically resembles

tuberculosis. After that, during the Arabic era Ibne Sina described accurately the clinical

features of the disease and mentioned two specific complications of the disease, namely

2

Introduction

gangrene and the collapse of sexual function. No further progress was made in the

understanding of Ziabetus until the 16th century AD when Von Hohenheim (Paracelsus)

reported that urine of Diabetic patients contained an abnormal substance and concluded

that this substance was salt and that Diabetes was due to the deposition of salt in the

kidneys causing thirst of the kidney and polyuria. In 1674 AD Thomas Willis claimed

that Diabetes was primarily a disease of the blood and not the kidneys, he proposed that

the sweetness first appeared in the blood and was later found in the urine. Cullen was the

first person who distinguished Diabetes into two types. In this classification, we find first

time a distinction between Diabetes, with the urine of “the smell; colour and flavor of

honey,” and Diabetes, with limpid but not sweet urine. In 1798 AD John Rollo was the

first who use the adjective “ Mellitus” to distinguish the condition from other polyuric

diseases. In 1889 AD, Oskar Minkowski and Josef Von Mering established the role of

the pancreatic disorders in causing Diabetes. In June 1921 AD, the endocrine role of the

pancreas in metabolism and development of Diabetes was clarified by Banting and Best,

when they repeated the work of Von Mering and Minkowski, and went a step further and

isolated the hormone insulin from bovine Pancreas.

Now in present era due to resemblance in clinical features of the disease Ziabetus Shakri

has been correlated with Diabetes Mellitus, which is a chronic disorder of carbohydrate

metabolism and glucose intolerance. It is characterized by high blood glucose level and

glycosuria resulting from dysfunction of pancreatic β cells and insulin resistance. The

defective β cells result in lack of total or partial synthesis of insulin. Heredity, age,

obesity, diet, sex, sedentary life style, socio-economic status, hypertension and various

stresses are the common factors supposed to be involved in the aetiology of Diabetes

3

Introduction

Mellitus. Although Diabetes Mellitus is a disorder of carbohydrate metabolism, but in

long term it also affects metabolism of protein, lipids and electrolytes and results in the

development of Diabetic complications like blindness, renal failure, coronary artery

disease, gangrene of lower extremities, stupor, coma etc. Due to these dreadful

complications, Diabetes has become a global problem in spite of advances in modern

sciences. It is considered as one of the most common non-communicable disease,

globally. According to IDF, about 246 million people are affected with this disease all

over the world in 2007 and this number may increase to 380 million by 2025. Although

the prevalence rate of the disease varies from country to country. However, WHO has

been projected India as the country with the fastest growing population of Diabetes

patients. Depending upon its aetiology and treatment Diabetes Mellitus can be divided

into four types among them two are main i.e. Type 1 or Insulin Dependent Diabetes

Mellitus (IDDM) and Type 2 or Non-Insulin Dependent Diabetes Mellitus (NIDDM).

Type 2 Diabetes Mellitus accounts for over 85-95% of all Diabetic population and is

characterised by insulin resistance and / or abnormal insulin secretion. Depending upon

the nature of the disease, insulin and certain synthetic drugs like Glibenclamide,

Metformin, Gliclazide, Glimepiride, and Glipizide etc are widely used in its management.

Although the initial response of these drugs are usually good but long term use of oral

hypoglycaemic agents frequently loosing efficacy and results in development of "insulin

resistance" and side effects like Hypoglycaemic reactions, Agranulocytosis, Aplastic

anaemia and Haemolytic anaemia.

Owing to dreadful complications of Diabetes Mellitus and lack of safe and effective drug

for its management, it becomes a thrust area for research, in every field of medical

4

Introduction

science. The researchers of different systems of medicine are continuously concentrating

themselves for the development of safe and effective antidiabetic drugs. As far as the

Unani system of medicine is concerned, Ziabetus Shakri is being treated since Greco-

Arab period. Unani physicians claim to possess many safe and effective antidiabetic

agents for the management of Ziabetus Shakri. Therefore, it is one of the areas which

have to be given priority in scientific research in Tibbe Unani. Tibbe Unani possesses

large number of mufrad and murakkab drugs for the management of Ziabetus Shakri.

Many important and therapeutically effective murakkab drugs have been described to be

useful in Ziabetus Shakri in standard qarabadeen; they have not been evaluated

scientifically so far, for their described effect. Recently several herbal single drugs have

been experimentally and clinically evaluated and reported as good hypoglycaemic agents.

However, the scientific study of compound formulation is largely ignored by the

scientists and physicians despite the fact that a good number of compound drugs have

been described in Unani literature to be effective in Ziabetus condition as large number of

physicians of Unani medicine are using them successfully since long.

Safoof Ziabetus is one such drug described in various qarabadeen to be effective in

Ziabetus Shakri further inquiry with Unani physicians revealed that the drug is highly

effective and possess least chances of toxicity and side effects.

In view of the above a single blind placebo study was designed to investigate the

hypoglycaemic effect of Safoof Ziabetus in the patients of Ziabetus Shakri.

Safoof Ziabetus contains Gurmar booti (Gymnema Sylvestre) and Gilo khushk

(Tinospora Cordifolia) in 1:1 ratio, in the form of fine powder. The Powder was filled in

5

Introduction

capsules of 1gm capacity and 6 capsules was given 3 times a day orally with water,

15 minutes before breakfast, lunch, and dinner for 45 days. Total daily dose of Safoof

Ziabetus given to each patient was 18 gm in three divided doses. The study was

conducted at National Institute of Unani Medicine Hospital, Bangalore. After completion

of the trial, the data were analysed for the efficacy of drugs.

The study work includes the detailed Introduction, Description of Ziabetus Shakri

(Introduction of the Disease), History, Anatomy & Physiology of Pancreas, Definition,

Prevalence, Classification, Pathogenesis, Clinical features, Complications, Diagnostic

criteria and Management of Ziabetus Shakri in the light of literature available in Unani as

well as Modern system of Medicine. The study work also includes the literature review of

Unani drugs used for the treatment, the description of Material and Methods, Results,

Discussion, Summary, Conclusion of the clinical trial and Bibliography which has been

numbered consecutively in the order in which they are first mentioned in the text.

Proforma and Master Charts of study work are attached at the end of the dissertation.

Abbreviations details used in the dissertation are given under the heading of abbreviation.

6

Objectives

OBJECTIVES

7

Objectives

OBJECTIVES OF THE STUDY

To evaluate the effect of “SAFOOF ZIABETUS” in the management of

Ziabetus Shakri.

To validate the Unani claim for “SAFOOF ZIABETUS”.

To help in development of a safe and efficacious drug for Ziabetus Shakri.

8

Review of Literature (Classification)

CLASSIFICATION

According to Unani System of Medicine Ziabetus can be divided into two types:

(A) Ziabetus har or Shakri

(B) Ziabetus barid

This classification is based upon the nature of the disease (4, 7, 9, 12, 15, 20).

While on the other hand, in modern system of medicine, although all forms of Diabetes

Mellitus are characterized by hyperglycemia, the pathogenic mechanisms by which

hyperglycemia arises differ widely. Some forms of Diabetes Mellitus are characterized by

an absolute insulin deficiency or a genetic defect leading to defective insulin secretion,

whereas other forms share insulin resistance as their underlying etiology. Recent changes

in classification reflect an effort to classify Diabetes Mellitus on the basis of etiology.

Etiologic Classification Of Diabetes Mellitus

I. Type 1 Diabetes: Cell destruction, usually leading to absolute insulin deficiency

A. Immune mediated

B. Idiopathic

II. Type 2 Diabetes: May range from predominantly insulin resistance with relative

insulin deficiency to a predominantly secretory defect with insulin resistance.

35


III. Other Specific Types

A. Genetic Defects Of Cell Function

1. Chromosome 12, HNF-1 (MODY3) 2. Chromosome 7, glucokinase (MODY2)

3. Chromosome 20, HNF-4 (MODY1) 4. Chromosome 13, insulin promoter factor-1

(IPF-1; MODY4) 5. Chromosome 17, HNF-1 (MODY5) 6. Chromosome 2, NeuroD1

(MODY6) 7. Mitochondria DNA 8. Others

B. Genetic Defects In Insulin Action

1. Type A insulin resistance 2. Leprechaunism 3. Rabson-Mendenhall syndrome

4. Lipoatrophic Diabetes 5. Others

C. Diseases Of The Exocrine Pancreas

1. Pancreatitis 2. Trauma / pancreatectomy 3. Neoplasia 4. Cystic fibrosis

5. Hemochromatosis 6. Fibrocalculous pancreatopathy 7. Others

D. Endocrinopathies

1. Acromegaly 2. Cushing’s syndrome 3. Glucagonoma 4. Pheochromocytoma

5. Hyperthyroidism 6. Somatostatinoma 7. Aldosteronoma 8. Others.

E. Drug Or Chemical-Induced

1. Vacor 2. Pentamidine 3. Nicotinic acid 4. Glucocorticoids 5.Thyroid hormone

6. Diazoxide 7. Adrenergic agonists 8.Thiazides 9. Dilantin 10. Interferon 11. Others

F. Infections

1. Congenital rubella 2. Cytomegalovirus 3. Others

36


G. Uncommon Forms Of Immune-Mediated Diabetes

1. “Stiff-man” syndrome 2. Anti–insulin receptor antibodies 3. Others

H. Other Genetic Syndromes Sometimes Associated With Diabetes

1. Down’s syndrome 2. Klinefelter’s syndrome 3. Turner’s syndrome 4.Wolfram’s

syndrome 5. Friedreich’s ataxia 6. Huntington’s chorea 7. Laurence-Moon-Biedl

syndrome 8. Myotonic dystrophy 9. Porphyria 10. Prader-Willi syndrome 11. Others

IV. Gestational Diabetes Mellitus (GDM) (120)

37

Review of Literature (Clinical Features)

CLINICAL FEATURES OF ZIABETUS SHAKRI

In classical Unani literature it is described that, the disease Ziabetus always clinically

presents itself by:

1. Increased frequency of Micturition with excessive thirst and dryness of mouth.

2. Ants and flies are attracted on urine. (Due to presence sugar).

3. Patients feel heat in the back around the waist (In case of abnormal hot

temperament of kidney).

4. Dryness all over the body (Due to shortage of fluid in body)

(1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 20, 104)

While according to modern system of medicine, Type 2 Diabetes Mellitus develops

slowly. Many people have Type 2 Diabetes for several years before the condition is

diagnosed, often through routine screening tests. Typically, the earliest symptoms are

increased thirst and frequent urination. That's because excess glucose circulating in

body draws water from tissues, making patients dehydrated. To quench thirst, patients

drink more water and other beverages which lead to more frequent urination.

Other Signs And Symptoms Of Type-2 Diabetes Mellitus Include:

Flu-like symptoms: Sugar is an important fuel. When it doesn't reach to body cells,

patients feel tired and weak.

Weight fluctuations: Because body is trying to compensate for lost fluids and sugar,

patients eat more than usual and gain weight which causes body cells to become more

43

Review of Literature (Clinical Features)

resistant to the action of insulin. But the opposite also can occur. Patients may eat more

than normal but still lose weight because muscle tissues don't get enough glucose to

generate growth and energy.

Blurred vision: High levels of blood sugar pull fluid from body tissues, including the

lenses of eyes. This affects your ability to focus. In some cases, Diabetes can lead to

blindness.

Slow-healing of sores or Frequent infections: Diabetes affects body's ability to heal

and fight infection. Bladder and vaginal infections can be a particular problem for

women.

Nerve damage (Neuropathy): Excess sugar in blood can damage the small blood

vessels to nerves. Patients may feel tingling and loss of sensation in hands and feet, as

well as burning pain in arms, hands, legs and feet.

Red, swollen, tender gums: Diabetes increases the risk of infection in gums and in the

bones that hold teeth in place. (21,109,171)

44

Review of Literature (Complications)

COMPLICATIONS OF ZIABETUS SHAKRI

In Ziabetus as the vicious cycle of large intake of fluid and frequent urination

developed, it affects almost all body parts. First, it weakened the liver due to which there

is deficiency of fluid and nutrition to all body parts which initially results in generalized

weakness, but with the passage of time it results in development of generalized wasting

and dryness all over the body (1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,21,104).

According To Modern Literature Complications Of Diabetes Mellitus Can Be

Divided Into Two Types:

Acute complications

Chronic complications

(1) Acute Complications

(A) Diabetic ketoacidosis.

(B) Nonketotic hyperosmolar coma.

(C) Hypoglycemia.

(D) Amputation

(2) Chronic Complications.

(A) Microvascular diseases

(a) Diabetic retinopathy

Severe vision loss .

Blindness.

45

http://en.wikipedia.org/wiki/Diabetic_retinopathy

http://en.wikipedia.org/wiki/Vision_loss

Review of Literature (Complications)

(b) Diabetic neuropathy

Abnormal sensation

Decreased sensation.

Diabetic foot .

(c) Diabetic nephropathy

Chronic renal failure.

(B) Macrovascular disease

(a) Atherosclerosis

(b) Coronary artery disease, leading to myocardial infarction or angina .

(c) Stroke (mainly ischemic type)

(d) Peripheral vascular disease, which contributes to intermittent claudication

(exertion-related foot pain) as well as diabetic foot.

(e) Diabetic myonecrosis

(f) Diabetic foot often due to a combination of neuropathy and arterial disease.

(21, 109, 172)

46

http://en.wikipedia.org/wiki/Diabetic_neuropathy

http://en.wikipedia.org/wiki/Diabetic_foot

http://en.wikipedia.org/wiki/Diabetic_nephropathy

http://en.wikipedia.org/wiki/Atherosclerosis

http://en.wikipedia.org/wiki/Coronary_artery_disease

http://en.wikipedia.org/wiki/Myocardial_infarction

http://en.wikipedia.org/wiki/Angina

http://en.wikipedia.org/wiki/Stroke

http://en.wikipedia.org/wiki/Peripheral_artery_occlusive_disease

http://en.wikipedia.org/wiki/Intermittent_claudication

http://en.wikipedia.org/wiki/Diabetic_myonecrosis

Review of Literature (Definition)

ZIABETUS SHAKRI (DIABETES MELLITUS)

In classical literature of Unani Medicine, Diabetes is described under the heading

of Ziabetus.It is defined by various Unani philosophers as following:

1. Ziabetus is a disease in which patient excretes water as such through urinary passage

soon after its intake, as that of food without digestion from the stomach and intestine

like in “Zalaqul -ama”. (1, 2, 5, 10, 13)

2. Ziabetus is a disease in which patient excretes water in the form of urine soon after its

intake, but there is no incontinence of urine as found in Salesul-baul. (3, 6, 14, 15, 16)

3. Ziabetus is a disease in which patient always feel thirst and when he drinks water,

excrete it out through urine soon after its intake.(4, 7, 8, 9, 11, 12, 17, 18, 19, 20, 104)

Now, after discovery of Insulin the concept of disease is totally changed. In modern

literature it is defined as:

4. Diabetes Mellitus is a chronic, hereditary disease characterized by an abnormally high

level of glucose in the blood and the excretion of sugar in urine. The basic defect is an

absolute or relative lack of insulin which leads to abnormalities of metabolism, not

only of carbohydrate but also of protein and fat. (105)

5. Diabetes Mellitus is a disorder in which the level of blood glucose is persistently raised

above the normal range. (106)

6. Diabetes Mellitus is a syndrome with metabolic, vascular and neuropathic components

that are interrelated. The metabolic syndrome is characterized by alterations in

28


carbohydrate, fat and protein metabolism secondary to absent or markedly diminished

insulin secretion and / or ineffective insulin action. The vascular syndrome consists of

abnormalities in both large vessels (Macroangiopathy) and small vessels

(Microangiopathy).The Macroangiopathic changes cause cerebrovascular accidents,

myocardial infarction and peripheral vascular disease. Although these large vessel

sequelae occur in people without Diabetes, but in Diabetic patients they appear earlier

and are more severe. The clinical expressions of the microangiopathic changes are

Diabetic retinopathy and nephropathy. (107)

7. Diabetes Mellitus is a disease of excess glucose in the plasma, Qualitative

abnormalities of carbohydrate and lipid metabolism, characteristic pathologic changes

in the nerves and small blood vessels and intensification of atherosclerosis. (108)

8. Diabetes Mellitus is a clinical syndrome characterized by hyperglycaemia due to

absolute or relative deficiency of insulin. Lack of insulin whether absolute or relative

affects the metabolism of carbohydrate, protein, fat, water and electrolytes. Chronic

hyperglycaemia leads to complications of Diabetes and affects most characteristically

the eye, the kidney, the nervous system, the cardiovascular system and others such as

intercurrent infections, Diabetic foot ulcers. (109)

9. Diabetes Mellitus is characterized by hyperglycaemia and other metabolic

derangements that are caused by inadequate action of insulin on body tissues, either

because of reduced circulating levels of insulin or resistance of target tissues to its

actions. (110)

29


10. The term Diabetes Mellitus describes a metabolic disorder of multiple aetiology

characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and

protein metabolism resulting from defects in insulin secretion, insulin action, or both.

The effects of Diabetes Mellitus include long term damage, dysfunction and failure

of various organs. Diabetes Mellitus may present with characteristic symptoms such

as thirst, polyuria, blurring of vision, and weight loss. In its most severe forms,

Ketoacidosis or a nonketotic hyperosmolar state may develop and lead to stupor,

coma and, in absence of effective treatment, death. Often symptoms are not severe,

or may be absent, and consequently hyperglycaemia sufficient to cause pathological

and functional changes may be present for a long time before the diagnosis is made.

The long term effects of Diabetes Mellitus include progressive development of the

specific complications of retinopathy with potential blindness, nephropathy that may

lead to renal failure, and / or neuropathy with risk of foot ulcers, amputation, Charcot

joints, and features of autonomic dysfunction, including sexual dysfunction. People

with Diabetes are at increased risk of cardiovascular, peripheral vascular and

cerebrovascular disease. Several pathogenetic processes are involved in the

development of Diabetes. These include processes which destroy the beta cells of the

pancreas with consequent insulin deficiency, and others that result in resistance to

insulin action. The abnormalities of carbohydrate, fat and protein metabolism are due

to deficient action of insulin on target tissues resulting from insensitivity or lack of

insulin. (111)

30


11. Diabetes mellitus is a metabolic cum-vascular syndrome of multiple aetiologies

characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat, and

protein metabolism resulting from defects in insulin secretion, insulin action or both. This

disorder is frequently associated with long term damage, which can lead to failure of

organs like eyes, kidneys, nerves, heart, and blood vessels. (112, 113, 22)

31

Review of Literature (Introduction of the Disease)

REVIEW OF LITERATURE

9


INTRODUCTION OF THE DISEASE

The term Ziabetus is a Greek word which means “to run through” or “Siphon”, is

characterized by hyperglycaemia, glycosuria, increased appetite, excessive thirst and

gradual loss of body weight. Dayasqoomas (1,2,3,4), Qaramees (1,3,4), Dawwarah

(1,2,4,5,6,7,8,9),Dolab (1,2, 3,4,5, 6, 7,8,9,10, 11, ,12), Zalaq-ul-kuliya (1,2, 3,4, 6, 7, 8,

9,11,12),Salesul-baul (5,6,9,12), Istisqae anmas (5,6,12),Barkarya (3,4,5,6,7), Moattasa

(5,7) and Attasa (12) are the synonyms commonly used for Ziabetus in Unani System of

Medicine. In Ziabetus, the patient excretes water as such through urinary passage soon

after its intake. The ratio of fluid taken and the urinary output remains the same (Zalqul

majari) as that of solid without digestion from the stomach and intestine, a condition

known in Unani medicine as 'Zalqul-ama'. There is excessive thirst more intake of water

and its rapid discharge as urine. The patient also experiences a feeling of heat in the back

around the waist and in the right side of the body. When the disease takes the body

completely in its grip dryness will develop all over the body rendering it weak.

There are four major causes described in most of the classical Unani literature,

responsible for the development of Ziabetus:

1. Sue mizaj har kuliya (Abnormal hot temperament of kidney).

(1,2,3,4,5,6,7,8,10,11,13,14,15,16,17,18,19)

2. Zoufe-kuliya (Weakness of kidney). (1,2,5,7,8,11)

3. Majari ka kushada ho jana (Dilatation of renal vessels). (1,2,5,7,8,11)

4. Sue mizaj barid of tamam badan / kuliya / jigar (Abnormal cold temperament of

body / kidney / liver). (1,2,3,4,5,6,7,8,10,11,14,15,17,18)

10


Among all above mentioned causes, most emphasis was given to abnormal hot

temperament of kidney by most of the eminent Unani physicians during the

description of Ziabetus. They also described that weakness of kidney and dilatation of

renal vessels occurs due to abnormal hot temperament of kidney. (1, 2, 5, 6, 7, 8, 10,

11, 13, 18)

Ziabetus Can Be Divided Into Two Types:

(A) Ziabetus har and (B) Ziabetus barid

(A) Ziabetus har: In this disease the patient feels very much thirst and passes white

coloured urine frequently and the urine contains sugar. In fact it is the Diabetes in

true sense. The excretion of sugar renders the body weak, the muscles degenerated

and become lean and thin and the general health is run down. (4, 7, 9, 12, 15, 20)

(B) Ziabetus barid: In this condition the patient feels acute thirst and passes white

coloured urine in large quantity but does not contain sugar. This type of Ziabetus can

be matched with Diabetes Insipidus. (4, 7, 9, 12, 15, 20)

Nowadays the accepted concept of Diabetes mellitus is that, it is a chronic

disorder of carbohydrate metabolism and glucose intolerance, characterized by high

blood glucose level and glycosuria resulting from dysfunction of pancreatic β cells and

insulin resistance. The defective β cells result in lack of total or partial synthesis of

insulin. Chronic hyperglycaemia also affects metabolism of protein and lipids. (21)

11


There are four types of Diabetes Mellitus depending upon its aetiology and

treatment among them two are main: Type-1 or Insulin Dependent Diabetes Mellitus

(IDDM) and Type-2 or Non-Insulin Dependent Diabetes Mellitus (NIDDM).

Type-1 Diabetes Mellitus: Type-1 Diabetes (formerly known as Insulin-Dependent

Diabetes, childhood Diabetes, or juvenile-onset Diabetes) is most commonly diagnosed

in children and adolescents, but can occur in adults, as well. It is characterized by β-cell

destruction, which usually leads to an absolute deficiency of insulin. Most cases of Type-

1 Diabetes are immune-mediated characterized by autoimmune destruction of the β-cells

in the Islets of Langerhans of the pancreas, destroying them or damaging them

sufficiently to reduce insulin production. However, some forms of Type-1 Diabetes are

characterized by loss of the β-cells without evidence of autoimmunity. (22)

Type -2 Diabetes Mellitus: This form of Diabetes, previously referred to as Non-Insulin

Dependent Diabetes, Type-2 Diabetes, or adult-onset Diabetes, is a term used for

individuals who have insulin resistance and usually have relative (rather than absolute)

insulin deficiency (23, 24, 25, 26). At least initially, and often throughout their lifetime,

these individuals do not need insulin treatment to survive. The specific aetiologies of

this form of Diabetes are not known, but many factors like heredity, age, obesity, diet,

sex, sedentary life style, socio economic status, hypertension and various stresses are

supposed to be involved in the aetiology of Diabetes Mellitus. Most patients of Type-2

Diabetes Mellitus are obese, and obesity itself causes some degree of insulin resistance

(27, 28). Patients who are not obese by traditional weight criteria may have an increased

percentage of body fat distributed predominantly in the abdominal region (29).

Ketoacidosis seldom occurs spontaneously in this type of Diabetes; when seen, it usually

12

http://en.wikipedia.org/wiki/Autoimmune_disorder

http://en.wikipedia.org/wiki/Islets_of_Langerhans

http://en.wikipedia.org/wiki/Pancreas


arises in association with the stress of another illness such as infection (30, 31, 32). This

form of Diabetes frequently goes undiagnosed for many years because the

hyperglycaemia develops gradually and at earlier stages is often not severe enough for

the patient to notice any of the classic symptoms of Diabetes (33, 34, 35). Nevertheless,

such patients are at increased risk of developing macro-vascular and micro-vascular

complications (35, 36, 37, 38, 39). Whereas patients with this form of Diabetes may have

insulin levels that appear normal or elevated, the higher blood glucose levels in these

Diabetic patients would be expected to result in even higher insulin values had their beta-

cell function been normal (40). Thus, insulin secretion is defective in these patients and

insufficient to compensate for the insulin resistance. The risk of developing this form of

Diabetes increases with age, obesity, and lack of physical activity (34, 41). It occurs

more frequently in women with prior GDM (Gestational Diabetes Mellitus) and in

individuals with hypertension or dyslipidemia, and its frequency varies in different

racial/ethnic subgroups (34, 35, 41). It is often associated with a strong genetic

predisposition, more so than is the autoimmune form of Type-1 Diabetes (42, 43).

However, the genetics of this form of Diabetes are complex and not clearly defined.

Classically, the age of onset of Type-2 Diabetes is above 40 years. However in

Indians it has been found to be a decade earlier than in the west. Occasional patients

might develop Type-2 Diabetes in the second decade of life. Obesity is not a common

feature in Type-2 Diabetes in India. Only about 50% of cases have a BMI > 25 kg / m2

while, 15-20 % of the patients are underweight. (21)

13

Review of Literature (Diagnostic Criteria)

DIAGNOSTIC CRITERIA

Revised criteria for diagnosing Diabetes Mellitus (Ziabetus Shakri) have been

issued by consensus panel of experts from the National Diabetes data group and the

world health organization. The revised criteria reflect new epidemiologic and metabolic

evidence and are based on the following premises:

1. The spectrum of fasting plasma glucose and the response to an oral glucose load varies

in normal individuals.

2. Diabetes Mellitus defined as the level of glycaemia at which Diabetes specific

complications are noted and not on the level of glucose tolerance from population based

viewpoint.

In the new diagnostic criteria the oral glucose tolerance test which was previously

recommended by the National Diabetes Data group has been replaced with the

recommendation that the diagnosis of Diabetes Mellitus be based on:

Two consecutive readings of fasting plasma glucose levels of 126 mg/dl

(7.0 mmol/L) or higher.

Other options for diagnosis include:

Two consecutive readings of casual plasma glucose concentration

(Random) 200 mg /dl (11.1 mmol / L) or higher with symptoms of

Diabetes i.e. polyuria, polydipsia or unexplained weight loss. Casual is

defined as any time of day without regard to time since last meal.

47

Review of Literature (Diagnostic Criteria)

Or

Finding of two consecutive readings of two hour post prandial plasma

glucose readings > 200 mg /dl during an oral glucose tolerance test.

Fasting plasma glucose is selected as the primary diagnostic test because it predicts

adverse outcomes (e.g. retinopathy) as well as the two hour post prandial blood glucose

test. But fasting plasma glucose is much more reproducible than oral glucose tolerance

test or the Random blood glucose test and easier to perform in a clinical setting.

Criteria For Testing For Diabetes Mellitus In Asymptomatic Undiagnosed Individuals:

1. Testing for Diabetes should be considered in all individuals at age 45 years and

above and, if normal, it should be repeated at 3 years intervals.

2. Testing should be considered at a young age or be carried out more frequently in

individuals who are

Obese ( > 120% desirable body weight or a BMI > 27 kg /m2 )

Habitually physically inactive.

Have a first degree relative with Diabetes.

Members of a high risk ethnic population.

Have delivered a baby weighing >9 lb (i.e.> 4.032 kg) or Have been diagnosed

with Gestational Diabetes Mellitus.

Hypertensive (BP > 140/90 mm Hg).

Have a HDL cholesterol level < 35 mg /dl (0.90 mmol /L) and / or a triglyceride

level > 250 mg /dl (2.82 mmol/L).

On previous testing, had Impaired Glucose Tolerance or Impaired Fasting

Glucose. ( 21, 22, 173)

48

Review of Literature (Gurmar Booti)

GURMAR BOOTI (GYMNEMA SYLVESTRE R.Br.)

55


GURMAR BOOTI (GYMNEMA SYLVESTRE R.Br.)

1. Unani Name Gurmar booti (174, 175, 176, 177, 178)

2. Botanical Name Gymnema sylvestre R.Br. (176, 177, 178, 179, 180, 181, 182)

3. Family Asclepiadaceae (176, 177, 178, 179, 180, 181, 182)

4. Vernaculars

Bengali ..........Mera-singi, Chhota-dudhilata.

English.......... Gymnema sylvestre, Periploca of the woods.

Gujrati...........Dhuleti, Mardashingi.

Hindi.............Gur-mar, Merasingi.

Kannada ........Sannagerasehambu.

Marathi..........Kavali, Kalikardori, Vakundi.

Sanskrit..........Meshashringi ( Ram’s horn ), Madhu nashini,

Sarpadarushtrika.

Tamil .............Adigam, Cherukurinja.

Telagu............Padapatri.

Unani.............Gurmar booti. (174, 175, 177, 179, 180, 181, 182)

56


5. Introduction

The description of Gurmar booti is not found in the classical text

books of Unani Medicine written by eminent scholars of Arab. However, Najmul Ghani

described this drug in his book “Khazainul Advia” with Indian reference. Gymnema

sylvestre is a shrubby climbing plant called Meshasringi, “ram’s horn” in Sanskrit, and

Gurmar booti in Hindi and Unani. It has been used for more than thousands of years in

India to treat Diabetes. Sushruta describes Gymnema sylvestre as a destroyer of

Madhumeha (Glycosuria) and other urinary disorders. On account of its property of

abolishing the taste of sugar it has been given the name of “Gurmar” meaning “sugar

destroying” and it is believed therefore, that it might neutralize the excess of sugar

present in the body of Diabetic patient. Its root also has been reported as a remedy for

snake bite for this purpose the powdered root being applied to the part bitten, and a

decoction given internally. In modern literature Gymnema sylvestre or Gurmar is first

described by Roxburgh under the name of “Asclepias geminate”, but he did not describe

anything about its medicinal properties. After Roxburgh, Mr.Edgeworth, noticed that on

chewing its leaves, it destroys the power of the tongue to appreciate the taste of sugar and

all saccharine substances. This property is later proved in 1887 AD by Dr. Hooper, who

says “After chewing one or two leaves it was proved undoubtedly that sugar had no taste

immediately afterwards”. But now it is a well established fact that this effect does not last

for 24 hours as stated, but for only one or two hours, after that time the tongue resumes

its appreciation of sweet taste. (177, 181, 182)

57


6. Habitat: Woody climber found in central and southern India, on the Western Ghats,

in the Goa territory, and in the tropical Africa (177, 178, 180, 181, 182).

7. Morphology:

A large woody much branched climber running over the tops of high

trees; young stems and branches pubescent, often densely so, terete. Leaves are 3.2-5.0

cm by 1.3-3.2 cm ,ovate, elliptic, or ovate-lanceolate, acute or shortly acuminate; upper

surface dark green, shining, under surface pale green, more or less pubescent on both

sides; venation transverse and reticulate with a marginal vein; petioles 6-13 mm long ,

pubescent. Flowers in pedunculate or nearly sessile cymes; peduncles densely pubescent,

shorter than the petioles and arising from between them, sometimes producing successive

umbels or whorls of flowers; pedicels 3-13 mm long, pubescent; bracts minute, ovate-

oblong, hairy ciliate. Calyx pubescent, divided to the base or nearly so; segments 2mm

long, oblong, obtuse, ciliolate. Corolla yellow,4-5 mm across; tube campanulate,1.5 mm

long, about equalling the lobes; lobes thick, ovate-deltoid, speading, recurved, glabrous;

corona of 5 processes inserted on the corolla-tube, alternate with its lobes, free at the

short deltoid subacute tip which protrudes above the sinus, the lower adnate portion

decurrent, channelled and with strongly ciliate margins. Style apex thick,

subhemispherical, much exserted beyond the anthers, pearly white. Follicles 6.3-7.5 by

0.8 cm, terete, rigid. Lanceolate, attenuated into a beak, glabrous, one follicle often

suppressed. Seeds 1.3 cm long, narrowly ovoid-oblong, flat, with a thin broad marginal

wing, brown, glabrous. The taste of plant is bitter, acrid. According to Unani literature

58


Gurmar booti is a shrubby climbing plant having dense branches. Its leaves are 4-5 inches

long and resembles with the leaves of Eagle Marmelos. On chewing leaves are bitter.

(174, 175, 177, 178, 179, 180, 182)

8. Parts Used: Leaves, Stem, Root. (174, 175, 176, 177, 178, 179, 180, 182)

9. Temperament:

Hot and Dry in second degree. (174, 175, 178)

10. Actions:

In Unani Literature : Muqawwie Meda (Stomachic), Qate Munashshiyat

( Anti-narcotic), Antidiabetic, Tiryaq (Antidote), Mulayyan

(Demulcent), Muharrike-Qalb wa Dorane-khoon (Stimulant to

Heart and Blood Circulation). (174, 175, 176, 177, 178)

In Modern Literature: Stomachic, Stimulant, Laxative, Diuretic, Astringent, Tonic,

Antiperiodic, Cooling, Alterative, Anthelmintic, Alexiteric,

Emetic, Expectorant .(179, 180, 181)

11. Uses:

It is commonly used as a remedy for Diabetes Mellitus and glycosuria. Its root

has long been used as a remedy for snake bite, its powder being dusted upon the wound,

or made into paste with water and applied and a decoction given internally. Leaves when

chewed paralyse the sense of taste for sweet and bitter substances for some time. A

59


decoction of leaves is useful for fever and cough. Leaves triturated and mixed with castor

oil are applied to swollen glands and to enlargement of internal viscera as the liver and

spleen. A mixture of leaves and black pepper is given for cholera. Leaves are also useful

in eye complaints, cures opacities of the lens, cornea, and vitreous body. It is also useful

in heart diseases, piles, leucoderma, inflammations, burning sensation, biliousness,

bronchitis, asthma, ulcers and used to relieve irritation in plague. (174, 175, 176, 177,

178, 179, 180, 181)

12. Phytochemical Studies:

The leaves contain hentriacontane, pentatriacontane, a-and ß-chlorophylls, phytin, resins,

tartaric acid, formic acid, butyric acid, anthraqui-none derivatives, inositol, d -quercitol

and "gymnemic acid". The leaves give positive tests for alkaloids. Flavonol glycosides,

kaempferol and quercetin have been isolated from the aerial parts of the plant (183).

Three new oleanane-type triterpene glycosides were isolated from the leaves of the plant.

Six oleanane-type saponins (184, 185). Few new tritepenoid saponins, gymnemasins A,

B, C and D were also isolated from the leaves of Gymnema sylvestre. (186, 187)

13. Important Formulations: Qurs Ziabetus khas, Qurs Ziabetus. (178,188)

14. Muzir : Non-toxic (177)

15. Musleh : Not mentioned in books

16. Badal : Not mentioned in books

17. Dose : 4-6 gms (177, 178)

60


18. Scientific Studies:

The hypoglycaemic action of Gymnema leaves was first documented in the late

1920s by Mhasker and caius (189). This action is attributed to members of a family of

substances called gymnemic acids (190, 191). According to research in healthy

volunteers, Gymnema leaves raise insulin levels (192, 193, 194). Based on animal

studies, this may be due to regeneration of the cells in the pancreas that secrete insulin

(195, 196, 197, 198) or by stimulation of β cell function and increasing the flow of

insulin from these cells (199, 200). Other animal researches shows that Gymnema can

also reduce glucose absorption from the intestine (201, 202), improve uptake of glucose

into cells, and prevent adrenal hormones from stimulating the liver to produce glucose,

thereby reducing blood sugar levels and increasing glucose tolerance (203, 204, 205, 206,

207, 208 ).Other animal studies have shown that extracts of Gymnema leaves can lower

serum cholesterol and triglycerides and prevent weight gain (209, 210, 211, 212, 213).

When placed directly on the tongue, gurmarin, another constituent of the leaves, and

gymnemic acid have been shown to block the ability in humans to taste sweets (214,215).

A preliminary trial in a group of type 1 and type 2 diabetics have shown promising results

with a dose of 800 mg per day of an extract standardized for 25 % gymnemic acid. (216)

61

http://www.purecaps.com/healthnotes.asp?org=pureencaps&ContentID=1399002

Review of Literature (History)

HISTORY

Ziabetus is known since the age of antiquity, where symptoms of Ziabetus were

described. It is commonly believed that the history of medicine began with the Greeks,

and before the time of Buqrat (460 BC), Ancient Egypt (Misri) was the first civilization

known to have an extensive study of medicine and to have left behind written records of

its practices and procedures. It is proved by the discovery of the Ebers papyrus in the

graves of thabes by famous German Egyptologist Georg Ebers in 1862 AD. The Ebers

papyrus is one of the most famous document relating to the ancient practice of medicine,

written about 1550 BC. Ebers papyrus contains descriptions of various diseases including

a polyuric state resembling Ziabetus shakri (44,45,46). Although the Unani physician

Buqrat (460 BC) “The father of medicine” did not specifically mentioned Ziabetus in his

writings, there are accounts in the Buqrat’s writings that are consistent with the sign and

symptoms of Ziabetus, like excessive urinary flow with wasting of the body (46).

Arsyatoos ( Aretaeus ) and Jalinoos (Galen) were followers of Buqrat. Arsyatoos ( 81-

138 AD ) provided the first accurate description of the symptoms of Ziabetus. He was the

first who use the term “Ziabetus” in connection with this ailment,which means “to run

through” or “Siphon”. He described the disease as “Ziabetus is a dreadful affliction, not

very frequently among men, being a melting down of the flesh and limbs into urine”

(45,47,48,49,50). Jalinoos (131-201 AD), a contemporary of Arsyatoos, the most

influential medical writer of all time,discussed Ziabetus in a number of his books. He

described the condition as rare, as he had only seen two cases, he referred to the ailment

as “Diarrhoea Urinosa ( Diarrhoea of urine )” and “dipsakos ( the thirsty disease)”

14


(45,46,51). However, the association of polyuria with a sweet tasting substance in the

urine was first reported in Sanskrit literature dating from the 5th - 6th century AD at the

time of Susruta, Charaka and Vaghbata. They described the urine of polyuric patients

as having the taste like honey, being sticky to touch and strongly attracting the ants. The

Indian description of that time also contains Ziabetus like conditions of two types:

congenital and late onset. Also, the Indians noticed the relation of Ziabetus to heredity,

obesity, sedentary life and diet. During the same era, Chinese and Japanese physicians

also described Ziabetus and the sweetness of urine of Ziabetus patients, which apparently

attracted dogs. They also observed that people with Ziabetus were prone to develop boils

and an affliction which clinically resembles tuberculosis (45,46,52). During the 9th -11th

centuries AD, Arabic medicine was at its peak of achievements and Arabian physicians

translated the works of Buqrat and Jalinoos and enriched them with latest knowledge of

that era. Two prominent physicians of this era who contributed to the knowledge of

Ziabetus were Shaikh-Ul-Rais Bu Ali Ibne Sina (960-1037 AD) and Musa Bin

Maimoon ( 1135 AD). Ibne Sina described accurately the clinical features of the disease

and mentioned two specific complications of the disease,namely gangrene and the

collapse of sexual function. While on the other hand Musa Bin Maimoon claimed to have

seen more than 20 cases. He proposed that Ziabetus was caused by the sweet water of

river nile and the prevailing heat that spreads over the kidneys (45,46). No further

progress was made in the understanding of Ziabetus until the 16th century AD. When the

swiss physician Von Hohenheim ( Paracelsus ) reported that urine of Ziabetus (Diabetic)

patients contained an abnormal substance which remained as a white powder after

evaporation, he concluded that this substance was salt and that Diabetes was due to the

15


deposition of salt in the kidneys causing thirst of the kidney and polyuria (45). The

modern history of Diabetes began with the Thomas Willi’s ( 1621-1675 AD )

observations of Diabetes in 1674 AD and Matthew Dobson’s experiments in 1776 AD

that conclusively established the diagnosis of Diabetes in the presence of sugar in the

urine and blood. Diabetes was no longer considered a rare ailment. Thomas Willis

referred to Diabetes as the “Pissing evil” and noted that in patients with Diabetes, “The

urine was wonderfully sweet, as if it were imbued with honey or sugar”. He claimed that

Diabetes was primarily a disease of the blood and not the kidneys. Willis proposed that

the sweetness first appeared in the blood and was later found in the urine. During the

same era Thomas Sydenham ( 1624-1689 AD ) speculated that Diabetes was a systemic

disease arising in the blood where “Chyle” was incompletely digested and its non-

absorbed residue had to be excreted. After Thomas Sydenham, Johann Conrada

Brunner ( 1653-1727 AD ) came very close to discovering pancreatic Diabetes when he

observed in 1682 AD that, After the incomplete removal of the pancreas from a dog,

“…..the animal made water very frequently and that he was very thirsty, drinking largely

of water in proportion to the discharge of urine” (45,46,53,54,55,56,57). Cullen was the

first person who distinguished Diabetes into two types. In this classification, we find first

time a distinction between Diabetes, with the urine of “the smell; colour and flavor of

honey,” and Diabetes, with limpid but not sweet urine (46). The concept of Thomas

Sydenham was further elaborated by Matthew Dobson (1735-1784 AD), who provided

experimental evidence that people with Diabetes pass sugar in their urine. He gently

heated two quarts of urine to dryness. The remaining residue was a whitish cake,which

Dobson wrote “ was granulated and broke easily between the fingers; it smelled sweet

16


like brown sugar, neither could it be distinguished from sugar, except that the sweetness

left a slight sense of coolness on the palate”. Moreover he concluded that this substance

had previously existed in the serum rather than being formed in the kidneys. He wrote

“this idea of the disease explains its emaciating effects from so large a proportion of the

alimentary matter being drawn off by the kidneys, before it is perfectly assimilated and

applied to the purpose of nutrition (58). In 1788 AD Thomas Cawley described that

Diabetes may follow damage to the pancreas, such as through calculus formation (59).

Twenty years after the Matthew Dobson, in 1797 AD Matthew Baillie stated that “upon

examination of the kidneys……it seemed probable that Diabetes depends, in a

considerable degree, upon a deranged action of the secretory structure of the kidneys, by

which the blood there is disposed to new combinations” the effect of which is the

production of “a saccharine matter”. He also proposed that “the chyle may be so

imperfectly formed, as to make the blood be more readily changed into a saccharine

matter, by the action of the kidneys” (60). In 1798 AD, a year after the Matthew Baillie,

“John Rollo” a surgeon, expressed his opinion that “ the Diabetes Mellitus” is a disease

of the stomach and its immediate cause is a morbid condition of stomach evolving from

vegetable substances containing saccharine matter, which is quickly separated as a

foreign body by the kidney”(61). Further he was the first who use the adjective

“Mellitus” to distinguish the condition from other polyuric diseases in which glycosuria

was absent and urine was tasteless. Rollo made other contributions to the study of

Diabetes,including descriptions of “cataract due to Diabetes” and odour of acetone on the

breath of some Diabetes patients (62). In 1815 AD, Michel Eugene Chevreul (1786-1889

AD) published his experimental findings on urine and stated that sweet substance found

17


in urine of Diabetes patients was to be identical to grape sugar (63). In 1839 AD, John

Elliotson speaks about “grief”, “chills” and, “excess of venery” as possible etiological

factors for Diabetes in his “Principles and practice of medicine” (64). In the first half of

the 19th century Claude Bernard (1813-1878 AD) discovered that the liver releases a

substance that affects blood sugar levels. In 1875 AD, he isolated a starch like substance

that he called “Glycogen”, which was the precursor of glucose, “the internal secretion” of

the liver. This observation established the liver’s role as a vital organ in Diabetes. He also

demonstrated that the central nervous system was involved in controlling the blood

glucose concentration. He also performed many systematic experiments on the pancreas

(46, 65, 66, 67). During mid 19th century AD, William Prout (1785-1859 AD) described

“exposure to cold”, “attacks of rheumatism and gout”, “The drinking of cold fluids while

heated”, and “mental anxiety and distress” as the most frequent exciting causes of

Diabetes. He was the first, who recognized the coma as a complication of Diabetes (68).

Further in 1869 AD, H.D.Noyes, observed that a form of “retinitis” developed in

glycosuric patients (45), during the same year, Paul Langrhans ( 1847-1888 AD) had

noticed small clusters of ductless cells in teased preparations of pancreas, he simply

described these structures without speculating as to their possible function. It was only in

1893 AD that Edouard Laguesse (1861-1927 AD ) suggested that these clumps of cells

,which he named the “islets of langerhans” in honour of langerhans and suggested that

they might constitute the endocrine tissue of the pancreas (45,46,69,70). In 1874 AD,

Prof.A.Kussmaul (1822-1902 AD) described the “air hunger” of ketoacidosis (71). In

1875 AD, Dickinson published a paper “Diabetes, in his diseases of the kidneys”, in

which he defined Diabetes as “a disease of the nervous system characterized by the

18


secretion of saccharine containing urine” (72). In 1877 AD, Etienne Lancereaux (1829-

1910 AD) demonstrated a causal relationship between Diabetes and lesions of the

pancreas (73), and his friend, Apollinaire Bauchardat (1806-1886 AD), began the

modern therapy of Diabetes by limiting carbohydrates in the diet, advocating fast days,

and using exercise to help control glycosuria (74). In 1889 AD, Oskar Minkowski (1858-

1931 AD) and Josef Von Mering (1849-1908 AD) demonstrated conclusively that

removal of the pancreas from a dog results in the development of fatal Diabetes. This

observation firmly established the role of the pancreatic disorders in causing Diabetes

(75,76,77). Further in 1901 AD, Eugene Undsay Opie’s ( 1873-1962 AD ) pathologic

study on Diabetes Mellitus established that Diabetes is caused by a lesion of the pancreas,

and the lesion is of such kind in which the islands of langerhans are destroyed or injured

(78). In 1908 AD, Georg L.Zuelzer (1870-1949 AD) and Nicolas Paulesco ( 1869-1931

AD ) had prepared potent pancreatic extract before 1921 AD. In 1909 AD, Jean De

Meyer gave the name “ insulin” derived from the latin word insula ( insula=island ), to

the glucose lowering hormone, whose existence at that time was still hypothetical , which

he postulated was produced by the islet tissue (79). Further Moses Barron ( 1883 AD)

give conclusion regarding the relationship of islets of langerhans to Diabetes “…..that the

islets secrete a hormone directly into the lymph or blood streams (Internal

secretion),which has a controlling power over carbohydrate metabolism” (80). The

finding of Moses Barron triggered the investigations of Frederick Grant Banting (1891-

1941 AD) and Charles Herbert Best (1899 AD). In December 1921 AD, they got success

in isolation of insulin and published the results of their research on “The internal

secretion of the pancreas” in which they were able to demonstrate the reversal of the

19


metabolic changes of Diabetes by injection of a potent extract of the pancreatic islands

(81,82,83). On 11th Jan 1922 AD, the first patient of Diabetes a 14 year old boy named

Leonard Thombson was treated with insulin (54, 84). In 1923 AD Eli Lilly begins

commercial production of insulin, and called it "Isletin Insulin." In 1925 AD Home

testing for sugar in the urine through Benedict’s solution was introduced. In 1927 AD an

oral medication called "horment" or "glukohorment" was developed as a replacement for

insulin, but side effects are unacceptable and very soon dropped out. In 1930s AD Insulin

was further refined to Protamine zinc insulin, a long-acting insulin that provide more

flexibility. In 1936 AD Himsworth divided Diabetics into two types based on "insulin

sensitivity." In 1940's AD neutral protamine Hagedorn insulin was introduced and the

connection was established between Diabetes and long-term complications of kidney and

eye diseases. In late 1940's AD Helen Free developed the "dip-and-read" urine test

(Clinistix) allowing instant monitoring of blood glucose levels. In 1951 AD Lawrence

and Bornstein measured the amount of insulin in the blood and noted that older and

obese patients with Diabetes have insulin, but those who were young have none. In 1955

AD Oral drugs that help lower blood glucose levels was introduced. In 1959 AD, Two

major types of diabetes are recognized: Type 1 (Insulin-Dependent) Diabetes and Type 2

(Non-Insulin-Dependent) Diabetes. During the1959-1960 AD Yallow and Berson

developed the radioimmunological assay (RIA) procedure, to measure insulin with much

greater precision than earlier techniques, for that Yallow received the Nobel Prize in 1977

AD. In 1964 AD, The first strips for testing blood glucose were used. In1970 AD, First

blood glucose meter (Ames) and Insulin pumps were introduced. During the same year

Laser therapy was used to slow down or prevent blindness due to Diabetes. In1973 AD,

20


U-100 insulin is introduced. In 1976 AD, the glycosylated haemoglobin (A1C) test was

introduced as a monitor of glycaemic control. The manufacturing of insulin changed

dramatically with the advent of DNA technology that allows synthesis of a genetically

engineered "human" type of insulin, and in 1978 AD, production of the first recombinant

DNA insulin was announced. In 1979 AD, Type 1 and Type 2 Diabetes are formally

recognized by the American Diabetes Association. Type 1 is also called Insulin

Dependent Diabetes Mellitus (IDDM), and Type 2 is called Non Insulin Dependent

Diabetes Mellitus (NIDDM). In 1983 AD, the first biosynthetic human insulin, and

"Reflolux", later known as "Accu-Chek"(allows blood glucose self-monitoring) was

introduced .In 1996 AD, the FDA approved the first recombinant DNA human insulin

analogue, lispro (Humalog). In 2001 AD, FDA approved Cygnus' first-generation model

of the GlucoWatch Biographer for use by adults - the first frequent, automatic and non-

invasive glucose monitor. In 2003 AD, the names Insulin Dependent Diabetes Mellitus

(IDDM) for Type 1 and Non Insulin Dependent Diabetes Mellitus (NIDDM) for Type 2

diabetes are formally dropped. Today Researchers are working on an insulin patch and

inhaled insulin, Genetic engineering is being used to manipulate cells so they secrete

insulin. A sensor-computer-pump system that mimics the insulin response of the normal

pancreas is being developed to function as an "artificial pancreas". Apart from these,

various researches are still going on, to explore new aspects of Diabetes and its

management. (85, 86, 87, 88, 89, 90, 91, 92)

21

Review of Literature (Management)

MANAGEMENT OF ZIABETUS SHAKRI (DIABETES MELLITUS)

The goals of management in people with Ziabetus Shakri (Diabetes Mellitus) are:

To normalise the elevated blood sugar level.

Relief from Diabetic symptoms and improvement in quality of life.

Prevention of acute complications.

Prevention of microvascular complications like retinopathy, neuropathy and

nephropathy.

Prevention of macrovascular complications like cardiovascular, cerebrovascular

and peripheral vascular disease.

Prevention of infections.

Therefore the complete treatment of people with Diabetes Mellitus requires

advocating a healthy life style, Diabetes education with focus on proper balanced diet and

increased physical activity to attain and maintain desired body weight. Also meticulous

attention is to be given to achieve normoglycaemia, control of hypertension and

management of dyslipidemia with the help of Diet, Exercise, Oral hypoglycaemic agents

and insulin.

49


1. Diabetes Education:

Diabetes education means empowering Diabetic patients with knowledge of Diabetes

and providing tools crucial for making them active partners in the Diabetes management,

these includes :

In depth information about Diabetes, its complications and treatment. Appropriate

self care skills.

Appropriate resources for self care.

A positive attitude.

Self monitoring skills.

2. Diet:

The aims of dietary management are to achieve and maintain ideal body weight,

euglycaemia and desirable lipid profile, prevent and postpone complications related to

Diabetes The dietary recommendations should be individualized according to person’s

ethnicity, cultural and family background, and personal preferences and associated co-

morbid conditions. It should be flexible in variety and preparation of food choices and

timing of meals according to person’s daily routine.

Dietary Recommendations:

A. Total Calorie Intake. The calorie requirements of Diabetic person depend on

physical activity and nutritional status as in a normal individual, unless there is

50


glycosuria. Individual with > 120% of ideal weight is considered overweight and <

90% of ideal weight is underweight.

The ideal body weight (IBW) is calculated by formula:

IBW= (height in cm – 100) x 0.9

The caloric intake of person with Diabetes should be altered gradually, preferably not

more than 500 Kcal per day.

B. Total Calorie Distribution:

(i) Carbohydrate (55-60% of total calorie requirement):

Avoid sugar, honey, jaggery and sweets.

Restrict processed refined foods like maida-based products.

Main source should be cereals, mixed coarse grains, whole pulses, salads and

soybeans.

Roots and tubers should be used sparingly.

(ii) Protein (10-15% of total calorie requirement):

Protein from vegetable sources, low fat milk and milk products, fish and lean meat is

preferable.

(iii) Fat (20-25% of total calorie requirement):

Saturated fat - <7% of total caloric intake (including ghee and butter).

51


Rest should be in from of MUFA and PUFA.

Trans-fatty acid (hydrogenated vegetable oils) should be avoided.

Dietary cholesterol should be minimal and in any case should not exceed 300mg

per day.

Use more than one edible oil.

Oils containing linoleic acid only such as ground nut, sesame, cotton seed, rice

bran and safflower should be used along with oils containing a-linoleic acid such

as soyabean, mustard, canola etc.

(iv) Fibers: Traditional Indian diet is rich in fibers. Fiber rich foods include whole

grains (ragi, jowhar, barley, oats etc.), whole pulses, soybean, green leafy vegetables and

fenugreek seeds.

(v) Fruits: Whole fruits are recommended in moderation (1-2 servings), however, very

sweet fruits and fruit juices should be avoided.

(vi) Common salt: Up to 6gm/day is permitted. Restrict pickles, papad, chatni and salty

processed foods

(vii) Alcohol: Alcohol intake is best avoided and if used, must be in moderation. It may

exacerbate, neuropathy, dyslipidemia, obesity and may worsen the control of Diabetes.

(viii) Artificial sweeteners: Use of artificial sweeteners in limited quantity is acceptable

but they are to be avoided during pregnancy and lactation.

(ix) Tobacco: Smoking and the use of tobacco in any form should be prohibited.

52


C. Dietary Modifications In Special Situations

(i) Nephropathy: Dietary protein should be restricted to 0.6 gm/kg, and salt to 4 gm/day.

(ii) Hypertension: Dietary salt should be restricted to minimum.

(iii) Dyslipidemia: Total fat intake should be curtailed and diet to be modified by

increasing MUFA and dietary fibers by reducing saturated fatty acids.

(iv) Infections and acute illness: In such conditions, fasting should be avoided and

adequate caloric intake must be ensured.

3. Physical Activity

Regular physical activity is an essential component of management in persons

with Type 2 Diabetes. A careful assessment of an individual should be made by physician

while incorporating an exercise program in the management. Exercise programme should

be individualized according to individual capacity and disabilities. Exercise must be done

regularly such as brisk walk for 30 - 60 minutes or its equivalent physical activity. The

best form of exercise recommended to a Diabetic is a stepwise increase of aerobic

exercises. There are several benefits from a regular exercise schedule. These include

improvement in insulin sensitivity, reduction of hypertension, reduction in weight,

improvement in lipid profile (reduces serum triglycerides and increases HDL particularly

HDL2 cholesterol), improvement in cardiovascular function, increase in bone density,

improvement in the sense of physical and mental well being and improvement in quality

of life.

53


Precautions During Exercise

Person with Diabetes and coronary artery disease should be prescribed

appropriate exercises after cardiac evaluation.

In proliferative Diabetic retinopathy, strenuous activity like diving, weight lifting

or bending may precipitate vitreous haemorrhage or retinal detachment. Walking

may be continued.

Person with Diabetes and overt nephropathy often have reduced capacity to

exercise.

Peripheral neuropathy results in loss of protective sensation in the feet. It is

advised to wear proper footwear. The person with Diabetes should be taught to

monitor for blisters and other damages to the feet before and after exercise.

Autonomic neuropathy may limit an individual's exercise capacity and increase

the risk of adverse cardiovascular events during exercise.

4. Oral Hypoglycemic Agents:

Oral hypoglycemic agents should be used in Type-2 Diabetes Mellitus in the

event of failure of diet and exercise. In Unani system of medicine certain drugs like Qurs

Dolabi, Safoof Tabasheer, Qurs Ziabetus, Qurs Nashkoor, Qurs Ziabetus khas, Safoof

Ziabetus are used, while in modern system of medicine various types of Oral

hypoglycemic agents are used like Tolbutamide, Glibenclamide, Glipizide, Metformin,

Phenformin etc. (112)

54

Review of Literature (Pancreas)

PANCREAS

The pancreas is a retroperitoneal gland, it is about 12 to 15 cm long and 2.5 cm

thick lies posterior to the greater curvature of the stomach. The pancreas consists of a

head, a body, and a tail and is connected to the duodenum by two ducts. Pancreatic

secretions pass from the secretory cells (Exocrine cells) in the pancreas into small ducts

that ultimately unite to form two large ducts that drain the secretions into the small

intestine. The larger of the two ducts is called the pancreatic duct (Duct of Wirsung). In

most people, the pancreatic duct joins the common bile duct from the liver and gall

bladder and enters the duodenum as a common duct called the Hepatopancreatic ampulla

(Ampulla of Vater). The smaller of the two ducts, the accessory duct (Duct of Santorini),

leads from the pancreas and empties into the duodenum about 2.5 cm superior to the

Hepatopancreatic ampulla. The pancreas is supplied by the pancreatic branches of the

splenic artery and pancreaticoduodenal arteries, and the venous drainage of pancreas is

via the pancreaticoduodenal veins which end up in the portal vein.

Histologically, the pancreas is composed of small clusters of glandular epithelial cells,

about 99 % of which are arranged in clusters called acini and constitute the exocrine

portion of the organ. The cells within acini secrete a mixture of fluid and digestive

enzymes called pancreatic juice. Remaining 1 % of the cells scattered amongst the acini

are the endocrine cells of the pancreas, in groups called the islets of Langerhans ,

arranged in clusters and cords and are crisscrossed by a dense network of capillaries. The

capillaries of the islets are lined by layers of endocrine cells, which are in direct contact

22

http://en.wikipedia.org/wiki/Islets_of_Langerhans


with blood vessels, by either cytoplasmic processes or by direct apposition. Islets of

Langerhans are composed of different kinds of cells:

Insulin-producing beta cells (50-80% of the islet cells).

Glucagon-releasing alpha cells (15-20%).

Somatostatin-producing delta cells (3-10%).

Pancreatic polypeptide-containing PP cells .

These cells are related with the regulation of blood glucose level. The levels of glucose in

the blood are monitored or regulated by different hormones liberated from these cells

with the help of negative feedback mechanism, to maintain the homeostasis. The most

important among them is insulin. Insulin is the “hormone of plenty”—it is released when

glucose is abundant and performs some important functions in the body.

Functions Of Insulin

In body it stimulates:

a) Muscle and fat cells to remove glucose from the blood

b) Body cells to breakdown glucose, releasing its energy in the form of ATP (via

glycolysis and the citric acid cycle)

c) The liver and muscles to store glucose as glycogen (short-term energy reserve)

d) Adipose tissues to store glucose as fat (long-term energy reserve) and inhibit fat

breakdown.

e) Cells to use glucose in protein synthesis.

23

http://en.wikipedia.org/wiki/Insulin

http://en.wikipedia.org/wiki/Beta_cell

http://en.wikipedia.org/wiki/Glucagon

http://en.wikipedia.org/wiki/Alpha_cell

http://en.wikipedia.org/wiki/Somatostatin

http://en.wikipedia.org/wiki/Delta_cell

http://en.wikipedia.org/wiki/Polypeptide

http://en.wikipedia.org/wiki/PP_cell


Glucagon is the main hormone opposing the action of insulin and is released when food

is scarce. Glucagon triggers glycogen breakdown, which releases energy (a catabolic

effect), and also helps the body to switch to using resources other than glucose, such as

fat and protein, whereas insulin triggers the formation of glycogen (an energy-requiring

process, or an anabolic effect). Blood glucose level varies according to the body needs

and is regulated by hormones within a narrow range i.e. from 70 to 140 mg/dl. The blood

glucose level can rise because of diet, breakdown of glycogen, or through hepatic

synthesis of glucose. Eating produces a rise in blood glucose, the extent of which depends

on a number of factors such as the amount and the type of carbohydrate eaten (i.e. the

glycemic index), the rate of digestion, and the rate of absorption. Because glucose is a

polar molecule, its absorption across the hydrophobic gut wall requires specialized

glucose transporters (GLUTS of which there are five types GLUTS 1, GLUTS 2, GLUTS

3, GLUTS 4, GLUTS 5). In the gut, GLUT2 and GLUT5 are the most common.

The liver is a major producer of glucose—it releases glucose from the breakdown of

glycogen and also synthesizes glucose from intermediates of carbohydrate, protein, and

fat metabolism. The liver is also a major consumer of glucose and can buffer glucose

levels. It receives glucose-rich blood directly from the digestive tract via the portal vein,

and quickly removes large amounts of glucose from the circulation so that even after a

meal, the blood glucose levels rarely rise above 140 mg/dl in a non-diabetic. On the other

hand the rise in blood glucose following a meal is detected by the pancreatic beta cells,

which respond by releasing insulin. Insulin increases the uptake and use of glucose by

tissues such as skeletal muscles and fat cells. This rise in glucose also inhibits the release

of Glucagon, inhibiting the production of glucose from other sources, e.g., glycogen

24


break down. Once when the glucose enters inside the cells, some of the glucose is used

immediately via glycolysis. This is a central pathway of carbohydrate metabolism

because it occurs in all cells in the body and because sugar can be converted into glucose

and enters this pathway. During the well-fed state, the high levels of insulin and low

levels of Glucagon stimulate glycolysis, which releases energy and produces

carbohydrate intermediates that can be used in other metabolic pathways. The liver and

muscles take up any glucose that is not used immediately where it can be converted into

glycogen (glycogenesis). Insulin stimulates glycogenesis in the liver by:

a) Stimulating hepatic glycogen synthetase (the enzyme that catalyzes glycogen

synthesis in the liver).

b) Inhibiting hepatic glycogen phosphorylase (the enzyme that catalyzes glycogen

breakdown in the liver).

c) Inhibiting glucose synthesis from other sources (inhibits gluconeogenesis).

On the other hand Insulin also encourages glycogen formation in muscles, through a

different method. In muscles, it increases the number of glucose transporters (GLUT4) on

the cell surface. This leads to a rapid uptake of glucose that is converted into muscle

glycogen. When glycogen stores are fully replenished, excess glucose is converted into

fat by a process called lipogenesis. Glucose is converted into fatty acids that are stored as

triglycerides (three fatty acid molecules attached to one glycerol molecule) for storage.

Insulin promotes lipogenesis by:

a) Increasing the number of glucose transporters (GLUT4) expressed on the surface

of the fat cells, causing a rapid uptake of glucose.

25


b) Increasing lipoprotein lipase activity, this frees up more fatty acids for triglyceride

synthesis.

In addition to promoting fat synthesis, insulin also inhibits fat breakdown by inhibiting

hormone sensitive lipase (an enzyme that breaks down fat stores). As a result, there are

lower levels of fatty acids in the blood stream. Insulin also has an anabolic effect on

protein metabolism. It stimulates the entry of amino acids into cells and stimulates

protein production from amino acids. While during fasting blood sugar level fall and

inhibits insulin secretion and stimulates Glucagon release. Glucagon opposes many

actions of insulin. Most importantly, Glucagon raises blood sugar levels by stimulating

the mobilization of glycogen stores in the liver, providing a rapid burst of glucose. In 10–

18 hours, the glycogen stores are depleted, and if fasting continues, Glucagon continues

to stimulate glucose production by favoring the hepatic uptake of amino acids and

glycerol. In addition to low blood glucose levels, many other stimuli stimulate Glucagon

release including eating a protein-rich meal (the presence of amino acids in the stomach

stimulates the release of both insulin and Glucagon, Glucagon prevents hypoglycemia

that could result from unopposed insulin) and stress (the body anticipates an increased

glucose demand in times of stress).The metabolism of fatty acids (from adipose tissue) is

a major source of energy for organs such as the liver. Fatty acids are broken down to

acetyl-CoA, which is channeled into the citric acid cycle and generates ATP. As

starvation continues, the levels of acetyl-CoA increase until the oxidative capacity of the

citric acid cycle is exceeded. The liver processes these excess fatty acids into ketone

bodies (3-hydroxybutyrate) to be used by many tissues as an energy source. The most

important organ that relies on ketone production is the brain because it is unable to

26


metabolize fatty acids. During the first few days of starvation, the brain uses glucose as a

fuel. If starvation continues for more than two weeks, the level of circulating ketone

bodies is high enough to be used by the brain. This slows down the need for glucose

production from amino acid skeletons, thus slowing down the loss of essential proteins.

(93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103)

27

Review of Literature (Pathogenesis)

PATHOGENESIS OF ZIABETUS SHAKRI

Pathogenesis Of Ziabetus Shakri (Diabetes Mellitus) In Unani System Of Medicine

In Unani system of medicine, ancient Philosophers explained the pathogenesis of

Ziabetus Shakri (Diabetes Mellitus) logically and rationally. The mainstay of Ziabetus is

the development of abnormal hot temperament in the kidney. This altered hot

temperament renders the renal vessels paralyzed and hence dilated. The morbid hot

temperament disturbs the normal functioning of kidney and reduces the Quwwate Masika

(Retentive power) of kidney. In contrast to the reduced retentive power, the morbid hot

temperament, on the other hand increases the Quwwate Jazba (Absorptive power) of

kidney. The excessive thrust of Quwwate Jazba pulls and absorbs the excessively large

amount of water from the liver but as unable to digest and retain the fluid due to weak

Quwwate Masika and strengthen Quwwate Dafia, the fluid ultimately passes out towards

the urinary bladder and finally in the form of urine large amount of fluid excreted. The

deficit of fluid thus created in the liver is compensated by excessive absorption of fluid

from the Urooqe Masariqa (Mesenteric vessels). The Urooqe Masariqa absorbs the fluid

from stomach, and stomach demands plentiful fluid from outside in form of excessive

thirst. The concatenation of this demand and supply thus established between the organs,

produces a vicious cycle resulting in large intake of fluid as due to thirst and thereof

excessive and frequent urination.(1, 2, 5, 6, 7, 8, 10, 11, 13, 18)

38


Pathogenesis Of Diabetes Mellitus Type 2 In Modern System Of Medicine

Type-2 Diabetes Mellitus known as maturity onset type of Diabetes till 1979 AD

and non insulin dependent Diabetes thereafter, it accounts for 85 to 95 % of all patients

with Diabetes mellitus. Pathogenesis of this primary form of Diabetes Mellitus is

complex and varied. The disorder evolves slowly in course of several years with a

prolonged subclinical phase. Two distinct factors that work in tandem for the evolution

and progress of the disorder are:

A. Insulin secretory dysfunction i.e. failure of pancreatic β cells to release as much

insulin as required for metabolic control under the prevailing situation “relative

insulin deficiency”.

B. Impaired insulin action manifest as decreased insulin sensitivity of the target cells

i.e. “insulin resistance”.

Both insulin secretory function and sensitivity to insulin action are modulated by

hereditary and environmental factors. (21)

1. Insulin Secretory Dysfunction: Impaired insulin secretion is a uniform finding

in Type-2 Diabetic patients and the development of beta cell dysfunction has been well

characterized in diverse ethnic populations (121, 122, 123, 124, 125, 126, 127, 128, 129,

130, 131, 132). Early in the natural history of type-2 Diabetes Mellitus, insulin resistance

with loss or reduction of Ist phase and prolongation of 2nd phase of insulin secretion is

well established (121, 122, 127, 129, 130, 131, 133, 134, 135, 136, 137), but glucose

tolerance remains normal because of a compensatory increase in insulin secretion (121,

122, 125, 126, 127, 129, 130, 131, 134, 135, 136, 138, 139, 140). Within the normal

39


glucose tolerant population, approximately 20-25 % of individuals are severely resistant

to the action of insulin (141). However, insulin secretion in these insulin resistant Non-

Diabetic individuals is increased in proportion to the severity of insulin resistance and

glucose tolerance remains normal (141). As the fasting plasma glucose concentration

rises from 80 to 140 mg /dl, the fasting plasma insulin concentration increases

progressively, up to two to three fold above that in normal glucose tolerant subjects. The

progressive rise in fasting plasma insulin level is an adaptive response of the pancreas to

maintain normal glucose homeostasis. However, when the fasting plasma glucose

concentration rises above 140 mg/dl, it causes glucotoxicity to β cells and affects insulin

gene transcription, leading to decreased insulin synthesis and secretion (122, 123, 126,

127, 136, 142, 143). Hyperglycaemia and hypoinsulinaemia causes lipotoxicity to β cells

by increasing plasma free fatty acid (FFA) levels which make situation worse, because

prolonged exposure of β cells to elevated plasma FFA levels leads to further inhibition of

insulin secretion. Increased fatty acyl CoA levels within the β cells also impair beta cell

function and causes apoptosis of beta cells (144, 145, 146). Apart from gluco-

lipotoxicity, some other factors contribute to beta cell dysfunction and leads to impaired

insulin secretion like Incretin deficiency and / or incretin resistance (147,148,149,150)

and hyper secretion of amylin (151). Apart from these acquired causes some genetic

factors are also implicated in inducing defect in β cell function. Monogenic mutations

leading to defects in insulin secretion have been documented in five types of maturity

onset type of Diabetes in the young (MODY) and two clusters with mitochondrial DNA

mutation thus for such patients may account for 1 % of Non-insulin dependent Diabetes

40


among the Caucasians. Specification of genetic loci in the rest still continues to remain as

nightmare for geneticists. (21)

2. Impaired Insulin Action Or Insulin Resistance: Insulin resistance implies decreased

peripheral uptake of glucose as well as inadequate suppression of hepatic glucose

production and lipolysis in response to insulin. Relatively high levels of insulin at fasting

and in response to secretogogues are indicative of insulin resistance. Insulin resistance is

well known in obesity (21), because obesity is an extremely important diabetogenic

influence and not surprisingly, approximately 80 % of Type-2 Diabetes Mellitus patients

are obese. (152)

Seats Of Insulin Resistance

A. Muscle: Skeletal muscles and adipose tissues required insulin for optimal glucose

uptake and utilization. In Type-2 Diabetes Mellitus, entry of glucose into myocytes

occurs only through mass action as available insulin fails to recruit more GLUT 4 for

facilitated transport of glucose across the cell membrane, and result in reduction of

glucose uptake. Further insulin mediated augmentation of glucose utilization is impaired

in muscles of patients with Type-2 Diabetes Mellitus. Late increase in the contents of

triglycerides in skeletal muscles has been implicated to induce insulin resistance in the

muscles. (21)

B. Liver: In Type-2 Diabetes Mellitus restraining effects of insulin in hepatic glucose

production (HGP) is impaired and leads to increase HGP during post absorptive and

fasting states.(21)

41


C. Adipose Tissue: Free fatty acids are stored as triglycerides in adipocytes and serve as

an important energy source during conditions of fasting. Insulin is a potent inhibitor of

lipolysis and restrains the release of FFA from the adipocytes by inhibiting the enzyme

hormone sensitive lipase. In Type-2 Diabetics the ability of insulin to inhibit lipolysis and

reduce the plasma FFA concentration is markedly reduced. Prolonged elevation of

plasma FFA concentration leads to insulin resistance in muscles and liver thus impair

insulin secretion. (121, 122, 153, 154, 155, 156, 157, 158, 159, 160, 161)

Cellular Mechanism Of Insulin Resistance: The stimulation of glucose metabolism by

insulin requires that the hormone must first bind to specific receptors that are present on

the cell surface of all insulin target tissues. After insulin has bound to and activated its

receptor “second messengers” are generated which initiate a series of events that

eventually result in the stimulation of intracellular glucose metabolism under the control

of insulin (121, 162, 163, 164, 165, 166, 167, 168). In Type-2 Diabetes Mellitus insulin

binding to target tissue is reduced due to decreased number of receptors without change

in insulin receptor affinity. In addition to the decreased number of cell surface receptors,

a variety of defects in insulin receptor internalization and processing also occurred.

(169,170)

42

Review of Literature (Prevalence)

PREVALENCE

Ziabetus (Diabetes) is now one of the most common non-communicable diseases

globally. It is a silent killer that kills one person every 10 seconds, and worldwide it kills

about 3.2 million every year. At least one in ten deaths among adults between 35-64 years

old is attributable to Diabetes (114). Further it is the fourth or fifth leading cause of death

in most developed countries and there is substantial evidence that it is epidemic in many

developing and newly industrialized nations (115, 116). Diabetes Mellitus is certain to be

one of the most challenging health problems in the 21st century (115, 116). Type 2

Diabetes Mellitus constitutes about 85 to 95% of all Diabetes in developed countries

(117), and accounts for an even higher percentage in developing countries. Type 2

Diabetes Mellitus is now a common and serious global health problem, which, for most

countries, has evolved in association with rapid cultural and social changes, ageing

populations, increasing urbanization, dietary changes, reduced physical activity and other

unhealthy lifestyle and behavioral patterns. (117)

Diabetes Status In 2003, 2007 And 2025 (115,116)

All diabetes 2003 2007 2025

Total world population (billions) 6.3 6.6 7.9

Adult population (billions) (20-79 years) 3.8 4.1 5.2

Number of people with diabetes (millions) (20-79 years)

194 246 380

World diabetes prevalence (%) (20-79 years) 5.1 6.0 7.3

Number of people with diabetes in India (millions) 35.5 40.9 69.9

32


Current Prevalence:

It is estimated that currently (2007) some 246 million people worldwide, or 6.0% in the

adult population, have diabetes and that this will increase to 380 million, or 7.3%, by

2025. The Western pacific region with 67 million and the European region with 53

million will have the highest number of people with Diabetes in 2007. However, in terms

of prevalence, it is the Eastern Mediterranean and Middle East region which has the

highest rate (9.2%) followed by the North American region (8.4%). (115, 116, 117)

By 2025 the Diabetic prevalence of the South and Central American region is expected to

be nearly as high (9.3%) as that of North America region (9.7%). The Western Pacific

region will continue to have the highest number of people with Diabetes, with some 100

million, representing an almost 50 % increase from 2007. (115, 116)

Age Distribution

The 40-59 year age group currently has the highest number of persons of Diabetes with

some 113 million (46 % of total world Diabetic population), of which more than 70 %

live in developing countries. (115, 116, 118)

Gender distribution

The estimates for both 2003 and 2025 showed a female predominance in the number of

persons with diabetes. The female numbers were about 10% higher than for males. (115)

33


Urban/Rural distribution

In 2003, the number of people with diabetes in urban areas was 78 million, compared to

44 million persons with diabetes in rural areas. By 2025, it is expected that this

discrepancy will increase to 182 million urban and 61 million rural persons with diabetes.

In India prevalence of diabetes in urban population is 5.9 % and in rural population it is

2.7 %. ( 115, 119)

34

Review of Literature (Gilo Khushk)

GILO KHUSHK (TINOSPORA CORDIFOLIA)

62


GILO KHUSHK (TINOSPORA CORDIFOLIA)

1. Unani Name : Gilo Khushk (174, 175, 217, 218, 219, 220, 221)

2. Botanical Name : Tinospora cordifolia (181, 182, 219, 220, 222, 223, 224)

3. Family : Menispermaceae (181, 182, 219, 222, 223, 224)

4. Vernaculars:

Arabic ……….......Jilo

Bengali………......Gadancha, Giloe, Gulancha, Guluncha, Nimgilo.

Ceylon……….......Chintil

China……….........K'uan Chu Hsing

French……….. .....Culancha

Goa………….........Amritvel, Amrityel

Gujarati……… ....Gado, Galo, Gulo, Gulwel

Hindi……….........Giloe, Gulancha, Gulbel, Gurach, Gurcha

Kannada…….......Amrytaballi, Madhuparne, Uganiballi

Malayalam…….....Amrytu, Peyamrytam, Sjttamrytu

Marathi……….....Ambarvel, Gharol, Giroli, Gulavela, Gulaveli, Guloe, Gulvel.

Nepal………….....Garjo

63


Persian……… .....Gulbel.

Punjab…………...Batindu, Garham, Garum, Gilo, Gilogularich, Zakhmihaiyat

Sanskrit………..... Amrita, Amritalata, Amritavallari, Amritavalli, Bhishaka-priya,

Chakralakshana,Chakrangi,Chandrahasa,Chandrapasa, Chchinna,

Chehinnaruha.

Sikkim……….......Gurjo

Tamil……….........Amridavalli, Amudam, Asasi, Kaippuchindil, Kunali.

Telugu……….......Duyutige, Guduchi, Iruluchi, Jivantika, Madhuka, Manapala,

Somida.

Uriya………….....Gulancha, Gulochi.

Unani ……............Gilo (174, 175, 181, 182, 217, 220, 221, 222, 223, 224)

5. Introduction:

A large, glabrous, deciduous climbing shrub found throughout tropical

India known as “Gilo” in Unani, and Guduchi in Sanskrit. In ancient era it is commonly

used as a Dafe Nobat (Antiperiodic) in fevers, and as a Muqawwi (Tonic) and Moaddil

(Alterative); it is also credited with Muqawwie Bah (Aphrodisiac) properties. The fresh

plant is said to be more efficient than the dry; it is taken with milk in Wajaul Mafasil

(Rheumatism), Hurqate Baul (Acidity of urine) and Sue Hazm (Dyspepsia). Its juice with

64


honey and pakhanbed is useful in Suzak (Gonorrhoea). In Gujarat, a necklace called

Kamala-ni-mala (Jaundice necklace) is made of small pieces of the stem, and is

supposed to cure that disease. The stem, if placed upon a bush in the open air, will retain

its vitality through the hot season, and when the rains commences, put forth leaves and

long whipcord-like roots, which soon reach the ground. A starch like substance is

prepared from its dry stem known as Sat Gilo. Tinospora cordifolia first time attracted the

Europeans during the early part of 19th century, by those who have tried it as a tonic,

antiperiodic and diuretic. Now at present it is an official part of Pharmacopoeia of India.

(174, 175, 181, 182, 220, 221, 222, 223, 224)

6. Habitat: Throughout tropical India, Ceylon and Burma. (181, 182, 220, 222, 223, 224)

7. Morphology

A woody climber, with perennial stems reaching 2 inches in diameter, with

a thick, soft, warted bark, the younger branches succulent with the bark smooth, giving

out adventitious roots sometimes many yards in length and excessively slender, which

lengthen downwards and at last reach the soil. Leaves alternate, on long flexuous

petioles, spreading, and 2—4 inches long, roundish-ovate, entire, cordate at the base,

acute at the apex, quite smooth, thin, somewhat glaucous beneath and resembles with the

betel leaves. Flowers dicecious, pedicellate, inconspicuous, yellow, in short, axillary,

long-stalked racemes, the male in small fascicles, the female solitary, bracts minute.

Male flowers :—Sepals 6 in two rows of 3- each, the outer short, roundish, the inner

twice as long, broadly obovate, concave, smooth; petals 6, opposite the sepals, and about

65


half the length of the inner ones, clawed below, somewhat 3-lobed above, with the lateral

lobes involute, stamens 6, longer than the petals, immediately in front of which they stand

and by which they are partially enwrapped, filaments much thickened at the end, anther-

cells oblong, widely separated below; no rudiment of carpels.

Female flowers :—Sepals as in the male ; petals oblong-spathulate ;stamens reduced to

small oblong scales in front of the petals; carpeis 3, distinct, opposite the outer sepals,

elevated on a thick gynophobe, ovary oblong-ovoid, smooth, style short, thick, stigma

dilated, tongue-shaped, laciniate.

Fruit of 3 (or more usually less by abortion) shortly stalked, subglobose drupes, with

an apiculus on one side marking the position of the style, about as large as a pea, red,

pulp scanty, putamen thin, bony, convex outside, with a deep, large, hollow process

extending to the middle of the fruit on the ventral surface, making the cavity horse-shoe-

shaped. Seed similar in form to the cavity which it fills, embryo enclosed in the copious

endosperm which is ruminated on the hollow, ventral surface, radicle rounded, superior,

cotyledons leafy, ovate, veined, very divaricated.(174,175,182,217,219,220,222,223,224)

8. Parts Used: Stem, Root and Leaves. (174,175,181,182,217,220,221,222,223,224)

9. Temperament: Hot and dry in first degree (Dry)

Hot and wet in first degree (fresh)

According to Sharif khan Murakkabul- quwa. (174,175,218,219,221)

66


10. Actions :

In Unani: Muqawwi (Tonic), Dafe Humma (Antipyretic), Dafe Nobat

(Antiperiodic), Muqawwie Meda (Stomachic), Katile Kirme

Shikam (Anthelmintic), Musaffie Khoon (Blood purifier),Mudire

Baul (Diuretic), Munaffise Balgham (Expectorant), Muqawwie

Bah (Aphrodisiac), Mushtahi (Appetiser), Dafe qae (Anti-emetic)

(174, 175, 217, 219, 220, 221).

In Modern: Anti-inflammatory, Adaptogenic, Antineoplastic, Antioxidant,

Hepatoprotective, Immunomodulator, Analgesic, Antispasmodic,

Hypoglycaemic. (181, 182, 222, 223, 224)

11. Uses:

• The stem is bitter stomachic, stimulates bile secretion, causes constipation, tonic,

and diuretic, enriches the blood, and cures jaundice, useful in skin diseases.

• The juice is useful in diabetes, vaginal and urethral discharges, Mild fevers and

enlarged spleen.

• Starch obtained from the roots and stems of plant known as Sate Gilo used in

chronic diarrhea and some form of chronic dysentery. But it is also a valuable

nutrient when there is intestinal irritability and inability to digest any kind of food.

In case of acid diarrhea due to acidity of the intestinal canal or acid dyspepsia. It

is also useful in relieving the symptoms of rheumatism.

67


• Freshly prepared juice from the green plant is a powerful diuretic so given to cure

urinary tract infections and gonorrhea. For Gonorrhea it is also given with

pakhanbed and honey.

• The root and stem of T. Cordifolia are prescribed in combination with other drugs

as an antidote to snake bite and scorpion sting. The juice and decoction of the root

are applied to the part bitten, poured frequently into the eyes and administered

internally by mouth at intervals of half an hour.

• The root is a powerful emetic and used for visceral obstructions and its watery

extract is used in leprosy.

• A decoction of Gilo leaves is used for the treatment of gout, and young leaves,

bruised in milk, are used as a liniment in erysipelas. The leaves are beaten with

honey and used for ulcers.

• Dried and powdered fruit with ghee or honey is prescribed as a tonic and also in

the treatment of jaundice and rheumatism. T. Cordifolia is also widely used in

India for treating diabetes mellitus. (174, 175, 181, 182, 217, 218, 219, 221, 222,

223, 224, 225, 226)

12. Phytochemical Studies

A large number of compounds have been isolated from the aerial parts and roots of

T. cordifolia. In the early 1900s, giloin, gilenin, and gilosterol were found in the plant

together with the bitter principles columbin, chasmanthin, and palmarin (227). More

recently, a wide variety of sesquiterpenes and diterpenes have been isolated from the

68


stems of the plant. The major isolated compounds include the following: Cordiofolisides

A, B, and C (new norditerpene furan glycosides) (228); tinocordifolin and

tinocordifolioside (daucane-type sesquiterpenes) (229,230); palmatosides C and F

(furanoid diterpene glucosides) (231); cordioside, tinosponone, and tinocordioside

(clerodane diterpenoids) (232, 233); tinosporaside (a novel 18-norclerodane diterpene

glucoside) (234), and tinocordiside (a new cadinane sesquiterpene glycoside) (235). In

addition, syringin, cordiol, cordioside, cordifoliosides A and B (new phenylpropene

disaccharides) were identified as the active principles with anticomplement and

immunomodulatory activities (236, 237). It has been shown that the stems of the plant

contain the alkaloid berberine, and cultures of stem callus from this plant have been

shown to have the capability of synthesizing this compound (238). Ecdysterone,

makisterone A, and 20β-hydroxyecdysone are the phytoecdysones isolated from the

aerial parts of the plant (239, 240, 241). Other constituents reported from T. cordifolia

include a new phenolic lignan and the following compounds: Octacosanol, nonacosan-15-

one, heptacosanol, β-sitosterol, tinosporidine, cordifol, cordifolone (242, 243),

magnoflorine, tembetarine (244), syringine, and syringine apiosylglycoside (245).The

roots of T. cordifolia contain isocolumbin, palmatine, tetrahydropalmatine, magnoflorine,

and jatrorrhizine. (246, 247)

12. Important Formulations: Safoof Sat-e-gilo (248), Safoof Gilo, Roghan Gilo (220).

13. Muzir: Little or no side effects. Toxicological studies on rabbit do not show any

Adverse effects. (249, 250)

14. Musleh: Tabasheer and Dana heel. (175)

69


15. Badal: Sat-e-gilo (175)

16. Doses:

Powder: 4-6 Masha [Masha = Gram] (174)

1-2 Tola [Tola = 10 Gram] (175)

Decoction: 2-3 Tola (175)

17. Scientific Studies:

Experimental trials on T.cordifolia shows that it exhibits insulin

like activity, decreases the blood glucose level, and inhibit adrenaline-induced

hyperglycaemia in rats and rabbits. It also reduces serum and tissue cholesterol,

phospholipids, and free fatty acids levels and also reduces levels of brain lipids in rats

(251, 252, 253). Its aq.extract is found to exhibit antispasmodic activity in rabbit and also

found to decrease Blood pressure and producing bradycardia temporarily in anaesthetised

dogs (223). T.cordifolia is reported to benefit the immune system in a variety of ways

(254). The alcoholic and aqueous extracts of T.cordifolia have been tested successfully

for immunomodulatory activity (255). It helps by increasing the effectiveness of WBC

and builds up the body’s immune system. It also has significantly reduced the mortality

from E.coli induced peritonitis in mice. In clinical study, it has afforded protection in

cholestatic patients against E.coli infection (256).

In animals, it exhibits anti-oxidant and anti-inflammatory properties (257, 258, 259), and

also found to kill the HeLa cells very effectively in vitro hence shows Antineoplastic

activity (249). The anti-stress and tonic property of the plant was clinically tested and it

70


was found that it brought about good response in children with moderate degree of

behaviour disorders and mental deficit (251). In other experimental trials it is found that

Tinospora cordifolia also exhibit Hepatoprotective property in goat, and in vitro

inactivating property against Hepatitis B and E surface antigen (260, 261). Other reported

properties of T.cordifolia includes Antimalarial, Antipyretic properties (246, 249, 258).

71

Methodology

METHODOLOGY

72

Methodology

MATERIAL AND METHODS

For the assessment of efficacy of Safoof Ziabetus the patients of Ziabetus Shakri

were selected from the National Institute of Unani Medicine Hospital, Bangalore. Before

conducting the trial, the proposed research project was submitted for the approval to the

Institutional Ethical Committee of National Institute of Unani Medicine, Bangalore, and

the same was approved by the Committee.

After obtaining ethical clearance, the patients were selected on the basis of detailed

history and pathological investigations. The findings were recorded on the prescribed

proforma designed for the study. The patients fulfilling the inclusion criteria were

included in the study after obtaining the informed consent in writing, while those patients

who did not qualify the inclusion criteria or came under exclusion criteria were excluded

from the study.

Criteria For The Selection Of Patients

1. Inclusion Criteria

A. All patients of Ziabetus Shakri confirmed by investigations.

B. Patients belonging to 30-60 years of age of either sex.

C. Patients able to participate in the study and ready to follow the instructions.

2. Exclusion Criteria

A. Patients below the age of 30 years and above the age of 60 years.

B. Female patients with pregnancy and lactation.

C. Patients with Cardiovascular diseases.

D. Patients with Renal diseases.

73

Methodology

E. Patients with Hepatic disorders.

F. Patients with Type-1 Diabetes Mellitus.

G. Patients having complications like Gangrene and Diabetic Ketoacidosis.

To exclude the patients from the study, detailed history, physical examination and the

following biochemical investigations were carried out:

• Kidney function test (Blood Urea, Serum Creatinine) was done to exclude renal

diseases.

• Liver function test (Serum Bilirubin, SGOT, SGPT, and Alkaline Phosphatase)

was done to exclude liver diseases.

• ECG was done to exclude Cardiac disorders (Angina, Myocardial Infarction etc.).

Following Investigations Were Carried Out In Patients Before The Treatment:

A. Haematological Investigations:

• Hb%

• TLC

• DLC

• ESR

B. Biochemical Investigations:

(i) Blood Sugar

• Fasting

• Post prandial

74

Methodology

(ii) Kidney Function Test

• Blood Urea

• Serum Creatinine

(ii) Liver Function Test

• Total Bilirubin

• SGPT (ALT)

• SGOT (AST)

• Alkaline Phosphatase

(iii) Serum Cholesterol

C. Urine Analysis

• Routine Examination

• Microscopic Examination

D. ECG

Assessment Of Mizaj (Temperament)

The temperament (Mizaj) of the patients was assessed evolving different parameters,

suggested by Unani authors for the purpose. Details of these parameters have been given

in the CRF proforma.

Clinical Evaluation Of The Disease

Patients suffering from Ziabetus Shakri were interrogated and subjected to complete

physical and clinical examination as per details given in the CRF proforma.

75

Methodology

Chief Complaints

The complaints which brought patient to the doctor were written in chronological order

with duration.

History Of Present Illness

A detailed history of development of present clinical symptoms Like Polyuria, Nocturia,

Polydipsia, Tiredness, General Weakness, Increased appetite, Wasting of muscles, Loss

of body Weight, Non-healing or Delayed healing of cuts and Wounds, Paraesthesia, Pain

in the limbs were recorded.

History Of Past Illness

All patients were thoroughly interrogated for history of past Illnesses like Obesity /

Overweight, Gestational Diabetes Mellitus, Pancreatitis, Hypertension, Ischemic heart

diseases etc. and the findings were noted.

Family History

History of specific diseases like Diabetes Mellitus, Hypertension, Ischemic heart

diseases, Stroke in family members like parents, brothers and sisters, were recorded.

General Physical Examination

General physical examination of all patients was done. Special emphasis was given to

examination of Pulse, Blood Pressure, Temperature, Respiratory rate, Weight, Pallor,

Oedema, Built, JVP, Cyanosis, and the eyes were observed for cataract.

76

Methodology

Systemic Examination

A. Cardiovascular System

The examination of Cardiovascular system was carried out and the findings

were recorded as follows:

(i) Inspection : To observe deformities, dilated vessels and impulses.

(ii) Palpation : To determine the site and character of apex beat, thrills and

other impulses.

(iii) Percussion : To determine area of cardiac dullness and other dullness’s.

(iv) Auscultation: At different areas to record heart sounds and other sounds like

murmurs, friction rub etc.

B. Respiratory System

The Respiratory System was thoroughly examined and the findings were

recorded as follows:

(i) Inspection : To observe shape and movements of chest and swelling or

lesion if any.

(ii) Palpation : To observe position of trachea, apex beat, movements of chest,

tenderness, vocal fremitus, swelling.

(iii) Percussion: To determine the percussion note of lungs, area of cardiac

dullness, upper border of liver dullness and other dullness’s.

(iv) Auscultation: To record breath sounds, vocal resonance and added

sounds.

77

Methodology

C. Digestive System :

The Digestive System was thoroughly examined and the findings were recorded as

follows:

(i) Inspection of :

(a) Mouth : To know the condition of teeth, tongue, and gums.

(b) Abdomen: For scar, distension, dilated veins, hernia, discolouration, masses

and movements.

(ii) Palpation and Percussion: To observe the condition of liver, spleen, kidney,

stomach, bladder etc.

(iii) Auscultation over the abdomen for bowel sounds and other added sounds.

D.Nervous System

The Nervous System was thoroughly examined for mental state, speech, neck

stiffness, cranial nerves, motor and sensory functions, reflexes and the findings

were recorded on the CRF Proforma.

E.Urogenital System

The Urogenital system was thoroughly examined by inspection, palpation,

percussion, and auscultation for any abnormality and the findings were recorded

on the CRF Proforma.

78

Methodology

Investigations Carried Out Before And After The Treatment:

Haematological Investigations

• Hb %

• TLC

• DLC

• ESR

Urine Examination

• Routine examination

• Microscopic examination

ECG

Specific Biochemical Investigations

Blood Sugar

• Fasting

• Postprandial

Kidney Function Test

• Blood Urea

• Serum Creatinine

Liver Function Test

• Total Bilirubin • SGOT (AST)

• SGPT (ALT) • Alkaline Phosphatase

Serum Cholesterol

79

Methodology

Investigations, Their Methods And Normal Values

S.No Investigation Method Normal Range

1. Hb % Sahli’s Method Male :13.5 – 16 gm %

Female :11.5 – 15 gm %

2. TLC Neubauer’s Method 4000-11000 cells/mm3

3. DLC Leishman’s stain Method Polymorphs 40 – 75 %

Lymphocytes 20 – 40 %

Eosinophils 01 – 06 %

Monocytes 02 – 08 %

Basophils 0 - 01 %

4. ESR Westergren's method Male :01 – 10 mm/1hr

Female :01 – 20mm/1hr

5. Blood Sugar Fasting GOD / POD Method 70 – 110 mg / dl

6. Blood Sugar Postprandial GOD / POD Method 110 – 140 mg / dl

7. Blood Urea Urease Method 10 – 50 mg / dl

8. Serum Creatinine Picrate Method Male : 0.6 - 1.4 mg / dl

Female:0.5 – 1.2 mg / dl

9. Total Bilirubin Jendrassik and Grof Method 0.1 – 1.2 mg / dl

10. SGOT (AST) UV Kinetic (IFCC) method 05 – 46 IU / L

11. SGPT (ALT) UV Kinetic (IFCC) method 05 – 50 IU / L

12. Alkaline Phosphatase PNPP Method Adults 60 – 170 IU / L

Child. 151 – 470 IU / L

13. S.Cholesterol Enzymatic Method 120-250 mg / dl

14. Urine Routine

Examination

Urine for Albumin Nitric Acid Test Nil

Urine for Sugar Benedict’s Sol. Test Nil

15. Urine Microscopic Exam Microscopic Method NAD

80

Methodology

After thorough clinical examination and laboratory investigations, 79 diagnosed

patients of Ziabetus Shakri were included in the study. Out of 79 patients, 29 patients did

not complete full course of treatment. Only 50 patients completed the treatment during

the study.

For the assessment of efficacy of Unani formulation (Safoof Ziabetus), patients of

Ziabetus Shakri were divided into two groups i.e. “Group A and Group B". Group A

contained 30 patients while Group B contained 20 patients. Group A was given the test

drug (Safoof Ziabetus) whereas Group B placebo.

Preparation Of The Drug

The ingredients of Safoof Ziabetus [Gurmar Booti (Gymnema Sylvestre), Gilo Khushk

(Tinospora Cordifolia)] (262) were supplied by National Institute of Unani Medicine

Pharmacy, Bangalore.

Proper identification of ingredients was done by Chief Pharmacist of NIUM Pharmacy, to

ensure the originality and authenticity of the drugs. After proper identification, the

ingredient of Safoof Ziabetus was cleared from all impurities and ground to fine powder,

under the guidance of Dr. Mohd. Nafis Khan, Chief Pharmacist, NIUM Pharmacy,

Bangalore and filled in capsules of 1 gm capacity.

Similarly placebo was supplied by NIUM Pharmacy, and identified by Chief Pharmacist.

After proper identification the placebo was filled in capsules in same way as the test drug.

Study Design

The research design used for the study was randomized single blind placebo diet control.

81

Methodology

SAFOOF ZIABETUS

PLACEBO

82

Methodology

Sample Size

Total 50 patients [30 pts in Group A (Test drug) and 20 pts in Group B (Placebo drug)]

were included in the study.

Duration Of Protocol

The total duration of protocol was 45 days.

Drug Dose And Dosage Schedule

The Safoof Ziabetus filled in capsules was given to Group A in a dose of 6 gm thrice a

day (i.e. Six Capsules of 1 gm each) orally with water,15 minutes before breakfast, lunch

and dinner for 45 days. Total daily dose of Safoof Ziabetus given to each patient was 18

gm in three divided doses. Group B was treated in same way as the test group but with

placebo.

The capsules given to both Groups i.e. Group A and Group B were identical in size,

shape and colour.

Diet

All the patients of Ziabetus Shakri included in the study were advised to take their

tailored made diet as per ICMR Guidelines, to achieve and maintain ideal body weight,

euglycaemia and desirable lipid profile to prevent or at least postpone the complications

related with Ziabetus.

83

Methodology

Exercise

All the patients of Ziabetus Shakri included in the study were advised to follow exercise

programme as per ICMR Guidelines to do regular physical activity. The exercise

programme was individualized according to individual capacity and disabilities.

Follow-Up

All the patients of Ziabetus Shakri included in the study, were kept under strict

observation and asked to come every fortnightly for proper follow-up and assessment of

subjective and objective parameters. Findings were recorded on the prescribed CRF

proforma.

Criteria For Assessment Of Results

To assess the response of treatment on patients of Ziabetus Shakri in Group A and Group

B, following subjective and objective parameters were used in the study:

Subjective Parameters

1. Polyuria

2. Nocturia

3. Polydipsia

4. Tiredness

5. General Weakness

6. Increased appetite

7. Wasting of muscles

8. Weight gain without any apparent reason

9. Non-healing or Delayed healing of cuts and wounds.

10. Paraesthesia

84

Methodology

11. Pain in limbs

12. Defective vision

13. Impotence

14. Pruritus vulvae

15. Balanitis

16. Nausea

17. Vomiting

18. Depression

19. Irritability

Objective Parameters

1. Blood Sugar Fasting

2. Blood Sugar Post Prandial

3. Urine for Sugar

Procedure Of Study

After thorough clinical examination of the patients and laboratory investigations,

seventy nine diagnosed patients of Ziabetus Shakri who fulfilled the inclusion criteria

were selected for the study. Out of these 29 patients did not complete full course of

treatment. Only 50 patients completed the treatment during the study.

For the assessment of efficacy of Unani formulation (Safoof Ziabetus), patients of

Ziabetus Shakri were divided into two groups i.e. “Group A and Group B". Group A

contained 30 patients and Group B contained 20 patients. Group A was given test drug

(Safoof Ziabetus) and Group B placebo in a dose of 6 gm thrice a day in capsule form

orally with water,15 minutes before breakfast, lunch and dinner, for the period of 45

85

Methodology

days. During the study each patient was advised to take their tailored made diet and to

follow exercise programme as per ICMR Guidelines.

All the patients included in the trial were asked to come to the hospital every fortnightly

for proper follow-up. During the complete course of study each patient visited the

hospital four times i.e. at 0 day, 15th day, 30th day, and 45th day. Complete laboratory

investigations (As mentioned in the CRF proforma) were carried out before and after the

treatment. Besides, Blood Sugar Fasting and Postprandial, Urine for Sugar, and thorough

clinical examination carried out on every visit. The findings were recorded on the

prescribed CRF proforma.

Statistical Analysis

After completion of study, obtained data was analysed with the help of Student’s‘t’ test.

86

Results

RESULTS

87

Results

RESULTS

The results regarding the incidence of Ziabetus Shakri according to Age, Sex,

Mizaj and the degree of efficacy of the test as well as that of placebo drug in various

subjective and objective parameters are as follows:

Incidence Of Patients Of Ziabetus Shakri According To Age

Table No.1 n = 50 Age Group in Years No. of Patients Percentage of Patients

31-40 15 30 %

41-50 19 38 %

51-60 16 32 %

Total 50 100 %

Out of 50 selected patients of Ziabetus Shakri, the highest number of patients i.e.

19 (38 %) were from the age group of 41 – 50 years and then 16 (32 %) patients were

found in the age group of 51 – 60 years, and the least 15 (30 %) patients were in the age

group of 31 – 40 years.

Incidence Of Patients Of Ziabetus Shakri According To Gender

Table No.2 n = 50 Gender No. of Patients Percentage of Patients

Male 25 50 %

Female 25 50 %

Total 50 100 %

So far the sex distribution of Ziabetus patients is concerned, out of 50 patients 25

(50 %) patients were male and 25 (50 %) patients were Female.

88

Results

Graph No.1


15

19

16

50

0

10

20

30

40

50

60

31‐40 41‐50 51‐60 Total

Age

No.

of P

atie

nts →

No. of Patients

Graph No.2 Incidence Of Ziabetus Patients According To Gender

25 25

50

0

10

20

30

40

50

60

Male Female Total

Gender

No.

of P

atie

nts →

MaleFemaleTotal

89

Results

Incidence Of Patients Of Ziabetus Shakri According To Mizaj (Temperament)

Table No.3 n = 50 Mizaj No. of Patients Percentage of Patients

Damvi 21 42 %

Balghami 17 34 %

Safravi 11 22 %

Saudavi 01 2 %

Total 50 100 %

The mizaj of the patients of Ziabetus was assessed as per the parameters given by

Ibne Sina. Accordingly, in our study 21 (42 %) patients were assessed as having Damvi

mizaj, while 17 (34 %) patients were of Balghami and 11 (22 %) patients were of Safravi

mizaj, whereas only 1(2%) patients had Saudavi mizaj.

90

Results

Graph No.3

Incidence Of Ziabetus Patients According To Mizaj (Temperament)

21 17

11

1

50

0

10

20

30

40

50

60

Damvi Balghami Safravi Saudavi Total Mizaj

No.

of P

atie

nts →

DamviBalghamiSafraviSaudavi Total

91

Results

Effect Of Treatment On Polyuria

Effect Of Safoof Ziabetus On Polyuria In Group A

Table No.4A n = 30 0 Days 15 Days 30 Days 45 Days Polyuria

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 3 10 % 2 6.66 % 0 0 % 0 0 %

Mild 8 26.6% 8 26.66% 9 30 % 7 23.33%

Absent 19 63.33% 20 66.66% 21 70 % 23 76.66%

Total 30 100 % 30 100 % 30 100 % 30 100 %

Effect Of Placebo On Polyuria In Group B

Table No.4B n = 20

0 Days 15 Days 30 Days 45 Days Polyuria

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 1 5 % 0 0 % 0 0 % 0 0 %

Mild 8 40 % 8 40 % 7 35 % 8 40 %

Absent 11 55 % 12 60 % 13 65 % 12 60 %

Total 20 100 % 20 100 % 20 100% 20 100 %

Mild→ Patient micturate more than 6 but less than 10 times during day hours.

Moderate→ Patient micturate more than 10 but less than 15 times during day hours.

Severe→ Patient micturate more than 15 during day hours.

92

Results

Graph No.4A


0 0 0 0

32

0 0

8 89

7

19 2021

23

30 30 30 30

0

5

10

15

20

25

30

35

0 Days 15 Days 30 Days 45 Days

Duration of Treatment →

No.

of P

atie

nts →

SevereModerateMildAbsentTotal

Graph No.4B


0 0 0 01

0 0 0

8 87

8

1112

1312

20 20 20 20

0

5

10

15

20

25



No.

of P

atie

nts →


93

Results

It is evident from Table No.4A and 4B that only 11 (36.66 %) patients in Group A

and 9 (45 %) patients in Group B had Polyuria at the beginning of trial. Whereas at the

end of the trial total 7 (23.33 %) patients in Group A and 8 (40 %) patients in Group B

had Polyuria. Hence, only 4 patients of Group A and 1 patient of Group B had shown

improvement.

Effect Of Treatment On Nocturia

Effect Of Safoof Ziabetus On Nocturia In Group A

Table No.5A n = 30 0 Days 15 Days 30 Days 45 Days Nocturia

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 1 3.33 % 0 0 % 0 0 % 0 0 %

Mild 13 43.3 % 8 26.6 % 6 20 % 3 10 %

Absent 16 53.3 % 22 73.3 % 24 80 % 27 90 %

Total 30 100 % 30 100 % 30 100 % 30 100 %

94

Results

Effect Of Placebo On Nocturia In Group B

Table No.5B n = 20 0 Days 15 Days 30 Days 45 Days Nocturia

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 1 5 % 1 5 % 0 0 % 1 5 %

Mild 7 35 % 5 25 % 6 30 % 5 25 %

Absent 12 60 % 14 70 % 14 70 % 14 70 %

Total 20 100 % 20 100 % 20 100 % 20 100 %

Mild→ Patient micturate more than 2 but less than 4 times during night hours.

Moderate→ Patient micturate more than 4 but less than 6 times during night hours.

Severe→ Patient micturate more than 6 times during night hours.

It is clear from the Table No. 5A and 5B that only 14 (46.66 %) patients in Group

A and 8 (40 %) patients in Group B had Nocturia at the beginning of trial. Whereas at the

end of the trial total 3 (10 %) patients in Group A and 6 (30 %) patients in Group B had

Nocturia. Hence, only 11 patients of Group A and 2 patients of Group B had shown

improvement.

95

Results

96

Graph No.5A

Effect of Safoof Ziabetus On Nocturia In Group A

0 0 0 01

0 0 0

13

8

6

3

16

22

24

27

30 30 30 30

0

5

10

15

20

25

30

35


Duration of Treatment→

No.

of P

atie

nts →


Graph No.5B

Effect of Placebo On Nocturia In Group B

0 0 0 01 1

01

7

56

5

12

14 14 14

20 20 20 20

0

5

10

15

20

25



No.

of P

atie

nts →


Results

Effect Of Treatment On Polydipsia

Effect Of Safoof Ziabetus On Polydipsia In Group A

Table No.6A n = 30 0 Days 15 Days 30 Days 45 Days Polydipsia

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 1 3.33 % 0 0 % 0 0 % 0 0 %

Mild 8 26.66% 6 20 % 4 13.33% 2 6.66 %

Absent 21 70 % 24 80 % 26 86.66% 28 93.33%

Total 30 100 % 30 100 % 30 100 % 30 100 %

Effect Of Placebo On Polydipsia In Group B

Table No.6B n = 20 0 Days 15 Days 30 Days 45 Days Polydipsia

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 1 5 % 0 0 % 1 5 % 1 5 %

Mild 1 5 % 2 10 % 3 15 % 3 15 %

Absent 18 90 % 18 90 % 16 80 % 16 80 %

Total 20 100 % 20 100 % 20 100 % 20 100 %

97

Results

Graph No.6B


0 0 0 01

01 11

23 3

18 18

16 16

20 20 20 20

0

5

10

15

20

25



No.

of P

atie

nts →


Graph No.6AEffect Of Safoof Ziabetus On Polydipsia In Group A

0 0 0 01

0 0 0

8

6

4

2

21

2426

28

30 30 30 30

0

5

10

15

20

25

30

35



No.

of P

atie

nts →

Severe ModerateMildAbsentTotal

98

Results

Mild→Patient drinks more than 6 but less than 8 glasses of water in 24 hours.

Moderate→Patient drinks more than 8 but less than 10 glasses of water in 24 hours.

Severe→ Patient drinks more than 10 glasses of water in 24 hours. (1 Glass=200 ml)

It is shown in Table 6A and 6B that only 9 (30 %) patients in Group A and 2

(10 %) patients in Group B had Polydipsia at the beginning of trial. Whereas the end of

the trial, total 2 (6.66 %) patients in Group A and 4 (20 %) patients in Group B had

Polydipsia. Thus, only 7 patients of Group A had shown improvement. On the contrary in

Group B Polydipsia had occurred in 2 more patients.

Effect Of Treatment On Tiredness

Effect Of Safoof Ziabetus On Tiredness In Group A

Table No.7A n = 30 0 Days 15 Days 30 Days 45 Days Tiredness

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 4 13.33% 0 0 % 0 0 % 0 0 %

Mild 22 73.33 % 23 76.66% 16 53.33% 12 40 %

Absent 4 13.33 % 7 23.33 % 14 46.66 % 18 60 %

Total 30 100 % 30 100 % 30 100 % 30 100 %

99

Results

Effect Of Placebo On Tiredness In Group B

Table No.7B n = 20 0 Days 15 Days 30 Days 45 Days Tiredness

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 1 5 % 0 0 % 0 0 % 0 0 %

Mild 14 70 % 17 85 % 17 85 % 18 90 %

Absent 5 25 % 3 15 % 3 15 % 2 10 %

Total 20 100 % 20 100 % 20 100 % 20 100 %

Mild → Feeling of tiredness more than normal during daily routine activity.

Moderate→ Feeling of tiredness which restricted the patient from performing daily routine

activity

Severe → Feeling of tiredness at rest.

It is evident from Table No. 7A and 7B, that 26 (86.66 %) patients in Group A

and 15 (75 %) patients in Group B had Tiredness at the beginning of trial. Whereas at the

end of the trial total 12 (40 %) patients in Group A and 18 (90 %) patients in Group B

had Tiredness. Thus, only 14 patients of Group A had shown improvement. On the

contrary in Group B Tiredness had occurred in 3 more patients.

100

Results

101

Graph No.7A


0 0 0 0

4

0 0 0

2223

16

12

47

14

18

30 30 30 30

0

5

10

15

20

25

30

35



No.

of P

atie

nts →


Graph No.7B


0 0 0 01

0 0 0

14

17 1718

5

3 32

20 20 20 20

0

5

10

15

20

25



No.

of P

atie

nts →


Results

Effect Of Treatment On General Weakness

Effect Of Safoof Ziabetus On General Weakness In Group A

Table No.8A n = 30 0 Days 15 Days 30 Days 45 Days General

Weakness No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 4 13.33% 0 0 % 0 0 % 0 0 %

Mild 15 50 % 18 60 % 18 60 % 17 56.66%

Absent 11 36.66 % 12 40 % 12 40 % 13 43.33 %

Total 30 100 % 30 100 % 30 100 % 30 100 %

Effect Of Placebo On General Weakness In Group B

Table 8B n = 20 0 Days 15 Days 30 Days 45 Days General

Weakness No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Severe 0 0 % 0 0 % 0 0 % 0 0 %

Moderate 0 0 % 0 0 % 0 0 % 0 0 %

Mild 12 60 % 13 65 % 14 70 % 15 75 %

Absent 8 40 % 7 35 % 6 30 % 5 25 %

Total 20 100 % 20 100 % 20 100 % 20 100 %

102

Results


0 0 0 0

4

0 0 0

15

18 1817

1112 12

13

30 30 30 30

0

5

10

15

20

25

30

35



No.

of P

atie

nts →

Graph No.8A


Graph No.8B


0 0 0 00 0 0 0

1213

1415

8 7

65

20 20 20 20

0

5

10

15

20

25



No.

of P

atie

nts →


103

Results

Mild→ Patient feels difficulty in performing only strenuous activity.

Moderate→ Patient feels difficulty in performing daily routine activity

Severe→ Patient feels exhausted and unable to do any work.

It is shown in Table 8A and 8B, that only 19 (63.33 %) patients in Group A and

12 (60 %) patients in Group B had General Weakness at the beginning of the study.

Whereas at the end of the study total 17 (56.66 %) patients in Group A and 15 (75 %)

patients in Group B had General Weakness. Hence, only 2 patients of Group A had

shown improvement. On the contrary in Group B General Weakness had occurred in 3

more patients.

104

Results

Effect Of Treatment On Different Subjective Parameters

Effect Of Safoof Ziabetus On Different Subjective Parameters In Group A

Table No.9A n = 30

0 Days 15 Days 30 Days 45 Days Parameters

Pres

ent

/

Abs

ent

No. of

Pts

% of

Pts.

No. of

Pts

% of

Pts.

No. of

Pts

% of

Pts.

No. of

Pts

% of

Pts.

Present 5 16.66% 2 6.66 % 0 0 % 0 0 % Increased

Appetite Absent 25 83.33% 28 93.33% 30 100 % 30 100 %

Present 6 20 % 6 20 % 6 20 % 6 20 % Wasting of

Muscles Absent 24 80 % 24 80 % 24 80 % 24 80 %

Present 3 10 % 0 0 % 0 0 % 0 0 % Weight gain

Absent 27 90 % 30 100 % 30 100 % 30 100 %

Present 3 10 % 3 10 % 3 10 % 3 10 % Non-healing

of wounds Absent 27 90 % 27 90 % 27 90 % 27 90 %

Present 20 66.66% 20 66.66% 20 66.66% 19 63.33% Paraesthesia

Absent 10 33.33% 10 33.33% 10 33.33% 11 36.66%

Present 23 76.66% 22 73.33% 16 53.33% 16 53.33% Pain in

Limbs Absent 7 23.33% 8 26.66% 14 46.66% 14 46.66%

Present 2 6.66 % 2 6.66 % 2 6.66 % 2 6.66 % Impotence

Absent 28 93.33% 28 93.33% 28 93.33% 28 93.33%

Present 2 6.66 % 1 3.33 % 0 0 % 0 0 % Nausea

Absent 28 93.33% 29 96.66% 30 100 % 30 100 %

Present 9 30 % 4 13.33% 2 6.66 % 2 6.66 % Irritability

Absent 21 70 % 26 86.66% 28 93.33% 28 93.33%

105

Results

Effect Of Placebo On Different Subjective Parameters In Group B

Table No.9B n=20

0 Days 15 Days 30 Days 45 Days Parameters Pr

esen

t /

Abs

ent

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

No. of

Pts.

% of

Pts.

Present 3 15 % 4 20 % 4 20 % 4 20 % Increased

Appetite Absent 17 85 % 16 80 % 16 80 % 16 80 %

Present 4 20 % 4 20 % 4 20 % 4 20 % Wasting of

Muscles Absent 16 80 % 16 80 % 16 80 % 16 80 %

Present 1 5 % 2 10 % 2 10 % 2 10 % Weight gain

Absent 19 95 % 18 90 % 18 90 % 18 90 %

Present 1 5 % 1 5 % 1 5 % 1 5 % Non-healing

of wounds Absent 19 95 % 19 95 % 19 95 % 19 95 %

Present 8 40 % 8 40 % 8 40 % 8 40 % Paraesthesia

Absent 12 60 % 12 60 % 12 60 % 12 60 %

Present 11 55 % 11 55 % 13 65 % 12 60 % Pain in

Limbs Absent 9 45 % 9 45 % 7 35 % 8 40 %

Present 3 15 % 3 15 % 3 15 % 3 15 % Impotence

Absent 17 85 % 17 85 % 17 85 % 17 85 %

Present 0 0 % 0 0 % 0 0 % 1 5 % Nausea

Absent 20 100 % 20 100 % 20 100 % 19 95 %

Present 3 15 % 6 30 % 7 35 % 7 35 % Irritability

Absent 17 85 % 14 70 % 13 65 % 13 65 %

106

Results

Graph No.9A

Effect Of Safoof Ziabetus On Following Subjective Parameters In Group A

5

2

0 0

6 6 6 6

3

0 0 0

3 3 3 3

20 20 2019

2322

16 16

2 2 2 22 1

0 0

9

4

2 2

0

5

10

15

20

25



No.

of P

atie

nts →

Increased AppetiteWasting of MusclesWeight gainNon-healing of woundsParaesthesiaPain in LimbsImpotenceNauseaIrritability

Graph No.9B

Effect Of Placebo On Following Subjective Parameters In Group B

3 4 4 44 4 4 4

1 2 2 2

1 1 1 1

8 8 8 8

11 11

13

12

3 3 3 3

0 0 0

1

3

6

7 7

0

2

4

6

8

10

12

14



No.

of P

atie

nts →

Increased AppetiteWasting of MusclesWeight gainNon-healing of woundsParaesthesiaPain in LimbsImpotenceNauseaIrritability

107

Results

Effect Of Treatment On Increased Appetite

It is evident from Table No. 9A and 9B that only 5 (16.66 %) patients in Group A

and 3 (15 %) patients in Group B had Increased Appetite at the beginning of trial.

Whereas at the end of the trial 0 (0%) patient in Group A and 4 (20 %) patients in Group

B had Increased Appetite. Hence, all patients i.e. 5 patients of Group A had shown

improvement. On the contrary in Group B Increased Appetite had occurred in 1 more

patient.

Effect Of Treatment On Weight Gain

It is evident from Table No. 9A and 9B that only 3 (10 %) patients in Group A

and 1 (5 %) patient in Group B had Weight gain at the beginning of trial. Whereas at the

end of the trial 0 (0%) patient in Group A and 2 (20 %) patients in Group B had Weight

gain. Thus, all the patients i.e. 3 patients of Group A had shown improvement by the

treatment. On the contrary in Group B Weight gain had occurred in 1 more patient.

Effect Of Treatment On Paraesthesia

It is evident from Table No. 9A and 9B that only 20 (66.66 %) patients in Group

A and 8 (40 %) patients in Group B had Paraesthesia at the beginning of trial. Whereas at

the end of the trial 19 (63.33 %) patients in Group A and 8 (40 %) patients in Group B

had Paraesthesia. Hence, only 1 patient of Group A had shown improvement. On the

contrary there was no improvement observed in the Paraesthesia in Group B.

108

Results

Effect Of Treatment On Pain In Limbs

It is evident from Table No. 9A and 9B that only 23 (76.66 %) patients in Group

A and 11 (55 %) patients in Group B had Pain in Limbs at the beginning of trial. Whereas

at the end of the trial 16 (53.33 %) patient in Group A and 12 (60 %) patients in Group B

had Pain in Limbs. Thus, only 7 patients of Group A had shown improvement. On the

contrary in Group B Pain in Limbs had occurred in one more patient.

Effect Of Treatment On Nausea

It is evident from Table No. 9A and 9B that only 2 (6.66 %) patients in Group A

and no patient in Group B had Nausea at the beginning of trial. Whereas at the end of the

trial no patient in Group A and 1 (5 %) patient in the Group B had Nausea. Hence, all

patients i.e. 2 patients of Group A had shown improvement by the treatment. On the

contrary in Group B Nausea had occurred in one more patients.

Effect Of Treatment On Irritability

It is evident from Table No. 9A and 9B that only 9 (30 %) patients in Group A

and 3 (15 %) patients in Group B had Irritability at the beginning of trial. Whereas at the

end of the trial 2 (6.66 %) patients in Group A and 7 (35 %) patients in Group B had

irritability. Thus, only 7 patients of Group A had shown improvement. On the contrary in

Group B Irritability had occurred in 4 more patients.

109

Results

Effect Of Treatment On Wasting Of Muscles, Non-Healing Or Delayed Healing Of

Cuts And Wounds and Impotence

Table No. 9A and 9B clearly showed that during the study, no effect was

observed on these symptoms.

Effect Of Treatment On Blood Sugar Levels

Effect Of Safoof Ziabetus On Blood Sugar Levels In Group A

Table No.10A n = 30 0 Days

15 Days 30 Days 45 Days Blood Sugar Calculated value

of in ‘t’ Mean Mean Mean Mean

mg / dl Fasting 173.23 133.43 124.96 116.4 9.31

Post prandial 249.53 208.7 194.4 182.3 7.42

Effect Of Placebo On Blood Sugar Levels In Group B

Table No.10B n = 20 0 Days 15 Days 30 Days 45 Days Blood Sugar Calculated value

of in Mean Mean Mean Mean

mg / dl ‘t’

164.2 Fasting 170.5 173.05 179.85 2.67

Post prandial 249.3 258.3 254.7 277.05 2.69

110

Results

Graph No.10A


173.23

133.43 124.96116.4

249.53

208.7194.4

182.3

0

50

100

150

200

250

300



Blo

od S

ugar

in m

g / d

l →

FastingPost prandial

Graph No.10B


164.2 170.5 173.05 179.85

249.3258.3 254.7

277.05

0

50

100

150

200

250

300



Blo

od S

ugar

in m

g / d

l→

FastingPost prandial

111

Results

Effect Of Treatment On Blood Sugar Fasting

It is evident from Table No.10A and 10B that before the treatment mean Blood

Sugar in the Fasting state was 173.23 mg/dl in Group A and 164.2 mg/dl in Group B.

Whereas at the end of the treatment it was reduced to 116.4 mg/dl (average reduction of

32.80 %) in Group A. On the contrary in Group B it was increased to 179.85 mg/dl

(average elevation of 9.53 %). On comparing Blood Sugar Fasting observations of

‘Group A’ with ‘Group B’ with the help of Student’s ‘t’ test, it was found significant

statistically (p<0.05). It means test drug reduces the Blood Sugar Fasting level

significantly as compared to placebo.

Effect Of Treatment On Blood Sugar Post Prandial

It is clearly shown in Table No.10A and 10B that before the treatment mean

Blood Sugar in the Post Prandial state was 249.53 mg/dl in Group A and 249.3 mg/dl in

Group B. Whereas at the end of the treatment it was reduced to 182.3 mg/dl (average

reduction of 26.94 %) in Group A. On the contrary in Group B it was increased to 277.05

mg/dl (average elevation of 11.13%). On comparing Blood Sugar Post Prandial

observations of ‘Group A’ with ‘Group B’ with the help of Student’s ‘t’ test, it was found

significant statistically (p<0.05). It means test drug reduces the Blood Sugar Post

Prandial level significantly as compared to placebo.

112

Results

Effect Of Treatment On Urine Sugar

Effect Of Safoof Ziabetus On Urine Sugar In Group A

Table No 11A n = 30 0 Days 15 Days 30 Days 45 Days Urine

Sugar No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

Nil 14 46.66 % 21 70 % 22 73.33% 23 76.66%

Traces 10 33.33 % 1 3.33 % 1 3.33 % 5 16.66 %

0.5% 3 10 % 3 10 % 2 6.66 % 2 6.66 %

1.0% 2 6.66 % 3 10 % 3 10 % 0 0 %

1.5% 0 0 % 1 3.33 % 1 3.33 % 0 0 %

2.0% 1 3.33 % 1 3.33 % 1 3.33 % 0 0 %

Effect Of Placebo On Urine Sugar In Group B

Table No.11B n = 20 0 Days 15 Days 30 Days 45 Days Urine

Sugar No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

No. of Pts.

% of Pts.

Nil 11 55 % 9 45 % 10 50 % 8 40 %

Traces 2 10 % 2 10 % 0 0 % 3 15 %

0.5% 1 5 % 2 10 % 3 15 % 5 25 %

1.0% 2 10 % 6 30 % 4 20 % 3 15 %

1.5% 3 15 % 1 5 % 1 5 % 1 5 %

2.0% 1 5 % 0 0 % 2 10 % 0 0 %

113

Results

Graph No.11A


14

2122

23

10

1 1

5

3 32 22

3 3

001 1

01 1 1

00

5

10

15

20

25



% o

f Sug

ar in

Uri

ne →

NilTraces0.50%1.00%1.50%2.00%

Graph No.11B


11

9

10

8

2 2

0

3

1

2

3

5

2

6

4

33

1 1 11 0

2

00

2

4

6

8

10

12



% o

f Sug

ar in

Uri

ne →

NilTraces0.50%1.00%1.50%2.00%

114

Results

It is clearly shown in Table No.11A and 11B that only 16 (53.33 %) patients in

Group A and 9 (45 %) patients in Group B had sugar in urine at the beginning of trial.

Whereas at the end of the trial 7 (23.33 %) patients in Group A and 12 (60 %) patients in

Group B had sugar in urine. Hence, only 9 patients of Group A had shown improvement.

On the contrary in Group B sugar in urine had appeared in 3 more patients.

Effect Of Treatment On Different Objective Parameters

Effect Of Safoof Ziabetus On Different Objective Parameters In Group A

Table No.12A n = 30 Mean Value

Mean ValueS.No Objective Parameters Calculated value of ‘t’

BT AT 1. Hb% (gm %) 11.86 11.85 0.13 2. TLC ( Cells/cu.mm) 5668.33 5846.33 0.61 3. DLC ( Cells/cu.mm)

Polymorph 53.06 54.53 0.76 Lymphocytes 42.26 41.26 0.44

Eosinophils 4.53 3.86 0.93 Monocytes 0.4 0.16 1.43 Basophils 0 0 0

4. ESR ( mm/1hr ) 25.33 24.13 0.43 5. Blood Urea (mg/dl) 19.23 20.46 0.99 6. Serum Creatinine (mg/dl) 0.65 0.69 1.25 7. Serum Bilirubin (mg/dl) 0.65 0.70 1.37 8. Alkaline

Phosphatase(IU/L) 112.46 122.26 1.47

9. SGOT (AST) (IU/L) 26.36 31.17 1.52 10. SGPT (ALT) (IU/L) 26.76 32.69 1.32 11. Serum Cholesterol (mg/dl) 201.9 196.66 0.70

115

Results

Effect Of Placebo On Different Objective Parameters In Group B

Table No.12B n = 20 Mean Value Mean Value

S.No Objective Parameters Calculated value of

‘t’ BT AT

1. Hb% (gm %) 12.2 11.98 0.39 2. TLC ( Cells/cu.mm) 5898 6228 1.04 3. DLC ( Cells/cu.mm)

Polymorphs 52.9 51.9 0.29 Lymphocytes 42.9 42.8 0.04 Eosinophils 3.9 4.05 0.34 Monocytes 0.3 1.05 1.92 Basophils 0 0 0

4. ESR ( mm/1hr ) 19.75 19.05 0.06 5. Blood Urea (mg/dl) 17.82 18.85 0.81 6. Serum Creatinine (mg/dl) 0.66 0.65 0.42 7. Serum Bilirubin (mg/dl) 0.66 0.65 0.25 8. Alkaline

Phosphatase(IU/L) 126.95 117.95 1.05

9. SGOT (AST) (IU/L) 21 33.25 1.42 10. SGPT (ALT) (IU/L) 22.9 38.8 1.37 11. Serum Cholesterol (mg/dl) 203.8 200.45 0.35

Effect Of Treatment On Hb%, TLC, DLC, ESR (Haemopoetic System), Blood Urea,

Serum Creatinine (Kidney Function Test), Serum Bilirubin, Alkaline Phosphatase,

SGOT, SGPT (Liver Function Test), Blood Cholesterol

It is evident from Table No.12A and 12B that average Hb%, TLC, DLC, ESR,

Blood Urea, Serum Creatinine, Serum Bilirubin, Alkaline Phosphatase, SGOT, SGPT,

Serum Cholesterol of group 'A' and group 'B' remained within normal limit before and

after the treatment. On comparing before and after observations of ‘Group A’ with

‘Group B’ with the help of Student’s ‘t’ test, it was found statistically insignificant

116

Results

(p<0.05). Thus, during the whole duration of study test as well as placebo drug has no

significant effect on all above mentioned safety parameters.

Effect Of Treatment On Weight Of The Patients

Effect Of Safoof Ziabetus On Weight Of Ziabetus Patients In Group A

Table No.13A n=30 Mean Weight

in kg

Mean Weight in

kg

Weight Reduction of

Weight in Kg

Calculated value

of

‘t’ BT AT

Trial Group

(n = 30)

63.88 62.48 1.4 (2.19 %) 8.78

Effect Of Placebo On Weight Of Ziabetus Patients In Group B

Table No.13B n=20 Mean Weight

in kg

Mean Weight

in kg

Weight Reduction of

Weight in Kg

Calculated value

of

‘t’ BT AT

Placebo Group

(n = 20)

60.42 59.55 0.87 (1.43 %) 3.47

It is evident from Table No.13A and 13B that before the treatment mean Weight

was 63.88 Kg in Group A and 60.42 Kg in Group B. Whereas at the end of the treatment

it was reduced to 62.48Kg (average reduction of 2.19 %) in Group A and 59.55 Kg

(average reduction of 1.43 %) in Group B. On comparing ‘before treatment’ and ‘after

treatment’ observations with the help of Student’s‘t’ test, it was found significant

statistically (p<0.05). It means treatment reduces Weight of diabetic patients

significantly.

117

Results

Graph No.12A


63.88

62.48

61.5

62

62.5

63

63.5

64

BT AT

Before and After Treatment →

Wei

ght i

n K

g→

Weight in Kg

Graph No.12B


60.42

59.55

59

59.2

59.4

59.6

59.8

60

60.2

60.4

60.6

BT AT

Before and After Treatment →

Wei

ght i

n K

g →

Weight in Kg

118

Discussion

DISCUSSION

119

Discussion

DISCUSSION

The Ziabetus Shakri (Diabetes Mellitus) is a major public health problem and

considered as one of the most common non-communicable disease, globally. About 246

million people are affected with this disease all over the world in 2007 and this number

may increase to 380 million by 2025. Although the prevalence rate of the disease varies

from country to country. However, WHO has been projected India as the country with the

fastest growing population of Diabetes patients. Due to its severe consequences Diabetes

become a silent killer that kills one person every 10 seconds, and world wide it kills 3.2

millions every year. Owing to its dreadful complications such as Diabetic Ketoacidosis,

Diabetic Retinopathy, Diabetic Neuropathy, Atherosclerosis, Coronary artery disease and

Stroke the researchers of different system of medicine are concentrating themselves for

the development of new antidiabetic drugs. A number of antidiabetic drugs have been

evaluated by the researchers of main stream medicine such as Glibenclamide, Metformin,

Gliclazide, Glimepiride, Glipizide etc. These drugs have been found to possess potent and

effective hypoglycaemic activity, but the long term use of these drugs frequently leads to

the development of various side effects such as Hypoglycaemic reactions,

Agranulocytosis, Aplastic anaemia, and Haemolytic anaemia .

As far as the Unani system of medicine is concerned, Unani physicians have been treating

Ziabetus Shakri since Greco-Arab period. They have claimed to possess many safe and

effective antidiabetic agents for the management of Ziabetus Shakri. Therefore, it is one

of the areas which have to be given priority in scientific research in Tibbe Unani. Many

important and therapeutically effective murakkab drugs have been described to be useful

120

Discussion

in Ziabetus Shakri in standard qarabadeen; they have not been evaluated scientifically so

far for their described effect. Recently several herbal single drugs have been

experimentally and clinically evaluated and reported as good hypoglycaemic agents.

However, the scientific study of compound formulation is largely ignored by the

scientists and physicians despite the fact that a good number of compound drugs have

been described in Unani literature to be effective in Ziabetus condition. Safoof Ziabetus

is one such drug described in various qarabadeen to be effective in Ziabetus Shakri.

In view of the above a single blind placebo study was designed to investigate the

hypoglycaemic effect of Safoof Ziabetus in the patients of Ziabetus Shakri.

The results and observations obtained from the trial were depicted in Tables and Graphs.

The discussions regarding the incidence of Ziabetus Shakri according to Age, Sex, Mizaj,

and the efficacy of drug in various subjective and objective parameters are as follows:


As it is evident from Table No. 1 that out of 50 selected patients of Ziabetus

Shakri, the highest number of patients i.e. 19 (38 %) were from the age group of 41 – 50

years and then 16 (32 %) patients were found in the age group of 51 – 60 years. While the

least 15 (30 %) patients were in the age group of 31 – 40 years. This finding coincides

with the findings described by Anonymous. (115,116)

121

Discussion

Incidence Of Patients Of Ziabetus Shakri According To Gender

As it is clear from the Table No.2 that out of 50 patients of Ziabetus Shakri, 25

(50 %) patients were male and 25 (50 %) patients were Female. This finding does not

coincide with the findings described by Anonymous (115). One of the reasons for such

difference might be the small number of patients in the study. The size of our study is too

small containing only 50 patients. Hence, the exact distribution pattern of the disease

according to gender probably could not be determined accurately through this study.

Incidence Of Patients Of Ziabetus Shakri According To Mizaj (Temperament)

The mizaj of the patients of Ziabetus was assessed as per the parameters given by

Ibne Sina. In our study 21 (42 %) patients were assessed as having Damvi mizaj, while 17

(34 %) patients were of Balghami and 11 (22 %) patients were of Safravi mizaj, whereas

only 1 (2%) patients had Saudavi mizaj. It clearly indicated that most of the patients had

har mizaj. These findings are inconformity with the findings suggested by Razi, Ibne

Sina, Jurjani, Al-Baghdadi, Majusi, M.A.Arzani, N.Samarqandi, and Ajmal Khan. (1, 3,

5, 11, 14, 16, 18, 19, 20).


It is evident from the table No.4A that only 11 (36.66 %) patients had Polyuria at

the beginning of trial. Out of these 3 (10%) patients had moderate and 8 (26.6 %) patients

had mild degree of Polyuria. After 15 days of treatment only 2 (6.66 %) patients had

moderate and 8 (26.6 %) patients had mild degree of Polyuria and after 30 days of

122

Discussion

treatment only 9 (30 %) patients had mild degree of Polyuria. Whereas after 45 days of

treatment only 7 (23.33 %) patients had mild degree of Polyuria.

The improvement in this symptom appears to be due to the effect of test drug which

reduced the blood glucose level and that in turn decreased the frequency of micturition

(Polyuria). The exact mechanism of hypoglycaemic activity of test can not be described

at the moment but as per the description of Unani literature it may be attributed mainly to

the blood purifying activity of both Gilo Khushk and Gurmar Booti. These findings are

inconformity with the findings suggested by Najmul Ghani, Kabeeruddin, Nadkarni,

Kritikar and Basu, Stanely P et al, Mhasker and caius, Shanmugasundaram et al.

(174,175,179,181,189,192,193,222,252)


It is shown in table No.4B that only 9 (45 %) patients had Polyuria at the

beginning of trial. Out of these, 1 (5 %) patient had moderate and 8 (40 %) patients had

mild degree of Polyuria. After 15 days of treatment 8 (40 %) patients had mild degree of

Polyuria while after 30 days of treatment only 7 (35 %) patients had mild degree of

Polyuria. Whereas at the end of the trial total 8 (40 %) patients had mild degree of

Polyuria.

The mild improvement in this symptom might be attributed to diet and exercise

prescribed as per ICMR guidelines.

123

Discussion

Effect Of Safoof Ziabetus On Nocturia In Group A

It is clear from the table No.5A that only 14 (46.66 %) patients of Ziabetus Shakri

had Nocturia at the beginning of the treatment. Out of these, 1 (3.33%) patient had

moderate degree and 13 (43.33 %) patients had mild degree of Nocturia. After 15 days of

treatment 8 (26.6 %) patients had mild degree of Nocturia. While after 30 days of

treatment only 6 (20 %) patients had mild degree of Nocturia. Whereas at the end of the

study only 3 (10 %) patients had Nocturia of mild degree. The improvement in this

symptom appears to be due to the effect of test drug which reduced the blood glucose

level and that in turn decreased the Nocturia. The exact mechanism of hypoglycaemic

activity of test drug can not be described at the moment but as per the description of

Unani literature it may be attributed mainly to the blood purifying activity of both Gilo

Khushk and Gurmar Booti. These findings are inconformity with the findings suggested

by Najmul Ghani, Kabeeruddin, Nadkarni, Kritikar and Basu, Stanely P et al, Mhasker

and caius, Shanmugasundaram et al.( 174,175,179, 181,189, 192,193, 222,252)

Effect Of Placebo On Nocturia In Group B

It is evident from the table No 5B that only 8 (40 %) patients of Ziabetus Shakri

had Nocturia at the beginning of the treatment. Out of these, 1 (5 %) patient had moderate

degree of Nocturia and 7 (35 %) patients had mild degree of Nocturia. After 15 days of

treatment 1 (5 %) patient had moderate degree and 5 (25 %) patients had mild degree of

Nocturia. While after 30 days of treatment only 6 (30 %) patients had mild degree of

Nocturia. Whereas at the end of the trial 1 (5 %) patient had moderate degree and 5

124

Discussion

(25 %) patients had mild degree of Nocturia. The mild improvement in this symptom

might be attributed to diet and exercise prescribed as per ICMR guidelines.

Effect Of Safoof Ziabetus On Polydipsia In Group A

As it is evident from table No.6A only 9 (30 %) patients had Polydipsia at the

beginning of trial. Out of these, 1 (3.33 %) patient had moderate and 8 (26.6 %) patients

had mild degree of Polydipsia. After 15 days of treatment 6 (20 %) patients had mild

degree of Polydipsia, while after 30 days of treatment only 4 (13.33 %) patients had mild

degree of Polydipsia.Whereas at the end of the trial only 2 (6.66 %) patients had mild

degree of Polydipsia.

The improvement in this symptom might be due to reduction in blood glucose

level and decreased frequency of micturition. This effect may be attributed to the

ingredients of the test drug; as Gilo khushk reduces the thirst and Gurmar booti reduces

the Polyuria as described by Anonymous. (177,222)


As it is clear from table No.6B only 2 (10 %) patients had Polydipsia at the

beginning of trial. Out of these, 1 (5 %) patient had moderate and 1 (5 %) patient had

mild degree of Polydipsia. After 15 days of treatment 2 (10 %) patients had mild degree

of Polydipsia, while after 30 days of treatment 1 (5 %) patient had moderate degree of

Polydipsia and 3 (15 %) patients had mild degree of Polydipsia. Whereas at the end of the

trial 1(5 %) patient had moderate and 3 (15 %) patients had mild degree of Polydipsia. It

clearly indicates that the placebo did not have any effect on this symptom. On the

125

Discussion

contrary in this group Polydipsia had occurred in two more patients during the study, it

might be due to fluctuation in the blood glucose level.


As it is shown in table No.7A total 26 (86.66 %) patients had Tiredness at the

beginning of trial. Out of these, 4 (13.33 %) patients had moderate and 22 (26.6 %)

patients had mild degree of Tiredness. After 15 days of treatment 23 (76.66 %) patients

had mild degree of Tiredness. While after 30 days of treatment only 16 (53.33 %) patients

had mild degree of Tiredness. Whereas at the end of the trial only 12 (6.66 %) patients

had mild degree of Tiredness.

Association of Tiredness with hyperglycaemia is now a well established and documented

fact. It can be inferred therefore that the improvement in the Tiredness of the patients is

mainly because of the improvement in diabetic condition of the patient. Further, since

Gilo and Gurmar has been reported to possess tonic, antioxidant, adaptogenic and

analgesic activities. The partial role of these effects in improving the Tiredness can not be

denied. These findings are inconformity with the findings suggested by Najmul Ghani,

Kabeeruddin, K.M.Nadkarni, Kirtikar and Basu, Dymock,W. et.al, Prince P, et al. ,

Mathew S, et al.(174, 175, 179, 181, 182, 222, 258, 259, 223)


As it is shown in table No.7B, 15 (75%) patients had Tiredness at the beginning

of trial. Out of these, 1 (5%) patient had moderate and 14 (70%) patients had mild degree

of Tiredness. After 15 and 30 days of treatment 17 (85%) patients had mild degree of

126

Discussion

Tiredness. Whereas at the end of the trial 18 (90%) patients had mild degree of Tiredness.

It clearly indicates that the placebo did not have any effect on this symptom. On the

contrary in this group Tiredness had occurred in three more patients during the study, it

might be due to fluctuation in the blood glucose level.


As evident from the table No.8A, total 19 (63.33 %) patients had General

Weakness at the beginning of trial. Out of these, 4 (13.33 %) patients had moderate and

15 (50 %) patients had mild degree of General Weakness. While after 15 and 30 days of

treatment 18 (60 %) patients had mild degree of General Weakness. Whereas at the end

of the study only 17 (56.66 %) patients had mild degree of General Weakness.

It is a well known and documented fact that in Ziabetus Shakri General Weakness

is mainly occurs due to reduction in utilisation of glucose. It is also documented that Gilo

khushk and Gurmar booti increases the utilisation of glucose, thereby improving the

General Weakness. Further, since Gilo has been reported to possess antioxidant, anti-

stress and tonic activity. The role of these effects in improving the General Weakness can

not be denied. (192,193,194,201, 202,203, 204,205, 251, 258,259)


As shown in table No.8B, total 12 (60%) patients had mild degree of General

Weakness at the beginning of trial. After 15 days of treatment 13 (65%) patients had mild

degree of General Weakness, while after 30 days 14 (70%) patients had mild degree of

General Weakness. Whereas after 45 days of treatment 15 (75%) patients had mild

127

Discussion

degree of General Weakness. It clearly indicates that the placebo did not have any effect

on this symptom. On the contrary in this group General Weakness had occurred in three

more patients during the study, it might be due to fluctuation in the blood glucose level.

Effect Of Safoof Ziabetus On Different Subjective Parameters In Group A

Out of 30 patients, 5 (16.66 %) patients were having Increased Appetite, 3 (10%)

patients were of Weight Gain before the treatment. During the study it was observed that

these two symptoms disappeared. Similarly, there were only 6 (20%) patients of Wasting

of Muscles, 3 (10%) patients of Non-healing of Wounds and 2 (6.66%) patients of

Impotence before the treatment. However, no improvement was observed in these

symptoms.

There were 20 (66.66%) patients of Paraesthesia, 23 (76.66%) patients of Pain in

Limbs and 9 (30%) patients of Irritability before the treatment. After 30 days of treatment

improvement was noted in only 7 (23.33%) patients of Pain in Limbs and 7 (23.33%)

patients of Irritability. At the end of the study Paraesthesia was absent in only one

patient. There were only 2 (6.66%) patients who complained of Nausea before the

treatment. One of them got relief after 15 days of treatment while other after 30 days .The

improvement in the symptom of Increased Appetite might be attributed to reduction in

blood sugar level, while improvement in Gaining of Weight might be attributed to diet

restriction and exercise programme advised to patients. The improvement in Paraesthesia

and Pain in the Limbs might be attributed to the analgesic property of Gilo khushk as

described in Wealth of India. As far as the improvement in Irritability was concerned it

might be occurred because of the overall improvement in health and feeling of wellness

128

Discussion

in patients. Improvement in the symptom of Nausea might be attributed to the anti-emetic

property of Gilo khushk as described in Najmul Ghani and Anonymous. (174, 222, 223)

Effect Of Placebo On Different Subjective Parameters In Group B

As evident from Table No. 9B out of 20 patients there were 3 (15 %) patients of

Increased Appetite, 1 (5%) patient of Weight Gain before the treatment. After 15, 30 and

45 days of treatment, there were 4 (20%) patients of Increased Appetite, 2 (10%) of

Weight Gain. Similarly, there were only 4 (20%) patients of Wasting of Muscles, 1 (5%)

patient of Non-healing of Wounds, 3 (15%) patients of Impotence and 8 (40%) patients of

Paraesthesia before the treatment. During the study no improvement was observed in

these symptoms.

There were 11 (55%) patients of Pain in Limbs, 3 (15%) patients of Irritability,

and no (0%) patient of Nausea before the treatment. After 15 days of treatment there

were 11 (55%) patients of Pain in Limbs, 6 (30%) patients of Irritability, and 0 patient of

Nausea, while after 30 days of treatment there were 13 (65%) patients of Pain in Limbs, 7

(35%) patients of Irritability and 0 patient of Nausea. Whereas at the end of the study

there were 12 (60%) patients of Pain in Limbs, 7 (35%) patients of Irritability and 1 (5%)

patient of Nausea. It indicates that the placebo did not have any effect on these

symptoms. On the contrary in this group all the above mentioned symptoms increases to

some extent, it might be due to fluctuation in the blood glucose level.

129

Discussion


It is evident from table No.10A, the mean Blood Sugar in the Fasting state was

173.23 mg/dl at the beginning of the treatment, while after 15 days and 30 days of

treatment it was reduced to 133.43 mg/dl and 124.96 mg/dl, respectively. Whereas at the

end of the study mean Fasting Blood Glucose level reduced to 116.4 mg/dl.

Similarly, the mean Blood Sugar in the Post Prandial state was 249.53 mg/dl at

the beginning of the treatment, while after 15 days and 30 days of treatment it was

reduced to 208.7 mg/dl and 194.4 mg/dl, respectively. Whereas at the end of the study

mean Post Prandial Blood Glucose level reduced to 182.3 mg/dl. The improvement in

Blood Sugar level during the state of Fasting and Post Prandial is attributed to the

hypoglycaemic activity of test drug contained Gilo Khushk and Gurmar booti.

Experimental and clinical studies shows that Gurmar booti and Gilo khushk

increases the insulin level, reduces the glucose absorption from the intestine, improves

uptake of glucose into the cells and prevents adrenal hormone from stimulating the liver

to produce glucose, thereby reducing Blood Glucose level and increasing the glucose

tolerance. Hence, the finding of Blood Glucose reduction during Fasting and Post

Prandial state is inconformity with the description of Najmul Ghani, Kabeeruddin,

Nadkarni, Kritikar and Basu, Stanely P et al, Mhasker and caius, Shanmugasundaram et

al., Hirata and co-workers,Yoshikawa et al, Chattopadhyay. (174, 175,179,181,189, 192,

193,194,202,206,207,222,252).

On comparing ‘before treatment’ observations of Blood Sugar Fasting and Post Prandial

with their corresponding ‘after treatment’ observations, with the help of Student’s ‘t’ test,

130

Discussion

it was found significant statistically (p<0.05). Hence trial drug has significant effect on

Blood Sugar Fasting and Post Prandial.


As it is evident from table No.10B, the mean Blood Sugar in the Fasting state was

164.2 mg/dl at the beginning of the treatment, while after 15 days and 30 days of

treatment it was increased to 170.5 mg/dl and 173.05 mg/dl, respectively. At the end of

the study mean Fasting Blood Glucose level increased to 179.85 mg/dl. Similarly, the

mean Blood Sugar in the Post Prandial state was 249.3 mg/dl at the beginning of the

treatment, while after 15 days and 30 days of treatment it was increased to 258.3 mg/dl

and 254.7 mg/dl, respectively. Whereas, at the end of the study mean Post Prandial Blood

Glucose level increased to 277.05 mg/dl. It clearly indicates that the placebo did not have

any effect on Blood Sugar levels. On the contrary in this group Blood Sugar levels i.e.

Fasting and Post Prandial increases during the study.

On comparing ‘before treatment’ observations of Blood Sugar Fasting and Post Prandial

with their corresponding ‘after treatment’ observations with the help of Student’s ‘t’ test,

it was found significant statistically (p<0.05). Hence, Placebo did not have any blood

glucose lowering effect.


As shown in table 11A out of 30 patients, 10 (33.33%) patients had sugar in urine

in traces at the start of the treatment. After 15 and 30 days there was only 1 (3.33%)

patient with sugar in urine. Whereas, at the end of the treatment there were only 5

131

Discussion

(16.66%) patients who had urinary sugar. Similarly, there were only 3 (10%) patients of

0.5%, 2 (6.66%) patients of 1% and 1 (3.33%) patient of 2% sugar in urine at the start of

the treatment. After 15 days of treatment there were 3 (10%) patients each of 0.5% and

1% sugar in the urine and 1 (3.33%) patient each of 1.5% and 2% sugar in urine. While

after 30 days of treatment there were 2 (6.66%) patients of 0.5%, 3 (10%) patients of 1%

and 1 (3.33%) patient each of 1.5% and 2% sugar in urine. Whereas at the end of the

study, there were 2 (6.66%) patients who had 0.5% sugar in the urine and no patient was

found to have 1%, 1.5%, and 2% sugar in urine. The improvement in urinary sugar level

is due to low level of sugar in the blood. As sugar in urine appears only when blood sugar

level exceeds the threshold value i.e.180 mg/dl and its quantity in the urine increases

proportionally as the sugar in blood increases..


As shown in table 11B out of 20, 2 (10%) patients had sugar in urine in traces at 0

and 15 days of treatment. While after 30 days no patient was found with sugar in urine.

Whereas at the end of the study, 3 (15%) patients had urinary sugar in traces. Similarly,

there were only 1 (5%) patient of 0.5%, 2 (10%) patients of 1% and 3 (15%) patients of

1.5% and 1 (5%) patient of 2% sugar in urine at the start of the treatment. After 15 days

of treatment there were 2 (10%) patients of 0.5%, 6 (30%) patients of 1%, 1 (5%) patient

of 1.5% and no patient of 2% sugar in urine. While after 30 days there were 3 (15%)

patients of 0.5%, 4 (20%) patients of 1%, 1 (5%) patient of 1.5% and 2 (10%) patients of

2% sugar in urine. Whereas at the end of the study, only 3 (15%) patients of traces, 5

132

Discussion

(25%) patients of 0.5%, 3 (15%) patients of 1%, and 1 (5%) patient of 1.5% were found.

Hence, the placebo has no effect on urinary sugar.

Effect Of Safoof Ziabetus On Different Objective Parameters In Group A

Effect On Haemopoetic System (Hb%, TLC, DLC, ESR)

Only slight variation was noted in parameters of Haemopoetic system, as shown

in Table No.12A. However, all the observations were still found within the normal limit.

On comparing ‘before treatment’ observations of each parameter with their

corresponding ‘after treatment’ observations with the help of Student’s‘t’ test, it was

found insignificant statistically (p<0.05). It may be concluded therefore that the test drug

does not posses any adverse effect on Haemopoetic system.

Effect On Kidney Function Test (Blood Urea, Serum Creatinine)

Only slight variation was observed in parameters of Kidney Function Test. As

evident from Table No.12A, all the observations were still found within normal limit. On

comparing ‘before treatment’ observations with their corresponding ‘after treatment’

observations with the help of Student’s‘t’ test, it was found insignificant statistically

(p<0.05). Hence trial drug has no adverse effect on Kidney Function Test.

133

Discussion

Effect On Liver Function Test (Serum Bilirubin, Alkaline Phosphatase, SGOT,

SGPT)

As shown in Table No.12A all the observations of Liver Function Test were

found within normal limit before and after the treatment. On comparing ‘before

treatment’ observations of all parameters with their corresponding ‘after treatment’


(p<0.05). Hence, it may be concluded that test drug has no adverse effect on Liver

Function Test.

Effect On Serum Cholesterol

Only slight variation was observed in S.Cholesterol level as shown in Table

No.12A. However, before and after observations were still found within normal limit. On

comparing ‘before treatment’ observation with ‘after treatment’ observation with the help

of Student’s‘t’ test, it was found insignificant statistically (p<0.05). Hence, it may be

concluded that test drug has no effect on Serum Cholesterol level.

Effect Of Placebo On Different Objective Parameters In Group B

As evident from Table No.12B, only slight variations were noted in all objective

parameters, but all the observations still found within normal limit. On comparing ‘before

treatment’ observations of each parameter with their corresponding ‘after treatment’


(p<0.05). Hence trial drug has no effect on these objective parameters.

134

Discussion


It is evident from the table No.13A, mean Weight of Group A patients before the

treatment was 63.88 kg and after treatment it reduced to 62.48 kg. This improvement might be

attributed to diet and exercise programme advised to the patients. On comparing ‘before treatment

observations of Weight with their corresponding after treatment observations with the help of

Student’s‘t’ test, it was found significant statistically (p<0.05).


As shown in table No.13B, mean Weight of Group B patients before the treatment

was 60.42 kg and after treatment it reduced to 59.55 kg. This improvement might be

attributed to diet and exercise programme advised to patients. On comparing before

treatment observations of Weight with their corresponding after treatment observations

with the help of Student’s‘t’ test, it was found significant statistically (p<0.05).

Although, the results of the present study are very encouraging and statistically

significant. But the duration of the study was only 45 days, which could not elaborate the

long term safety and efficacy of the Safoof Ziabetus. Hence, the long term study (Phase

III and IV Clinical Trial) is required to further explore the safety and efficacy of this

formulation and to make it a standard formulation for the long term management of

Ziabetus Shakri.

135

Conclusion

CONCLUSION

136

Conclusion

CONCLUSION

The clinical study on Ziabetus Shakri and review of literature presented in this

dissertation provide certain important and fruitful information regarding the usefulness of

Unani formulation in the management of Ziabetus Shakri. Ziabetus (Diabetes) has

become a global problem in spite of advances in modern sciences and considered as one

of the most common non-communicable disease globally. It is a major cause of disability

through its complications like blindness, renal failure, coronary artery disease, gangrene

of lower extremities. Owing to these complications, the researchers of different system of

medicine are concentrating themselves for the development of the new antidiabetic drugs.

The different antidiabetic drugs has been already evaluated by main stream of medicine

such as Glibenclamide, Metformin, Glipizide etc., these drugs have very much potent and

effective hypoglycaemic action, but the long term use of these drugs resulted in

development of various side effects like Hypoglycaemic reactions, Aplastic anaemia, and

Haemolytic anaemia. Hence, there is an increasing interest among diabetic patients and

health professionals in using alternative medicinal systems such as Unani system of

Medicine for the management of Ziabetus Shakri. Unani drugs are available in abundance

in surrounding and can provide safe, stable, standardise and efficacious treatment. The

therapeutic application of Unani drugs is based upon evidence handed down from

generation to generation and achieves their importance through experience and not by

experiments. Nevertheless their clinical efficacy is beyond doubt. Hence, Tibbe Unani

possesses large number of mufrad and murakkab drugs for the management of Ziabetus

Shakri; but they have not been evaluated scientifically so far for their described effect.

Hence, scientific evaluation of compound Unani drugs on the modern scientific approach

137

Conclusion

of research and treatment is quite necessary. Keeping this fact in mind a clinical trial was

conducted on the "Clinical evaluation of Safoof Ziabetus in management of Ziabetus

Shakri.” Safoof Ziabetus was selected from a long list of compound Unani formulations

used by the Unani physicians for the management of Ziabetus Shakri. It contains Gurmar

booti (Gymnema Sylvestre) and Gilo khushk (Tinospora Cordifolia) in equal quantity.

The trial was conducted on 50 newly diagnosed patients of Ziabetus Shakri [divided into

two groups "Group A (30 Patients) and Group B (20 Patients)"] at National Institute of

Unani Medicine Hospital, Bangalore. Group A was given the test drug (Safoof Ziabetus)

whereas Group B placebo in a dose of 6 gm thrice a day in capsule form orally with

water,15 minutes before breakfast, lunch, and dinner along with planned diet and exercise

for the period of 45 days. Study reveals that the Ziabetus Shakri is relatively more

common in person having age 40 years and above with har mizaj.

As evident from results and discussion, the cases treated with Safoof Ziabetus

showed good response; the results were encouraging and statistically significant.

Moreover, the drug was found relatively safe, as the safety parameters (Haemogram,

LFT, KFT and S.Cholesterol) remained within normal limits during the study. Since the

duration of the study was only 45 days, therefore the long term safety and efficacy of

Safoof Ziabetus can not be elaborate at the moment but for short term use, it was found

safe. Hence, long term study (Phase III and IV Clinical Trial) will be required to assess

the long term perspectives of test drug for its safety and toxicity and to make it a standard

formulation for the long term management of Ziabetus Shakri.

138

Summary

SUMMARY

139

Summary

SUMMARY

The term Ziabetus is a Greek word which means “to run through” or “Siphon”,

was first used by Arsyatoos,characterized by hyperglycaemia, glycosuria, increased

appetite, excessive thirst and gradual loss of body weight . It is a disease in which, patient

excretes water as such through urinary passage soon after its intake. The ratio of fluid

taken and the urinary output remains the same (Zalaqul majari) as that of solid without

digestion from the stomach and intestine, a condition known in Unani medicine as

'Zalaqul-ama'. There is excessive thirst more intake of water and its rapid discharge as

urine. When the disease takes the body completely in its grip there occurs dryness all

over the body rendering it weak. Sue mizaj har kuliya, Zoufe-kuliya, Majari ki

kushadgi,and Sue mizaj barid of tamam badan / kuliya / jigar ,are the four major causes

described in most of the classical Unani literature, responsible for the development of

Ziabetus. Now in present era due to resemblance in clinical features of the disease

Ziabetus Shakri has been correlated with Diabetes Mellitus, which is a chronic disorder

of carbohydrate metabolism and glucose intolerance. It is characterized by high blood

glucose level and glycosuria resulting from dysfunction of pancreatic β cells and insulin

resistance. Owing to its dreadful complications such as Diabetic Ketoacidosis, Diabetic

Retinopathy, Diabetic Neuropathy, Atherosclerosis, Coronary artery disease, Stroke etc.,

now Diabetes has become a global problem in spite of advances in modern sciences, and

prevails all over the world, and considered as one of the most common non-

communicable disease globally. In present study, the Introduction of Ziabetus Shakri,

History, Anatomy & Physiology of Pancreas, Definition, Prevalence, Classification,

140

Summary

Pathogenesis, Clinical features, Complications, Diagnostic criteria and Management has

been discussed in detail.

Age: The highest number of patients i.e. 19 (38 %) were found in the age group of 41–50

years showing higher incidence after 40 years.

Gender: 25 (50 %) patients were male and 25 (50 %) patients were Female, showing

equal incidence of disease in both sexes.

Mizaj (Temperament): The highest number of patients i.e. 21(42%) were of Damvi

Mizaj, showing higher incidence in har mizaj.

Effect Of Treatment On Different Subjective Parameters Of Ziabetus Shakri

[Group A contain 30 Patients and Group B contain 20 Patients]

Effect Of Treatment On Polyuria: Only 4 (36.36 %) patients of Group A and 1

(11.11 %) patients of Group B had shown improvement by the treatment.

Effect Of Treatment On Nocturia: Only 11 (78.57 %) patients of Group A and 2 (25 %)

patients of Group B had shown improvement by the treatment.

Effect Of Treatment On Polydipsia: Only 7 (77.77 %) patients of Group A had shown

improvement by the treatment. On the contrary in Group B Polydipsia had occurred in 2

more patients.

Effect Of Treatment On Tiredness: Only 14 (53.84 %) patients of Group A had shown

improvement by the treatment. On the contrary in Group B Tiredness had occurred in 3

(20 %) more patients.

Effect Of Treatment On General Weakness: Only 2 (10.52 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B General Weakness had

occurred in 3 (25 %) more patients.

141

Summary

Effect Of Treatment On Increased Appetite: All patients i.e. 5 (100 %) patients of

Group A had shown improvement by the treatment. On the contrary in Group B Increased

Appetite had occurred in 1 (33.33 %) more patients.

Effect Of Treatment On Weight Gain: All the patients i.e. 3 (100 %) patients of Group

A had shown improvement by the treatment. On the contrary in Group B Weight Gain

had occurred in 1 more patients.

Effect Of Treatment On Paraesthesia: Only 1 (5 %) patient of Group A had shown

improvement by the treatment. On the contrary no improvement was observed in the

Paraesthesia in Group B.

Effect Of Treatment On Pain In Limbs: Only 7 (30.43 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B Pain in Limbs had

occurred in one (9.09 %) more patients.

Effect Of Treatment On Nausea: All patients i.e.2 (100 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B Nausea had occurred

in one more patients.

Effect Of Treatment On Irritability: Only 7 (77.77 %) patients of Group A had shown

improvement by the treatment. On the contrary in Group B Irritability had occurred in 4

more patients.


Cuts And Wounds, Impotence: During the study, no effect was observed on these

symptoms.

142

Summary

Effect Of Treatment On Different Objective Parameters Of Ziabetus Shakri

Effect Of Treatment On Blood Sugar Fasting: During the study average reduction of

56.83 mg/dl (32.80 %) in Group A, and average elevation of 15.65 mg/dl (9.53 %) in

Group B was recorded in Blood Sugar Fasting and statistically it was found significant.

Effect Of Treatment On Blood Sugar Post Prandial: During the study average

reduction of 67.23 mg/dl (26.94 %) in Group A, and average elevation of 27.75 mg/dl

(11.13%) in Group B was recorded in Blood Sugar Post Prandial and statistically it was

found significant.

Effect Of Treatment On Urine Sugar: Only 9 (56.25 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B, sugar in urine had

appeared in 3 (33.33 %) more patients

Effect Of Treatment On Hb%, TLC, DLC, ESR, Blood Urea, Serum Creatinine,

Serum Bilirubin, Alkaline Phosphatase, SGOT, SGPT, Serum Cholesterol

It was observed that average Hb%, TLC, DLC, ESR, Blood Urea, Serum

Creatinine, Serum Bilirubin, Alkaline Phosphatase, SGOT, SGPT, Serum Cholesterol of

group 'A' and group 'B' remained within normal limit before and after the treatment. On

comparing before and after observations of ‘Group A’ with ‘Group B’ with the help of

Student’s ‘t’ test, it was found statistically insignificant (p<0.05). Thus, during the whole

duration of study test as well as placebo drug has no significant effect on all above

mentioned safety parameters.

Effect Of Treatment On Weight Of The Patients: During the study, average reduction

of 1.4 Kg (2.19 %) in Group A and 0.87 Kg (1.43 %) in Group B was recorded and found

significant statistically (p<0.05).

143

Summary

SUMMARY

139

Summary

SUMMARY

The term Ziabetus is a Greek word which means “to run through” or “Siphon”,

was first used by Arsyatoos,characterized by hyperglycaemia, glycosuria, increased

appetite, excessive thirst and gradual loss of body weight . It is a disease in which, patient

excretes water as such through urinary passage soon after its intake. The ratio of fluid

taken and the urinary output remains the same (Zalaqul majari) as that of solid without

digestion from the stomach and intestine, a condition known in Unani medicine as

'Zalaqul-ama'. There is excessive thirst more intake of water and its rapid discharge as

urine. When the disease takes the body completely in its grip there occurs dryness all

over the body rendering it weak. Sue mizaj har kuliya, Zoufe-kuliya, Majari ki

kushadgi,and Sue mizaj barid of tamam badan / kuliya / jigar ,are the four major causes

described in most of the classical Unani literature, responsible for the development of

Ziabetus. Now in present era due to resemblance in clinical features of the disease

Ziabetus Shakri has been correlated with Diabetes Mellitus, which is a chronic disorder

of carbohydrate metabolism and glucose intolerance. It is characterized by high blood

glucose level and glycosuria resulting from dysfunction of pancreatic β cells and insulin

resistance. Owing to its dreadful complications such as Diabetic Ketoacidosis, Diabetic

Retinopathy, Diabetic Neuropathy, Atherosclerosis, Coronary artery disease, Stroke etc.,

now Diabetes has become a global problem in spite of advances in modern sciences, and

prevails all over the world, and considered as one of the most common non-

communicable disease globally. In present study, the Introduction of Ziabetus Shakri,

History, Anatomy & Physiology of Pancreas, Definition, Prevalence, Classification,

140

Summary

Pathogenesis, Clinical features, Complications, Diagnostic criteria and Management has

been discussed in detail.

Age: The highest number of patients i.e. 19 (38 %) were found in the age group of 41–50

years showing higher incidence after 40 years.

Gender: 25 (50 %) patients were male and 25 (50 %) patients were Female, showing

equal incidence of disease in both sexes.

Mizaj (Temperament): The highest number of patients i.e. 21(42%) were of Damvi

Mizaj, showing higher incidence in har mizaj.

Effect Of Treatment On Different Subjective Parameters Of Ziabetus Shakri

[Group A contain 30 Patients and Group B contain 20 Patients]

Effect Of Treatment On Polyuria: Only 4 (36.36 %) patients of Group A and 1

(11.11 %) patients of Group B had shown improvement by the treatment.

Effect Of Treatment On Nocturia: Only 11 (78.57 %) patients of Group A and 2 (25 %)

patients of Group B had shown improvement by the treatment.

Effect Of Treatment On Polydipsia: Only 7 (77.77 %) patients of Group A had shown

improvement by the treatment. On the contrary in Group B Polydipsia had occurred in 2

more patients.

Effect Of Treatment On Tiredness: Only 14 (53.84 %) patients of Group A had shown

improvement by the treatment. On the contrary in Group B Tiredness had occurred in 3

(20 %) more patients.

Effect Of Treatment On General Weakness: Only 2 (10.52 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B General Weakness had

occurred in 3 (25 %) more patients.

141

Summary

Effect Of Treatment On Increased Appetite: All patients i.e. 5 (100 %) patients of

Group A had shown improvement by the treatment. On the contrary in Group B Increased

Appetite had occurred in 1 (33.33 %) more patients.

Effect Of Treatment On Weight Gain: All the patients i.e. 3 (100 %) patients of Group

A had shown improvement by the treatment. On the contrary in Group B Weight Gain

had occurred in 1 more patients.

Effect Of Treatment On Paraesthesia: Only 1 (5 %) patient of Group A had shown

improvement by the treatment. On the contrary no improvement was observed in the

Paraesthesia in Group B.

Effect Of Treatment On Pain In Limbs: Only 7 (30.43 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B Pain in Limbs had

occurred in one (9.09 %) more patients.

Effect Of Treatment On Nausea: All patients i.e.2 (100 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B Nausea had occurred

in one more patients.

Effect Of Treatment On Irritability: Only 7 (77.77 %) patients of Group A had shown

improvement by the treatment. On the contrary in Group B Irritability had occurred in 4

more patients.


Cuts And Wounds, Impotence: During the study, no effect was observed on these

symptoms.

142

Summary

Effect Of Treatment On Different Objective Parameters Of Ziabetus Shakri

Effect Of Treatment On Blood Sugar Fasting: During the study average reduction of

56.83 mg/dl (32.80 %) in Group A, and average elevation of 15.65 mg/dl (9.53 %) in

Group B was recorded in Blood Sugar Fasting and statistically it was found significant.

Effect Of Treatment On Blood Sugar Post Prandial: During the study average

reduction of 67.23 mg/dl (26.94 %) in Group A, and average elevation of 27.75 mg/dl

(11.13%) in Group B was recorded in Blood Sugar Post Prandial and statistically it was

found significant.

Effect Of Treatment On Urine Sugar: Only 9 (56.25 %) patients of Group A had

shown improvement by the treatment. On the contrary in Group B, sugar in urine had

appeared in 3 (33.33 %) more patients

Effect Of Treatment On Hb%, TLC, DLC, ESR, Blood Urea, Serum Creatinine,

Serum Bilirubin, Alkaline Phosphatase, SGOT, SGPT, Serum Cholesterol

It was observed that average Hb%, TLC, DLC, ESR, Blood Urea, Serum

Creatinine, Serum Bilirubin, Alkaline Phosphatase, SGOT, SGPT, Serum Cholesterol of

group 'A' and group 'B' remained within normal limit before and after the treatment. On

comparing before and after observations of ‘Group A’ with ‘Group B’ with the help of

Student’s ‘t’ test, it was found statistically insignificant (p<0.05). Thus, during the whole

duration of study test as well as placebo drug has no significant effect on all above

mentioned safety parameters.

Effect Of Treatment On Weight Of The Patients: During the study, average reduction

of 1.4 Kg (2.19 %) in Group A and 0.87 Kg (1.43 %) in Group B was recorded and found

significant statistically (p<0.05).

143

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170

Annexures (Proforma)

CLINICAL EVALUATION OF SAFOOF ZIABETES IN

MANAGEMENT OF ZIABETES SHAKRI

PROFORMA _______________________________________________________________________

Case No…… OPD/IPD No. Regd.No.

Name: …………………………….....Father/Husband’s Name…….......................

Age/Sex : …………………….................Religion:………………………….............

Marital status:…………………..............................................................................

Occupation:………………………... Monthly income:…………………................

Address:…………………………………………………………………….....................................................................................................................................................

Date of starting Treatment :………..... Date of stopping Treatment:………......

Chief complaints:

1. 2. 3. 4. 5.

History Of Present Illness: …………………………………………………............................................................

………………………………………………………………………...............................

History Of Past Illness:……………………………………………….........................

……………………………………………………………………………….....................

Past History Of Gestational Diabetes:………………………………........................

Family History Of Diabetes Mellitus:………………………………..........................

Treatment History :…………………………………………………............................

………………………………………………………………………………....................

171


Personal History:

Appetite o Good o Fair o Poor

Diet

o Veg o Non –veg

Habit o Smoking o Alcohol intake

o Tobacco Chewing o Pan Chewing

Menstrual / Obstetrical History:……………………………………............... ………………………………………………………………………………..........

GENERAL PHYSICAL EXAMINATION

Look ………………........Cyanosis ………. ……….Clubbing …………..........

Built………………….....Paller……………………....Oedema…………...........

Expression………….....Icterus………………….......Dehydration………........

Lymphadenopathy………....JVP…………………...Weight …………............

Vitals :

Pulse B.P. Temp R.R.

SYSTEMIC EXAMINATION

CARDIOVASCULAR SYSTEM Inspection……………………………………………………………………….

Palpation…………………………………………………………………………..

Percussion…………………………………………………………………………

Auscultation………………………………………………………………………..

172


RESPIRATORY SYSTEM

Inspection………………………………………………………………………….

Palpation…………………………………………………………………………..

Percussion…………………………………………………………………………

Auscultation……………………………………………………………………….

DIGESTIVE SYSTEM

Inspection………………………………………………………………………….

Palpation…………………………………………………………………………

Percussion…………………………………………………………………………

Auscultation………………………………………………………………………. NERVOUS SYSTEM

Mental state.................................................................................................

Speech..........................................................................................................

Neck stiffness..............................................................................................

Cranial nerves.............................................................................................

Motor and Sensory functions.......................................................................

Reflexes........................................................................................................

UROGENITAL SYSTEM

Inspection……………………………………………………………………….

Palpation………………………………………………………………………...

Percussion………………………………………………………………………

Auscultation……………………………………………………………………..

173


INVESTIGATIONS

S.NO INVESTIGATION BEFORE TREATMENT AFTER TREATMENT

1. Hb%

2. TLC

3. DLC

4. ESR

5. Blood sugar fasting

6. Blood sugar post prandial

7. Blood Urea

8. Serum Creatinine

9. Serum bilirubin

10. Alkaline Phosphatase

11. SGOT (AST)

12. SGPT (ALT)

13. Serum Cholesterol

14 URINE Colour Appearance Reaction Sp.gravity Protein Glucose RBC Pus cells Cast Bacteria Epithelial Cells Crystals

15. ECG

16. Weight

174


FOLLOW-UP CHART

S.No Subjective Parameter 0 Day 15 Days 30 Days 45 Days

1. Polyuria

2. Nocturia

3. Polydipsia

4. Tiredness

5. General weakness

6. Increased appetite

7. Wasting of muscles

8. Wt.gain without any apparent reason

9. Non-healing or Delayed healing of cuts & wounds

10. Paraesthesia

11. Pain in the limbs

12. Defective vision

13. Impotence

14. Pruritus vulvae

15. Balanitis

16. Nausea

17. Vomiting

18. Depression

19. Irritability

S.No Objective Parameter 0 Day 15 Days 30 Days 45 Days

1. Urine for sugar

2. Blood sugar fasting

3. Blood sugar PP

175


ASSESSMENT OF MIZAJ (TEMPERAMENT)

SIGNS OF TEMPERAMENT PARAMETERS DAMVI

(SANGUINE) BALGHAMI

(PHLEGMATIC) SAFRAVI (BILIOUS)

SAUDAVI (MELANCHOLIC)

COMPLEXION Ruddy(Reddish/Wheay brown)

Chalky (Whitish)

Pale (Yellowish)

Purple (Blackish)

BUILT Muscular & Broad

Fatty & Broad Muscular &Thin Skeletal

TOUCH Hot & Soft Cold & Soft Hot & Dry Cold & Dry

MO

RPH

OLO

GIC

AL

HAIR Black & Lusture,Thick,R

apid Growth

Black & Thin Slow Growth

Brown & Thin Rapid Growth

Brown & Thin Slow Growth

MOVEMENT Active Dull Hyperactive Less Active

DIET (MOST LIKED)

Cold & Dry Hot & Dry Cold & Moist Hot & Moist

WEATHER (MOST SUITABLE)

Spring Summer Winter Autumn

SLEEP Normal (6-8 hours)

In Excess Inadequate Insomnia

PHY

SIO

LOG

ICA

L

PULSE Normal in Rate (70-80/min)

Large in Volume

Slow in Rate (70/min)

Normal in Volumes

Rapid in Rate (80-100/min)

Normal in Volume

Slow in Rate (60-70/min)

Sig. of the Student. Sig. of the attending Consultant.

176

1 26373 44 F Average ─ ve 0 + + - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 + - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 + - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 + - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

2 1201 40 F Obese ─ ve 0 ++ + ++ ++ ++ +ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 + - + + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve30 + - + + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 + - - - + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

3 1256 35 F Obese ─ ve 0 + + + ++ + +ve +ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve15 + + + + + -ve +ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve30 + + + + + -ve +ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve45 + + + + + -ve +ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve

4 24525 36 M Average ─ ve 0 + + - ++ ++ +ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve15 + - - + - +ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + - -ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + - -ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

5 20701 40 M Average ─ ve 0 - - - + - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - - - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

6 26755 51 M Thin + ve 0 - + - - - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 - - - - - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

7 1285 55 F Obese ─ ve 0 + - + + ++ -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 - - + + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

S.N

o.

Tem

pera

men

t

Abr : Mild (+),Modeerate (++), Severe (+++), Absent(-)

Noc

turia

-ve-ve

OP

D/IP

D N

o.

Age

in y

ears

F/H

of D

iabe

tes

Mel

litus

Sex

Bui

lt

-ve-ve

Day

s

Pol

yuria

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

Occ

upat

ion

Gen

.Wea

knes

s

Was

ting

of M

uscl

es

-ve

-ve

-ve-ve

-ve

-ve

-ve

-ve-ve-ve

-ve

-ve

Irri

tabi

lity

-ve

Vom

iting

Dep

ress

ion

Bal

aniti

s

Nau

sea

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n-ve-ve

-ve

-ve

-ve-ve-ve

-ve

-ve-ve

Master Chart of Group A (Safoof Ziabetus) - Subjective Parameters

Hou

sew

ife

Bal

gham

i

Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Par

aest

hesi

a

Non

-Hea

ling

of W

ound

Inc

reas

ed A

ppet

ite

Mol

viH

ouse

wife

Hou

sew

ifeE

mpl

oyee

Dam

viD

amvi

Dam

viB

algh

ami

Con

duct

orH

ouse

wife -ve

Bal

gham

iSa

fravi

177

29 37614 46 M Obese + ve 0 - + + + - -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - + + + - -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - + - + - -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - + - + - -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

30 1714 53 M Obese + ve 0 - - - - - -ve -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve15 - - - - - -ve -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve30 - - - + - -ve -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve45 - - - + - -ve -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve


Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Non

-Hea

ling

of W

ound

Par

aest

hesi

a

Gen

.Wea

knes

s

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n

S.N

o.

OP

D/IP

D N

o.

Irri

tabi

lity

Bal

aniti

s

Nau

sea

Vom

iting

Dep

ress

ion

Sho

pkee

p e

Dam

vi

Pol

ydip

sia

Occ

upat

ion

Tem

pera

men

t

Day

s

Pol

yuria

Noc

turia

Driv

er

Bal

gham

i Inc

reas

ed T

iredn

ess

Inc

reas

ed A

ppet

ite

Was

ting

of M

uscl

es

-ve

-ve

-ve

Age

in y

ears

-ve

Sex

Bui

lt

F/H

of D

iabe

tes

Mel

litus

-ve

-ve

185

-ve


-ve

8 1354 58 F Obese ─ ve 0 ++ ++ + ++ ++ -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 ++ + + + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve30 + + + + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve45 + + + + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve

9 28745 46 M Average ─ ve 0 - - - + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - - + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

10 30127 48 M Obese ─ ve 0 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - - + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - + -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

11 30415 60 M Average ─ ve 0 - - - + - -ve -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve15 - - - + - -ve -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve30 - - - - + -ve -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve

12 1440 50 F Obese ─ ve 0 + + + + + +ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve +ve15 + - - + + -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 + - - + + -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

13 1449 47 F Obese ─ ve 0 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

14 30099 56 M Average + ve 0 - - - + - -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - - - -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

179

Saf

ravi

Dam

vi D

amvi

Saf

ravi

Bal

gham

i D

amvi

Hou

sew

ife F

arm

er L

and

lord

labo

ur H

ouse

wife


-ve

-ve-ve-ve-ve-ve-ve

Ste

nogr

ap -ve-ve-ve-ve


Hou

sew

ife

Bal

gham

i

Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Non

-Hea

ling

of W

ound

Par

aest

hesi

a

Gen

.Wea

knes

s

Irri

tabi

lity

-ve-ve-ve

Bal

aniti

s

Nau

sea

Vom

iting

Dep

ress

ion

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n

-ve-ve

+ve-ve

-ve-ve-ve-ve

-ve-ve-ve-ve

S.N

o.

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

Occ

upat

ion

Tem

pera

men

t

Day

s

Pol

yuria

F/H

of D

iabe

tes

Mel

litus

OP

D/IP

D N

o.

Age

in y

ears

Sex

Bui

lt

Noc

turia

-ve-ve

Inc

reas

ed A

ppet

ite

Was

ting

of M

uscl

es

22 32627 55 F Obese ─ ve 0 + + - + - -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 + + - + - -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 + + - + - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 + - - + - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

23 1589 52 F Obese + ve 0 - - - + - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

24 32606 48 F Obese + ve 0 ++ + + - + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve15 ++ + - - + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve30 + + - - + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve45 + - - - + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve

25 33310 46 M Average + ve 0 - + + + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 - + + + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve30 - - + + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

26 34531 35 F Obese + ve 0 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve30 - - - - + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve

27 1641 58 F Obese ─ ve 0 - - - + - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

28 1680 42 F Obese ─ ve 0 + + - + - -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 + - - + - -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 + - - - - -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

S.N

o.

Tem

pera

men

t

Day

s

183

-ve-ve

Inc

reas

ed A

ppet

ite

Was

ting

of M

uscl

es

Sex

Bui

lt

F/H

of D

iabe

tes

Mel

litus

OP

D/IP

D N

o.

Age

in y

ears

-ve

Hou

sew

ife

Dam

vi

Gen

.Wea

knes

s

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

Occ

upat

ion

Noc

turia

Pol

yuria

-ve-ve-ve-ve-ve-ve-ve-ve-ve-ve-ve

Irri

tabi

lity

-ve-ve-ve

Bal

aniti

s

Nau

sea

Vom

iting

Dep

ress

ion

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n


Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Non

-Hea

ling

of W

ound

Par

aest

hesi

a

-ve-ve-ve-ve


-ve

-ve-ve-ve-ve-ve-ve

Hou

sew

ifeH

ouse

wife

Sar

ee d

yeH

ouse

wife

Hou

sew

ifeH

ouse

wife

Bal

gham

i D

amvi

Bal

gham

i D

amvi

Bal

gham

i B

algh

ami

1 25748 35 M Obese ─ ve 0 + - + + + +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve15 + - + + + +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve30 + - + + + +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve45 + - + + + +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve

2 26258 48 M Average ─ ve 0 ++ - ++ ++ - +ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 + - + + - +ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 + - ++ + - +ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 + - ++ + - +ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

3 26725 45 M Obese + ve 0 + + - + + -ve -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve15 + - - + + -ve -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve30 + - - + + -ve -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve45 + - - + + -ve -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve

4 28641 50 F Obese ─ ve 0 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve

5 30215 45 M Average ─ ve 0 - - - + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

6 30716 32 F Average + ve 0 - + - + - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve15 - + - + - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - + - + - -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - + - + - -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

7 31343 42 M Average ─ ve 0 - - - - - -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve15 - - - + - -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve +ve30 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve +ve45 - - - + + -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve +ve

187Abr : Mild (+),Modeerate (++), Severe (+++), Absent(-)

-ve-ve

Dam

vi D

amvi

Saf

ravi

Hou

sew

ifeS

hopk

eepe

Bal

gham

i D

amvi

Def

ectiv

e V

isio

n

Ser

vice

Aut

o dr

iver

Hou

sew

ifeS

aree

dye

-ve-ve

Master Chart of Group B (Placebo) - Subjective Parameters

Farm

er

Dam

vi

Wei

ght G

ain

with

out

any

reas

on

Non

-Hea

ling

of W

ound

Par

aest

hesi

a

Gen

.Wea

knes

s

Inc

reas

ed A

ppet

ite

Im

pote

nce

Irri

tabi

lity

+ve +ve +ve

Bal

aniti

s

Nau

sea

Vom

iting

Dep

ress

ion

Pru

ritus

Vul

vae

Pai

n in

Lim

bs-ve-ve

-ve-ve-ve-ve

-ve-ve-ve-ve

-ve-ve-ve-ve

-ve-ve-ve-ve

S.N

o.

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

Occ

upat

ion

Tem

pera

men

t

Day

s

Pol

yuria

OP

D/IP

D N

o.

Noc

turia

-ve-ve

Age

in y

ears

Sex

Bui

lt

F/H

of D

iabe

tes

Mel

litus

Was

ting

of M

uscl

es

+ve

Bal

gham

i

15 1468 57 M Average ─ ve 0 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

16 1496 50 F Thin + ve 0 - + + + + +ve +ve -ve +ve +ve +ve -ve -ve -ve +ve -ve -ve -ve15 - + - + + +ve +ve -ve +ve +ve +ve -ve -ve -ve +ve -ve -ve -ve30 - - - - + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve +ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

17 27944 40 F Obese + ve 0 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

18 30920 40 F Thin + ve 0 - - - + + -ve +ve -ve +ve -ve +ve -ve -ve -ve +ve -ve -ve +ve15 - - - + + -ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - - + -ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve +ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

S.N

o.

Tem

pera

men

t

Day

s

-ve-ve

Inc

reas

ed A

ppet

ite

Was

ting

of M

uscl

es

Sex

Bui

lt

F/H

of D

iabe

tes

Mel

litus

OP

D/IP

D N

o.

Age

in y

ears

-ve

Nil Dam

vi

Gen

.Wea

knes

s

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

Occ

upat

ion

Noc

turia

Pol

yuria

-ve-ve-ve-ve-ve-ve-ve-ve-ve

+ve

Irri

tabi

lity

-ve-ve-ve

Bal

aniti

s

Nau

sea

Vom

iting

Dep

ress

ion

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n


Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Non

-Hea

ling

of W

ound

Par

aest

hesi

a

-ve

Hou

sew

ifeH

ouse

wife

Hou

sew

ife H

ouse

wife

Sau

davi

Bal

gham

i D

amvi

Dam

vi

19 1541 60 F Obese + ve 0 + + - - + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 + + - + + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 + + - - + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 + - - - + -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

+ve-ve-ve-ve

+ve

Hou

sew

ifeH

ouse

wife

Dam

viB

algh

ami20 1495 60 F Obese ─ ve 0 - - - + + -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

15 - - - + + -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve -ve +ve +ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

21 32072 45 M Obese + ve 0 - - - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - - - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve

181

-ve-ve-ve-ve


+ve-ve-ve-ve

loom

wor

kH

ouse

wife

Bal

gham

iBa

lgha

mi

8 30914 43 M Average ─ ve 0 + + - + + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve15 + + - + + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve30 + + - + + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve45 + + - + + -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve

9 31737 36 F Obese + ve 0 + + - + - -ve -ve -ve -ve +ve +ve -ve +ve -ve -ve -ve -ve -ve15 + - - + - -ve -ve -ve -ve +ve +ve -ve +ve -ve -ve -ve -ve -ve30 + - - + - -ve -ve -ve -ve +ve +ve -ve +ve -ve -ve -ve -ve -ve45 + - - + - -ve -ve -ve -ve +ve +ve -ve +ve -ve -ve -ve -ve -ve

10 1576 45 F Average + ve 0 - - - + - -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve30 - - - + + -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve45 - - - + + -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve

11 28896 40 M Average + ve 0 - - - + + -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve +ve30 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve +ve45 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve +ve

12 33697 60 M Thin ─ ve 0 - - - - + -ve +ve -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve15 - - - - + -ve +ve -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve30 - - - - + -ve +ve -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve45 - - - - + -ve +ve -ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve

13 35138 55 F Average + ve 0 - - - - + -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve15 - - - - + +ve -ve +ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve30 - - - + + +ve -ve +ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve45 - - - + + +ve +ve +ve -ve -ve +ve +ve -ve -ve -ve +ve -ve -ve +ve

14 34860 38 M Average + ve 0 + + - + + -ve +ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve15 + + - + + -ve +ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve30 + + + + + -ve +ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve45 + + + + + -ve +ve -ve -ve -ve -ve +ve -ve -ve -ve -ve -ve -ve +ve

189

Saf

ravi

Saf

ravi

Dam

vi S

afra

vi S

afra

vi

Tailo

rLa

bour

Hou

sew

ifeTe

ache

r

-ve


Bus

ines

s

Bal

gham

i Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Irri

tabi

lity

-ve

Vom

iting

Dep

ress

ion

-ve-ve

Bal

aniti

s

Nau

sea

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n

Non

-Hea

ling

of W

ound

Par

aest

hesi

a

-ve-ve-ve-ve

Gen

.Wea

knes

s

Inc

reas

ed A

ppet

ite

Was

ting

of M

uscl

es

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

Occ

upat

ion

Bui

lt

F/H

of D

iabe

tes

Mel

litus

S.N

o.

OP

D/IP

D N

o.

Age

in y

ears

Sex

Noc

turia

Tem

pera

men

t

Day

s

Pol

yuria


Hou

sew

ife

Bal

gham

i

Hou

sew

ife

15 1686 32 M Average + ve 0 + ++ - - + -ve +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve15 + ++ - + + -ve +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve30 + + + + + -ve +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve45 + ++ + + + -ve +ve -ve -ve +ve -ve -ve -ve -ve -ve -ve -ve -ve

16 35200 32 M Average + ve 0 + - - - - +ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve15 + - - - - +ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve30 - - - - - +ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve45 + - - - + +ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve -ve

17 35899 52 M Obese ─ ve 0 - + - + - -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve15 - + - + - -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve30 - + - - - -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve45 - + - + - -ve -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve

18 36284 60 M Average + ve 0 - - - + + -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve30 - - - + + -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve45 - - - + + -ve -ve +ve -ve +ve +ve -ve -ve -ve -ve -ve -ve +ve

19 40143 50 F Obese + ve 0 - + - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve15 - + - + - -ve -ve -ve +ve -ve +ve -ve -ve -ve -ve -ve -ve -ve30 - + - + - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve45 - + - + - -ve -ve -ve +ve +ve +ve -ve -ve -ve -ve -ve -ve +ve

20 43094 38 F Average ─ ve 0 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve15 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve30 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve45 - - - + + -ve -ve -ve -ve +ve +ve -ve -ve -ve -ve -ve -ve -ve

Bui

lt

F/H

of D

iabe

tes

Mel

litus

Noc

turia

S.N

o.

OP

D/IP

D N

o.

Age

in y

ears

Sex

Occ

upat

ion

Tem

pera

men

t

Day

s

Pol

yuria

Gen

.Wea

knes

s

Inc

reas

ed A

ppet

ite

Was

ting

of M

uscl

es

Pol

ydip

sia

Inc

reas

ed T

iredn

ess

-ve-ve-ve

-ve-ve-ve-ve

Irri

tabi

lity

-ve-ve-ve

Bal

aniti

s

Nau

sea

Vom

iting

Dep

ress

ion

Pai

n in

Lim

bs

Def

ectiv

e V

isio

n

-ve


Labo

ur

Saf

ravi

Im

pote

nce

Pru

ritus

Vul

vae

Wei

ght G

ain

with

out

any

reas

on

Non

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ling

of W

ound

Par

aest

hesi

a

Dam

vi D

amvi

-ve

Ser

vice

Sar

ee d

yeB

usin

ess

Hou

sew

ife -ve-ve

Saf

ravi

Dam

vi

-ve

-ve-ve

-ve-ve

-ve

191

Saf

ravi

Hou

sew

ife


-ve-ve-ve-ve

P L E M B

Master Chart of Group A (Safoof Ziabetus) - Objective Parameters

192

Pos

t Pra

ndia

l in

mg/

dl

WNL

308 T

otal

leuc

ocyt

e co

unt

Hae

mog

lobi

n in

gm

%

/ A

fter t

reat

men

t (A

T)

Bef

ore

Trea

tmen

t (B

T)

Urin

e fo

r Sug

ar

Ery

thro

cyte

Sed

imen

tatio

n R

ate

Diff

eren

tial L

euco

cyte

cou

nt

BT 588.5 4200

S

erum

Bilir

ubin

in m

g/dl

Alk

alin

e P

hosp

hata

se in

IU/L

Blo

od U

rea

in m

g/dl

Wei

ght i

n K

g

EC

G

S

GO

T in

IU/L

S

GP

T in

IU/L

Blo

od C

hole

ster

ole

in m

g/dl

Urin

e fo

r Alb

umin

e

Day

s

Ser

um C

reat

inin

e in

mg/

dl

S.N

o.

Blo

od S

u gar

Blo

od S

ugar

fast

ing

inm

g/dl

38 4 0 0 20 17 0.6 0.48 127 22 13 148 Traces 581 0 Traces

15 1.0%30 2.0%45 1.0%

192187313170144 164

WNL

WNL

260

BT 10

308204415

BT

AT

588.5

8.5

4200

4500

6500

38

26

3066

74

4

0

4

0

0

0

0

0

0

20

30

60

17

25

21

0.6

0.6

0.7

0.48

0.59

0.9

127

106

75

22

64

37

13

125

39

148

162

197

Traces

Nil

Nil

58

57

68.52 0 Nil

15 Nil30 Nil45 Nil

144101

164

WNL

WNL

BT

AT

10

10

131138130250166

93

BT

72

12.5 5950

7200 62

44

6500 3066

32

54

4

6

2

0

0

0

0

0

0

60

40

10

21

11

19

0.7

0.6

0.6

0.9

1.2

0.56

75

117

126

37

78

46

39

49

69

197

192

187

Nil

Traces

Traces

68.5

66

533 0 Traces

15 1.0%30 Nil45 0.5% WNL244

WNL

201

250166137 273

290124

113109

BT

AT

BT 11

12.5

12.5

3950

6600

5950

42

54

44 54

44

52

2

2

6

0

0

0

0

0

0

10

10

5

19

21

10

0.6

0.7

0.5

0.56

0.4

0.64

126

143

82

46

27

18

69

29

26

187

193

158

Traces

Traces

Nil

53

51

644 0 Nil

15 Nil30 Nil45 Nil

WNL

WNL

201

138142179

938885

135

113

BT

BT

AT

135 11

13

11

3850

5700

3950

60

48

42 52

50

34

6

2

6

0

0

0

0

0

0

5

30

5

10

13

14

0.5

0.6

0.7

0.64

1

0.71

82

110

65

18

29

28

26

30

19

158

197

143

Nil 64

Nil

Nil

63

625 0 Nil

15 Nil30 Nil45 Nil WNL

WNL

135137376

92239

150

179135BT114 145

AT

BT 12.5

13

13

5050

4900

3850

50

58

60 34

36

46

6

6

4

0

0

0

0

0

0

5

15

15

14

22

10

0.7

0.6

0.5

0.71

0.54

0.86

65

71

64

28

21

25

19

23

18

143

174

205

Nil

51

Nil

Nil

62

606 0 Traces

15 2.0%30 1.0%45 0.5% WNL309

345160186

376197206

239340331

BT 12.5

12

12AT

BT 4850

5700

5050

40

34

50 46

56

54

4

10

4

0

0

2

0

0

0

15

10

10

10

12

17

0.5

0.5

0.6

0.86

0.77

0.56

64

122

126

25

20

18

18

24

14

205

189

272

51

Nil

Traces

Nil

WNL

50.5

547 0 Traces

15 0.5%30 0.5%45 Nil

160164

345186157

Abr : WNL = With in Normal Limit 178

298246251 12AT

12BT

5350

4850

64

40 54

32

4

2

2

2

0

0

10

15

17

15

0.6

0.6

0.56

0.6

126

102

18

20

14

14

272

212 Traces

Traces

WNL

54

53.5

P L E M B


60Traces30067451560.60.6243000256

S.N

o.

Blo

od S

ugar

Blo

od S

ugar

fast

ing

inm

g/dl

Day

s

Blo

od U

rea

in m

g/dl

Ser

um C

reat

inin

e in

mg/

dl

Ery

thro

cyte

Sed

imen

tatio

n R

ate

Tot

al le

ucoc

yte

coun

t

Hae

mog

lobi

n in

gm

%

Wei

ght i

n K

g

EC

G

S

GO

T in

IU/L

S

GP

T in

IU/L

Blo

od C

hole

ster

ole

in m

g/dl

Urin

e fo

r Alb

umin

e

S

erum

Bilir

ubin

in m

g/dl

Alk

alin

e P

hosp

hata

se in

IU/L

6000193

BT219

/ A

fter t

reat

men

t (A

T)

Bef

ore

Trea

tmen

t (B

T)

Urin

e fo

r Sug

ar

WNL

Diff

eren

tial L

euco

cyte

cou

nt

4211

Pos

t Pra

ndia

l in

mg/

dl

8 0 Nil15 Nil30 Nil45 Nil

60

57

67

Traces

Traces

Nil

300

289

194

67

76

25

45

55

27

156

138

89

0.6

0.63

1.2

0.6

0.7

0.6

24

28

19

30

70

20

0

0

0

0

0

0

2

4

2

9200

7250

56

24

48BT

187

13.5 50

7211.5

600019397

101BT

AT

219

WNL

4211

WNL

16714780

142 1989 0 Nil15 Nil30 Nil45 Nil

74

67

66

Nil

Nil

Traces

192

194

188

23

25

24

19

27

16

136

89

143

1.02

1.2

1.53

0.7

0.6

0.6

18

19

14

5

20

15

0

0

0

0

0

0

6

2

250

50

7250 48

444850

4750

BT

AT

13

8475

170

13.5

13 48

50

BT246

WNL

97 156112

WNL

142 198

15210 0 0.5%

15 Traces30 Nil45 Nil

74

73

60

Nil

Traces

Nil

192

197

151

23

23

15

19

27

18

136

109

113

1.02

1.02

0.48

0.7

0.7

0.6

18

20

19

5

5

5

0

0

0

0

1

0

6

4

6

50

38

5242

52

444850

4350

6050

13

13

13

BT290

170BT

AT

1589291

182

246221139137 WNL

WNL

11 0 Traces15 Nil30 Nil45 Nil

78

60

59

Traces

Nil

+ 217

151

160

19

15

21

16

18

30

131

113

150

0.52

0.48

0.6

0.6

0.6

0.7

26

19

22

35

5

5

0

0

0

0

0

0

6

6

658

36

52

36

42

586600

4000

11

12.5

435013BT

AT

187290

108119 163

136196

BT

114143

182

WNL

WNL12 0 Nil

15 Nil30 Nil45 Nil

78

78

67

Traces

Nil

Traces

217

211

260

19

21

45

16

19

71

131

154

81

0.52

0.74

0.66

0.6

0.6

0.7

26

16

22

35

40

25

0

0

0

0

0

0

6

2

4

36

32

5046

66

58660011

6250

5500

12.5

12AT

BT

109196228 BT153132193

6796

101

143

WNL

WNL


62

67

65

Nil

Traces

+ 173

260

218

20

45

30

18

71

34

137

81

142

0.63

0.66

1.3

0.7

0.7

0.6

23

22

20

30

25

10

0

0

0

0

0

0

4

4

438

38

50

58

58

46

4500

4600

625012.5

AT

BT

BT12196

111158

12.5

13

193807598

132

101

WNL

WNL


62

62

Nil

Nil

173

113

20

18

18

36

137

211

0.63

0.56

0.7

0.6

23

16

30

15

0

0

0

0

4

2

38

4652

58

5950

4500BT116121126

158

180

11.5AT

12.5

Abr : WNL = With in Normal Limit

1099094

132

WNL

P L E M B Pos

t Pra

ndia

l in

mg/

dl

WNL

Ery

thro

cyte

Sed

imen

tatio

n R

ate

Tot

al le

ucoc

yte

coun

t

Hae

mog

lobi

n in

gm

%

/ A

fter t

reat

men

t (A

T)

Bef

ore

Trea

tmen

t (B

T)

Urin

e fo

r Sug

ar

Diff

eren

tial L

euco

cyte

cou

nt

173BT 4610.5 7100

S

erum

Bilir

ubin

in m

g/dl

Alk

alin

e P

hosp

hata

se in

IU/L

Blo

od U

rea

in m

g/dl

Ser

um C

reat

inin

e in

mg/

dl

Wei

ght i

n K

g

EC

G

S

GO

T in

IU/L

S

GP

T in

IU/L

Blo

od C

hole

ster

ole

in m

g/dl

Urin

e fo

r Alb

umin

e

Day

s

270

S.N

o.

Blo

od S

ugar

Blo

od S

ugar

fast

ing

inm

g/dl

50 2 2 0 25 11 0.6 1.1 60 46 22322 Nil

Master Chart of Group B (Placebo) - Objective Parameters

681 0 1.0%

15 1.0%30 1.5%45 1.0% WNL

WNL

340351209

121 201

264

11.5

8500

5000

173181230

BT

AT

4610.5

12.5

7100270

BT 62

46

50

52

34

2

2

4

2

0

0

0

0

0

25

20

5

11

11

21

0.6

0.4

0.6

1.1

0.6

0.73

60

64

75

46

23

20 32

223

187

207

22

28

Nil

Traces

Nil

68

69

63.52 0 Nil

15 Nil30 Nil45 0.5% WNL

WNL

121 201

245184

124 239 11.5 5000

BT298

121134174

BT

AT 13.5

14 5700

6900 50

62

44

34

46

54

4

4

2

0

0

0

0

0

0

5

10

5

21

29

9.5

0.6

0.8

0.6

0.73

0.12

0.58

75

63

76

20

22

18

32

26

32

207

230

Nil

Nil

Traces248

63.5

62

743 0 1.5%

15 1.5%30 1.0%45 1.5%

WNL

WNL202

BT

AT112

298261227234168

174192114

BT 11

13

14

7100

7010

5700

52

66

44 54

32

42

2

2

6

0

0

0

0

0

0

5

10

70

9.5

17

10

0.6

0.6

0.5

0.58

0.72

0.41

76

136

64

18

16

21 22

32

19

Traces

Nil

Nil

248

276

132 64

74

724 0 Nil


WNL

108117126165

BT

180214214

112161168

BT

AT

13

11.2

11

4800

6700

7100

58

50

52 42

44

36

6

6

6

0

0

0

0

0

0

70

34

20

10

13

19

0.5

0.5

0.7

0.41

0.5

0.49

64

70

103

21

19

29

22

22

28 169

Nil

140

132 64

Nil

Traces

63

515 0 Nil

15 1.0%30 0.5%45 Traces WNL

WNL

216199104

165231 336

252261210

BT

AT

214

BT 11

12.5

13

7550

4500

4800

66

42

58 36

50

30

6

8

4

0

0

0

0

0

0

20

25

40

19

25

21

0.7

0.9

0.7

0.49

0.44

0.45

103

124

155

29

16

26

19

28

19 230

248

169 Traces

Nil

64 Nil

51

496 0 Nil


104117117101184

58

WNL

40 2257

210

AT

BT

204218199

BT

13

11

11

6750

5020

7550

62

66 30

28

4

5

0

5

0

0

0

0

40

30

5

21

19

12

0.7

0.6

0.6

0.45

0.7

0.79

155

160

122

16

18

19

16

22

248 64

Nil

Nil

Nil

61

59

210

216247 0 Traces

15 1.0%30 2.0%45 0.5%

184260204177

Abr : WNL = With in Normal Limit58

58

WNL

40

38

2257

BT334298258 14AT

13

7680

6750

4

0

0

0

0

5

5

12

24

0.6

0.7

0.79

0.56

122

98

22 Nil

Nil

188

59

58.5

216

42 21336

24

P L E M B


Pos

t Pra

ndia

l in

mg/

dl

/ A

fter t

reat

men

t (A

T)

Bef

ore

Trea

tmen

t (B

T)

Urin

e fo

r Sug

ar

WNL

S

erum

Bilir

ubin

in m

g/dl

Alk

alin

e P

hosp

hata

se in

IU/L

EC

GDiff

eren

tial L

euco

cyte

cou

nt

119BT 5013

2565000

Wei

ght i

n K

g

S

GO

T in

IU/L

S

GP

T in

IU/L

Blo

od C

hole

ster

ole

in m

g/dl

Urin

e fo

r Alb

umin

e

Blo

od U

rea

in m

g/dl

Day

s

Ser

um C

reat

inin

e in

mg/

dl

Ery

thro

cyte

Sed

imen

tatio

n R

ate

Tot

al le

ucoc

yte

coun

t

Hae

mog

lobi

n in

gm

%

S.N

o.

Blo

od S

ugar

Blo

od S

ugar

fast

ing

inm

g/dl

46 4 0 0 10 13 0.5 0.76 154 22 24 189 Nil 578 0 Nil

15 0.5%30 Nil45 Nil

230251139

187 228

WNL

WNL

119123114

BT

AT

5013256

12.5

5000

BT

240

12 44

525050

4750

46

38

56

4

4

0

0

6

0

0

0

0

10

10

20

13

22

25

0.5

0.7

0.7

0.76

0.8

0.48

154

144

120

22

21

22

24

23

20

189

190

239

Nil

Nil

Nil

57

55

669 0 Nil

15 Nil30 1.0%45 Nil

187 228

225

147 171210

WNL

WNL

280

BT

AT

BT

12

11.5 60

44170162170

11 7100

5600

54

4750 56

40

40

0

0

6

0

0

0

0

0

0

20

5

30

25

14

20

0.7

0.5

0.6

0.48

0.64

0.62

120

136

90

22

32

19

20

38

24

239

275

145

Nil

Traces

+

66

66

5710 0 Nil


WNL

151170

280162218267

BT

AT

107122

BT291

17011

7010

5000

13

10.5

7100

44

32

54 40

58

48

6

10

8

0

0

0

0

0

0

30

55

5

20

22

18

0.6

0.9

0.6

0.62

0.7

0.44

90

126

208

19

21

12

24

29

16

145

193

158

+ + Nil

57

56

6011 0 1.5%

15 1.0%30 1.0%45 0.5%

WNL

WNL

170

BT

383399161

208114

185298

BT

AT

342291

12

13

701013

484050

6500 44

44 48

46

48

8

8

2

0

2

2

0

0

0

5

7

20

18

16

19

0.6

0.6

1.1

0.44

0.5

0.8

208

176

180

12

14

16

16

18

22

158

160

240

Nil

Nil

60

59.5

Nil 5112 0 Nil

15 Nil30 Nil45 Nil

WNL

WNL80

101144

145161194

195 BT161114

110

AT

BT 5700

5000

11

12

12

50

52

484050 48

46

48

2

2

2

2

0

0

0

0

0

20

30

25

19

24

21

1.1

0.8

0.9

0.8

0.48

0.73

180

118

111

16

23

18

22

26

40

240

145

225 Nil

Nil 51

51

58

Traces13 0 Nil

15 Nil30 2.0%45 0.5% WNL

WNL

267

144 194149210228 293

369

196287

BT

14

11.5AT

BT 5600

6000

570011

52

56

50

42

46

48

2

2

2

0

0

0

0

0

0

5

25

20

17

21

19

0.6

0.9

0.7

0.82

0.73

1.03

134

111

110

16

18

30

10

40

34

177

225

241

Nil

Nil

Nil 54

58

5914 0 2.0%

15 Traces30 0.5%45 0.5% WNL

267

Abr : WNL = With in Normal Limit

247223252

369287369423

190

13.5AT

14BT

6000

5600

56

52 46

44

2

0

0

0

0

0

5

10

17

13

0.6

0.6

0.82

0.75

134

141

16

16

10

20

177

164

Nil

Traces

54

54

P L E M B


62 Nil2261421610.670.7298000432

S.N

o.

Blo

od S

ugar

Blo

od S

ugar

fast

ing

inm

g/dl

Day

s

Pos

t Pra

ndia

l in

mg/

dl

302

Wei

ght i

n K

g

EC

G

S

GO

T in

IU/L

S

GP

T in

IU/L

Blo

od C

hole

ster

ole

in m

g/dl

Urin

e fo

r Alb

umin

e

Alk

alin

e P

hosp

hata

se in

IU/L

Blo

od U

rea

in m

g/dl

Ser

um C

reat

inin

e in

mg/

dl

S

erum

Bilir

ubin

in m

g/dl

WNL

Bef

ore

Trea

tmen

t (B

T)

Ery

thro

cyte

Sed

imen

tatio

n R

ate

Diff

eren

tial L

euco

cyte

cou

nt

188BT

Tot

al le

ucoc

yte

coun

t

Hae

mog

lobi

n in

gm

%

/ A

fter t

reat

men

t (A

T)

6412.5 4800

Urin

e fo

r Sug

ar

15 0 Traces15 Nil30 0.5%45 0.5%

62

60.5

51

Nil

Nil

Traces

226

224

267

14

29

18

21

26

20

61

98

62

0.67

0.77

0.49

0.7

1.4

0.8

29

43

29

80

45

20

0

0

0

0

0

2

4

2

8

32

52

5832

46

BT

246302

WNL

WNL

188113119

BT

AT

6412.5

12

4800

11.5

8500

4250

227192109

274 38316 0 1.0%15 0.5%30 Nil45 0.5%

66 Nil

51

50

Traces

Nil

267

187

179

18

18

19

20

22

21

62

65

121

0.49

0.6

0.57

0.8

0.7

0.6

29

22

14

20

35

40

0

0

0

2

0

0

8

10

2

46

38

5832

44

604400

BT

AT109157119

207 259179

BT 10.5

WNL

WNL

11.5

12 4560

4250

162

274 383

19717 0 Nil

15 Nil30 Nil45 Nil

66

65

47

Nil

Nil

Traces

179

160

206

19

10

31

21

28

23

121

130

76

0.57

0.59

0.68

0.6

0.6

0.5

14

12

22

40

25

30

0

0

0

0

0

0

2

2

8

38

40

467150 46

58

60

4000

4400

BT307

11910699

BT

AT106203

13

11.5

10.5

WNL

WNL

162247154148

18 0 1.0%15 Nil30 Nil45 Nil 46.5

76

47

Nil

Traces

212 + 209

206

84

18

31

73

25

23

79

145

76

0.68

0.6

0.68

0.6

0.6

0.5

16

19

22

10

20

30

0

0

0

0

2

0

8

6

8

40

42

46

50

6400

7150

52

46

520012

BT

AT

159307

141176295

BT

20373

10084

18211.5

13

WNL

WNL

19 0 Traces15 Nil30 1.0%45 0.5%

76

75

68

215

295

212

Traces

Nil

+ 18

18

20

25

23

22

145

173

96

0.6

0.54

0.62

0.6

0.6

0.6

19

17

12

20

10

35

0

0

0

2

0

0

6

0

4

42

42

30

58

50

667200

5600

5200

11.5

11.5

12295

BT

BT

AT

196238216148125

182122

WNL

WNL

170137

20 0 Nil15 Nil30 Nil45 Nil 67

72

68

Nil

Nil239

295 Nil

21324

26

20

26

24

22

105

162

96

0.6

0.58

0.62

0.6

0.5

0.6

16

14

12

20

10

35

0

0

0

0

2

0

4

4

4

44

32

30

62

52

66

5200

7200

12

11.5148154

BT

AT

BT

130296

148

13 6000

11494

103202

125

WNL

WNL21 0 0.5%

15 1.0%30 Nil45 Nil

72

71

Nil239

Nil

26

32

24

29

162

130

0.58

0.8

0.5

0.6

14

19

10

5

0

0

2

0

4

2

32

6038

62210170162

BT296

1067495

Abr : WNL = With in Normal Limit12.5AT

13

4900

6000

235

202

WNL

182

P L E M B


Pos

t Pra

ndia

l in

mg/

dl

WNL

Ery

thro

cyte

Sed

imen

tatio

n R

ate

Tot

al le

ucoc

yte

coun

t

Hae

mog

lobi

n in

gm

%

/ A

fter t

reat

men

t (A

T)

Bef

ore

Trea

tmen

t (B

T)

Urin

e fo

r Sug

ar

Diff

eren

tial L

euco

cyte

cou

nt

119BT 6611.5 5800

Alk

alin

e P

hosp

hata

se in

IU/L

Blo

od U

rea

in m

g/dl

Ser

um C

reat

inin

e in

mg/

dl

S

erum

Bilir

ubin

in m

g/dl

S

GO

T in

IU/L

S

GP

T in

IU/L

Blo

od C

hole

ster

ole

in m

g/dl

Urin

e fo

r Alb

umin

e

Day

s

211

S.N

o.

Blo

od S

ugar

Blo

od S

ugar

fast

ing

inm

g/dl

34 0 0 0 25 24 0.8 0.68 180 23 21 221 Nil 64

Wei

ght i

n K

g

EC

G

22 0 Nil15 Nil30 Nil45 Nil WNL

WNL

14814312378

113 180

11910298

BT

AT

6611.5

12.5

5800

11.5BT

211

5500

6400

34

38

3660

54

0

6

4

0

2

0

0

0

0

25

9

35

24

21

16

0.8

1.17

0.6

0.68

0.32

0.64

180

86.8

96

23

27.2

27

21

30.9

24

221

205

122

Nil

Nil

Traces

64

63.5

6123 0 Nil


WNL

95113 180

139143146

BT 12

11.5

10 66

BT

AT 6280261

9174

20164

6400

6150

3660

22

32

4

12

4

0

0

0

0

0

0

35

50

30

16

26

18

0.6

0.6

0.6

0.64

0.61

0.71

96

92

119

27

18

34

24

22

47

122

120

113

Traces

Traces

+

61

60

6324 0 0.5%

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Hamid Ali.pdf

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