RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE,
KARNATAKA
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
BANGALORE, KARNATAKA
SYNOPSIS
OF
DISSERTATION
" STUDY OF LIPID PROFILE IN
TYPE 2 DIABETES MELLITUS
IN A.I.M.S , RURAL SETUP-
A COMPARATIVE STUDY"
Submitted by
Dr. MITHUN SOMAIAH C.S. M.B.B.S
POST GRADUATE
GENERAL MEDICINE (M.D)
Under the guidance of
Dr. SHASHIKANTHA M.B.B.S M.D
PROFESSOR
DEPARTMENT OF GENERAL MEDICINE
DEPARTMENT OF GENERAL MEDICINE
ADICHUNCHANAGIRI INSTITUTE OF MEDICAL SCIENCES,
B.G.NAGARA-571448
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
1
NAME OF THE CANDIDATE
AND ADDRESS
(in block letters)
Dr. MITHUN SOMAIAH C.S.
P.G (GENERAL MEDICINE)
ADICHUNCHUNAGIRI INSTITUTE OF
MEDICAL SCIENCES.B.G NAGARA,
MANDYA DISTRICT -571448
2.
NAME OF THE INSTITUTION
ADICHUNCHANAGIRI INSTITUTE OF
MEDICAL SCIENCES, B.G.NAGARA.
3.
COURSE OF STUDY AND SUBJECT
M.D. ( GENERAL MEDICINE)
4.
DATE OF ADMISSION TO COURSE
24th May, 2010
5.
TITLE OF THE TOPIC
" STUDY OF LIPID PROFILE IN
TYPE 2 DM IN A.I.M.S RURAL SETUP-
A COMPARATIVE STUDY”
6.
BRIEF RESUME OF INTENDED WORK
6.1 NEED FOR THE STUDY
6.2 REVIEW OF LITERATURE
6.3 OBJECTIVES OF THE STUDY
APPENDIX-I
APPENDIX-IA
APPENDIX-IB
APPENDIX-IC
7
MATERIALS AND METHODS
7.1 SOURCE OF DATA
7.2 METHOD OF COLLECTION OF DATA : (INCLUDING SAMPLING PROCEDURE
IF ANY)
7.3 DOES THE STUDY REQUIRE ANY INVESTIGATION OR INTERVENTIONS TO
BE CONDUCTED ON PATIENTS OR OTHER ANIMALS, IF SO PLEASE DESCRIBE
BRIEFLY.
7.4 HAS ETHICAL CLEARENCE BEEN OBTAINED FROM YOUR INSTITUTION IN
CASE OF 7.3
APPENDIX-II
APPENDIX-IIA
APPENDIX-IIB
YES
APPENDIX-IIC
YES
8.
LIST OF REFERENCES
APPENDIX – III
9.
SIGNATURE OF THE CANDIDATE
10.
REMARKS OF THE GUIDE
WITH THE RISING NUMBER OF DIABETICS IN INDIA, THE FOLLOW UP OF
LIPID PROFILE HAS CERTAINLY EMERGED AS AN IMPORTANT PROGNOSTICATION
TOOL TO ASSESS CARDIOVASCULAR RISK FACTORS IN THESE PATIENTS SO AS
TO REDUCE MOBIDITY AND MORTALITY IN THEM. HENCE THE STUDY WILL GIVE
US AN INSIGHT INTO RISK STRATIFICATION WHICH CAN BE CORELATED WITH
THE ALTERATIONS IN LIPID PROFILE
11
NAME AND DESIGNATION
(in Block Letters)
11.1 GUIDE
Dr. SHASHIKANTHA . M.B.B.S, M.D
PROFESSOR,
DEPARTMENT OF GENERAL MEDICINE
AIMS, B.G. NAGARA-571448
11.2 SIGNATURE OF THE GUIDE
11.3 CO-GUIDE (IF ANY)
-
11.4 SIGNATURE
-
11.5 HEAD OF DEPARTMENT
Dr JAGANNATHA. K M.B.B.S,M.D
PROFESSOR and HOD
DEPARTMENT OF GENERAL MEDICINE
AIMS, B.G. Nagara-571448
11.6 SIGNATURE
12
12.1 REMARKS OF THE CHAIRMAN
AND PRINCIPAL
12.2 SIGNATURE
APPENDIX-I
6 . BRIEF RESUME OF THE INTENDED WORK:
APPENDIX –I A
6.1. NEED FOR THE STUDY:
Diabetes as a metabolic disorder is rising at an alarming rate
all over the world and has
been a reason for concern due to the complications associated
with it . With India having
the highest number of diabetic patients in the world, the sugar
disease is posing an
enormous health problem in the country. Calling India the
diabetes capital of the
world, the International Journal of Diabetes in Developing
Countries says that there
is alarming rise in prevalence.
The International Diabetes Federation estimates that the number
of diabetic
patients in India more than doubled from 19 million in 1995 to
40.9 million in 2007.
It is projected to increase to 69.9 million by 2025. Currently,
up to 11 per cent
of India’s urban population and 3 per cent of rural population
above the age of 15
have diabetes. Diabetes affects all people in the society, not
just those who live with
it. The World Health Organization estimates that mortality from
diabetes and heart
disease cost India about $210 billion every year and is expected
to increase to $335
billion in the next ten years. These estimates are based on lost
productivity, resulting
primarily from premature death.
Various studies have shown that the high incidence of diabetes
in India is
mainly because of sedentary lifestyle, lack of physical
activity, obesity, stress and
consumption of diets rich in fat, sugar and calories.
Dyslipidemia is commonly seen in diabetes. Type 2 diabetes
mellitus is one of
the most common secondary cause of hyperlipidemia.The
relationship between
hyperlipidemia and vascular complication of diabetes has long
been of interest
because both tend to occur with greater frequency in type 2
diabetes mellitus. Insulin
resistance and obesity combine to cause dyslipidemia.and
hyperglycemia and
hyperlipidemia has additive cardiovascular risk..
Diabetes,particularly type 2 diabetics
have higher lipid levels than non-diabetics and those patients
with poor diabetic
control exaggerate this11.
.
There are several reasons for this association. Firstly, insulin
plays an important role in
the regulation of intermediary lipid metabolism (Nikkila, E.A,
1974) and fluctuations in the
degree of diabetic control thus produce a variable effect on
plasma lipoprotein metabolism.
Secondly, many non-insulin dependent diabetic patients are
obese, and obesity leads to the
development of hyperlipidemia(Bierman, E.L1968). Thirdly
,although diabetes and
hyperlipidemia represent different genetic disorders, each of
these disorders is common in the
population and the two disorders may co-exist by chance in
thesame individual (Brunzell, J.D 1975).
Hence identification, critical evaluation, follow up of serum
lipid profile in type 2
diabetes mellitus continue to be important and help in the
prognostication of
cardiovascular risk.
APPENDIX –I B
6.2 REVIEW OF LITERATURE
HISTORY AND REVIEW OF LITERATURE
Diabetes mellitus is a group of metabolic diseases in which a
person has high blood
sugar, either because the body does not produce enough insulin,
or because cells do not
respond to the insulin that is produced resulting in polyuria(
frequent urination), polydipsia
(increased thirst) and polyphagia( increased hunger).
The term diabetes was coined by Aretaeus of Cappadocia. It was
derived from the
Greek verb, itself formed from the prefix dia-, "across, apart,"
and the verb bainein, "to walk,
stand." The verb diabeinein meant "to stride, walk, or stand
with legs asunder"; hence, its
derivative diabētēs meant "one that straddles," or specifically
"a compass, siphon." The sense
"siphon" gave rise to the use of diabētēs as the name for a
disease involving the discharge of
excessive amounts of urine. Diabetes is first recorded in
English, in the form diabete, in a
medical text written around 1425. In 1675, Thomas Willis added
the word mellitus, from the
Latin meaning "honey", a reference to the sweet taste of the
urine. This sweet taste had been
noticed in urine by the ancient Greeks, Chinese, Egyptians,
Indians, and Persians. In 1776,
Matthew Dobson confirmed that the sweet taste was because of an
excess of a kind of sugar in
the urine and blood of people with diabetes.
Sushruta (6th century BCE) identified diabetes and classified it
as Medhumeha. He
further identified it with obesity and sedentary lifestyle,
advising exercises to help "cure" it.
The ancient Indians tested for diabetes by observing whether
ants were attracted to a person's
urine, and called the ailment "sweet urine disease" (Madhumeha).
The Chinese, Japanese and
Korean words for diabetes are based on the same ideographs which
mean "sugar urine
disease".
Medicine first recognized the existence of abnormal fatty
content of the
circulating blood through the milky appearance observed during
the days when blood
letting was widely practiced. The term lipemia was formulated by
Babington in the 18th
century, when he showed that fats were responsible for giving
this milky appearance
to the serum.The presence of lactescent serum with diabetes was
first noted by Mariet
in 1799 and in 1958 by Thannhauser.S.J.
Owing to lack of research facilities no further advance was made
till the
beginning of the 20th century. The deficiency in knowledge was
made evident in 1903
when Fischer reviewed the subject. He listed all the conditions
where doctors had
earlier observed milky appearance of blood. These included
apoplexy, peritonitis,
malaria, jaundice, leprosy, etc. He finally retained diabetes
and alcoholic lipaemia as
being genuine. In the years that followed data accumulated about
hyperlipemia
accompanying diabetes. Man and Peters (1935) found that
triglyceride was the
primary lipid to be elevated. Harries et al (1952) found
elevations of serum lipid levels
in diabetic acidosis.
More recently, Chaturvedi et al1(2001) found elevation in
triglyceride rich VLDL
to be a common abnormality. In a study of Lowy A.D et al (1957)
found a significant
increase in the incidence of hyperlipidemia in association with
poor diabetic control.
In a study of the significance of blood lipid alterations in
diabetes mellitus,
Mazzone,T et al (2000) 2 measured plasma triglyceride and
cholesterol levels in a
large series of diabetic and non-diabetic subjects of all ages.
Their results showed that
plasma triglycerides increase with age in diabetics but not in
nondiabetics, while
cholesterol levels increase with age in both groups.
Bagdade et.al. (1967) 3 studied five patients with chronic
symptomatic diabetes
and minimal ketoacidosis who had marked hyperlipidemia and
concluded that diabetic
lipemia can be considered to be a reversible form of dietary fat
induced lipemia
secondary to chronic insulin deficiency.
Nikkila EA and Hormila P (1978) 4, concluded that the average
serum lipid and
lipoprotein pattern of insulin treated chronic diabetic patients
was not_more
atherogenic than non-diabetic subjects of similar age and sex.
On the contrary the
increase in HDLc levels which they found, should make them less
liable to develop
coronary heart disease. Thus they felt that the increased
incidence of cardiovascular
disease in type II diabetes must be accounted for by some other
factors.
Chance et.al. (1969)5 studied serum lipids and lipoproteins in
135 diabetic
children prior to treatment and found elevated serum total
lipids in 64% of the patients
and elevated cholesterol in 43%. Abnormal lipoprotein patterns
were found in 77%, the
commonest anomaly being increase in pre P-lipoprotein.
Strisower E H et al (1958)6 found significant increase in serum
cholesterol, LDL
and VLDL values in poorly controlled insulin treated diabetics,
which returned to
normal on achieving rigid control
Dewind et. al. (1952) carried out studies in patients with
advanced diabetic
atherosclerosis and found no obvious correlation between any of
the lipid fractions
although the mean serum cholesterol values were significantly
higher in diabetics than
in non-diabetic elderly controls.
Hokanson JE, et al (1996) 7 stated that plasma triglyceride is
an independent
risk factor for the development of cardiovascular disease.
Sharma D et.al. (1970)8 studied serum lipid profile in type 2I
diabetic patients
below 40 years of age and found significant elevations in the
level of serum
cholesterol, phospholipids, esterified fatty acids and
triglyceride as compared to a
control group.
In the study of Barr et al (1951) HDL concentrations were
Strikingly reduced
in some atherosclerotic diabetic patients. In a recent Study of
HDLc in diabetics by
P.K.Bijlani et.al. (1983), it was found that the HDLc values in
diabetics and subjects
with impaired glucose tolerance were significantly lower than
normal controls. Females
in all groups had higher HDLc than males. Higher HDLc values
were also observed in
diabetics on insulin therapy and with better glycemic
control.
V.J. Retnam et al (1983) 9 reported hyperlipoproteinemia in a
study of 152
adult diabetics on treatment. They found that 20 out of 70
controlled patients and 48
of 82 uncontrolled patients had hyperlipoproteinemia.
Over the past years there has been increasing awareness on the
part of the
physicians and general population of the potential benefits of
detecting and treating
hypercholesterolemia. This is particularly important in
diabetics for two reasons:
1.There already is an increased risk of premature coronary heart
disease
In patients with diabetes independent of raised plasma
cholesterol levels.
2.Alterations in plasma lipoprotein metabolism are common in
diabetes
as they tend to exaggerate any pre-existing tendencies towards
elevated lipid levels.
The new recommendations by the National Cholesterol Education
Program
have provided guidelines for practicing physicians in treatment
of
hypercholesterolemia. These guidelines can be easily applied to
patients with diabetes
and optimal. care of diabetic patients require that these
recommendations be followed.
However it is also important to understand the effect of
diabetes on lipoprotein
metabolism,because in many cases it may be more appropriate to
make a change in
diabetic treatment rather than treat the hyperlipidemia.
DYSLIPIDEMIA AND DIABETES
Dyslipidemia is a relatively common problem in patients with
poorly
controlled diabetes mellitus. It has been estimated that the
frequency of elevated
plasma lipid levels in diabetic patients is between 20 and 90 %.
(Billimoria, J.D 1976,
Chance.G.W 1969, Chase. H.P 1976) 5 . Diabetes,particularly type
2 diabetics have
higher lipid levels than non-diabetics and those patients with
poor diabetic control
exaggerate this. There are several reasons for this
association.
Firstly, insulin plays an important role in the regulation of
intermediary lipid
metabolism (Nikkila, E.A, 1974) and fluctuations in the degree
of diabetic control thus
produce a variable effect on plasma lipoprotein metabolism.
Secondly, many non-insulin dependent diabetic patients are
obese, and obesity
leads to the development of hyperlipidemia(Bierman, E.L1968).
Third,although
diabetes and hyperlipidemia represent different genetic
disorders, each of these
disorders is common in the population and the two disorders may
co-exist by chance
in the same individual (Brunzell, J.D 1975).
TYPE 2 DIABETES AND ITS EFFECT ON LIPID PROFILE
The most common abnormality in type-2 diabetes is
hypertriglyceridemia
caused by increase in VLDL. The effect of type-2 diabetes on TG
is moderate and
increases in plasma TO >500 mg/dl is caused by the
coexistence of a genetic form of
hypertriglyceridmeia aggravated by the hyperglycemia.
Type-2 diabetes causes both overproduction and impaired
clearance of
VLDL triglyceride. The mechanism of overproduction of VLDL - TG
most likely is
because of increased flow of glucose and free fatty acids to the
liver. The removal
defect is caused by impaired lipoprotein lipase activity, but is
minimal except in poorly
controlled type-2 diabetes. VLDL overproduction and lipoprotein
lipase levels can be
controlled with normalization of glucose levels .
There is also increased production of VLDL apoprotein -B which
may be
related to obesity.
Plasma LDLc in type-2 diabetes is increased because of
decreased
clearance of LDL.In some individuals with type-2 diabetes, LDL
production is low
because of impaired conversion of VLDL to LDL. These patients
have normal LDL
levels but increased levels of VLDL.
HDLc in type-2 diabetes is consistently low, especially HDL2.
Studies have
shown that an inverse relation between HDLc and arterial disease
is present. They
increase with diabetic treatment, but often remain low. The
mechanism appears to be
both increased catabolism and reduced production,the former
being related to
increased hepatic lipase activity. Insulin is more effective
than sulphonylureas in
raising HDLc levels.
HYPERLIPIDEMIC SYNDROMES ASSOCIATED WITH DIABETES
& CHYLOMICRONEMIA SYNDROME IN DIABETES
Diabetic lipemia is a rare but well recognized manifestation of
uncontrolled
diabetes. It is characterized by the development of gross
lipemia caused by
accumulation of chylomicrons and VLDL in patients with chronic
hyperglycemia.
Usually patients develop eruptive xanthomas, lipemia retinalis,
chronic abdominal pain
or pancreatitis. The lipemia corrects with insulin treatment and
is thought to be caused
by decreased lipoprotein lipase activity secondary to insulin
deficiency.
In many individuals with type-2 diabetes, insulin treatment
ameliorates the
severe hypertriglyceridemia but does not return plasma lipid
values to normal; these
individuals often have hypertriglyceridemic relatives,
suggesting the coexistence of a
familial form of hypertriglyceridemia. For this group of
patients the term
"chylomicronemia syndrome" 10 is used, which describes
development of
hypertriglyceridemia resulting from the interaction of genetic
and secondary forms of
hyperlipidemia.
Studies of triglyceride metabolism in patients with type-2
diabetes and
hypertriglyceridemia show both overproduction and impaired
clearance of VLDL and
triglycerides. Both improve with treatment, but do not
necessarily return to normal.
These patients appear to have abnormality of lipoprotein
metabolism, which is
aggravated by poorly controlled diabetes. They require
lipid-lowering therapy along
with treatment for diabetes.
PRIMARY DIABETES AND SECONDARY HYPERLIPIDEMIA
This is frequently seen during poor diabetic control and is
characterized by mild
to moderate hyperlipidemia. Most of these patients rarely
develop increases in TG
>500mg\dl and often only mild to moderate
hypercholesterolemia, both of which return
to normal levels after treatment with insulin or oral
hypoglycemic drugs.
Occasionally patients develop secondary hypercholesterolemia
alone, even with
good diabetic control because of carbohydrate restricted and
high fat diet which was
prescribed earlier change in diet to more prudent fat or low
cholesterol approach often
controls this secondary hyperchoIesterolemia (American Diabetes
Association). 11 This
group of patients represents a primary from of diabetes and a
secondary form of
hyperlipidemia due to either poor diabetic control,primarily
affecting the triglycerides or
high fat diet.
PRIMARY HYPERLIPIDEMIA AND SECONDARY GLUCOSE INTOLERANCE
An increased incidence of abnormal glucose tolerance has been
reported in
individuals with various primary forms of hyperlipidemia
(Glueck, C.J1969).
One reason for this maybe that obesity is common in patients
with_primary form of
hyperlipidemia and this may also result in glucose intolerance
(Bierman, E.L1968).
A second reason may be related to the fact that insulin
resistance is often observed in
patients with endogenous onset of hypertriglyceridemia
(Steiner.G 1981, Olefsky, J.M
1974)12 and this may increase the likelihood of developing
glucose intolerance and/or
overt diabetes.
The clinical significance of this association is that treatment
of hyperlipidemia
frequently results in amelioration of glucose intolerance. Thus
primary emphasis in the
treatment of this group of patients should be directed towards
treatment of
hyperlipidemia and they do not require specific treatment for
diabetes.
PRIMARY DIABETES MELLITUS AND PRIMARY HYPERLIPIDEMIA
The association of primary forms of diabetes mellitus and
hyperlipidemia is
greater than would be expected by chance alone. Brunzell et al
(1975) studied the
frequency of diabetes in adults, first degree relatives of
patients with familial forms of
hypertriglyceridemia. In the families with both familial
hypertriglyceridemia and
diabetes, diabetes occurred with equal frequency in normolipemic
and hyperlipemic
relatives.
Similar findings were found in families of individuals with
only
hypertriglyceridemia, but in them the overall frequency of
diabetes in the relatives
were much lower. These findings suggested diabetes is frequently
associated with
hypertriglyceridemia. Genetic hypertriglyceridemia does not
carry an increased risk of
diabetes. Thus diabetes and genetic forms of
hypertriglyceridemia appear to be
independent entities which may happen to coexist by chance in
the same individllal.
These investigators further evaluated diabetic patients with
either familial forms
or sporadic forms of hypertriglyceridemia with regard to their
response to diabetic
treatment. They observed that the triglyceride levels before
treatment were much
higher in patients with a coexistent familial form of
hypertriglyceridemia compared to
those with sporadic forms.
CLINICAL FEATURES
The most common hyperlipidemia in diabetes is
hypertriglyceridemia which is
characterized by increased VLDL-TG.
Fasting plasma triglyceride is in the range of 200 -800 mg/dl.
The plasma is
opalescent on inspection if Tg concentration is more than 300
mg%.
At times there is associated fasting chylomicronemia, usually
increasing fasting
plasma TG to more than 1000mg%. The plasma becomes more
opalescent with a
layer of chylomicrons floating on the top of the plasma.
The clinical signs and symptoms of hypertriglyceridemia are as
follows:
Signs:
Eruptive xanthomas
Hepatosplenomegaly
Hyperuricemia
Sjogren-like syndrome
Symptoms:
• Abdominal pain (mostly due to pancreatitis )
• Arthralgia
• Peripheral neuropathy
Although these manifestations are said to occur with increased
VLDL alone,
they are ordinarily seen with chylomicronemia.
The characteristic skin lesions are eruptive xanthomas which are
small, firm,
non-tender papules with a yellow tip on an erythematous base,
erupting over a
period of several weeks. When hypertriglyceridemia is severe and
diabetes is in poor
control, they are usually seen on the buttocks and extensor
surface of the
extremeties.They rarely involve the face and resolve in months
if hypertriglyceridemia
is controlled.
Xanthelasma is a distinctive type of xanthoma that occurs on
eyelids. They
begin as small yellow macules that thicken to form oval foamy
plaques.
Lipemia retinalis is blanching of retinal arteries and
veins.
Treatment of diabetic dyslipidemia in adults is as follows:
LDLc lowering
· First choice-HMG CoA reductase inhibitors
· Second choice- Bile-acid binding resin
VLDLc lowering
- Behavorial changes such as weight loss, increased physical
activity and smoking cessation.
- Nicotinic acid or fibrates
Triglyceride lowering
· Glycemic control first prioirty
· Fibric acid derivatives (gemfibrozil, fenofibrate)
Statins
COMBINED HYPERLIPIDEMIA-
FIRST CHOICE
· Improved glycemic control plus high dose statins
SECOND CHOICE
· Improved glycemic control plus statins, fibric acid
derivative
THIRD CHOICE
· Improved glycemic control plus statins, nicotinic acid
· Improved glycemic control plus resin plus fibric acid
derivative
· Estrogen should be the first line of therapy in post
menopausal women with high cholestrol levels.Estrogens decrease
LDLc levels and raise HDLc levels,but also increase triglyceride
levels
APPENDIX –IC
6.3 AIMS AND OBJECTIVES OF STUDY:
TO STUDY THE LIPID PROFILE IN PATIENTS OF
TYPE-2 DIABETES MELLITUS IN A.I.M.S , RURAL SETUP
AS A CASE-CONTROL STUDY.
APPENDIX-II
7.0 MATERIALS AND METHODS
APPENDIX-II A
7.1 SOURCE OF DATA
Study Design : A COMPARATIVE study
Study Period
: 24 months (November 2010 to November 2012)
Source of Data:
The subjects for the study are selected from patients who were
admitted to
Sri .Adichunchanagiri Research centre and Hospital, B.G.Nagar,
Nagamangla taluk, Mandya
attached to the Sri.Adichunchanagiri institute of medical
sciences,B.G.Nagara, Mandya.
APPENDIX- II B
7.2 METHOD OF COLLECTION OF DATA
SAMPLE SIZE : TOTAL: 100
CASE: 50
CONTROL: 50
INCLUSION CRITERIA:
1) Patients with Type 2 diabetes mellitus
2) Duration of Diabetes more than 4 years.
.
EXCLUSION CRITERIA
1) Type -2 diabetes patients with concomittant diseases or
condition effecting the lipid levels liken hypothyrodism, on
lipostatic drugs, thiazides etc.
2) Type-1 DM patients
METHODOLOGY:
- A detailed history, careful physical examination,
- Routine Blood & Urine examination.
- Biochemical analysis for Fasting blood sugar, post prandial
blood sugar.
- Fasting lipid profile
Serum Triglycerides
Total Cholesterol
HDLc , LDLc, VLDLc
APPENDIX – II C 7.3 Does the study require any investigation or
intervention to be conducted on the patients or animals , if so
please describe briefly
YES
Investigation :
Blood sampling and preparation of serum.
The blood samples will be drawn in the fasting state. The
venepuncture will be done
in the cubital fossa. Torniquet shall be used but will be
released just before sampling to
avoid artificial increase in the concentration of serum lipids.
About 10 ml of blood will be
drawn using perfectly dry and sterile syringes and the blood
shall be transferred to dried
glass vials.
Serum has to be seperated within 2 hrs of collection to prevent
artifical changes in
concentration of HDL. The blood has to be centrifuged at 5000
rpm for 10 minutes. The
supernatant clean serum will then be pipetted out using dry
piston pipettes with
disposable tips and stored in dry thin walled vials . The
samples shall be analysed
the same day. Care shall be taken to exclude the haemolysed
serum.
Laboratory procedure:
1.Estimation of Total cholesterol
Method - CHOD - DAP method
Principle - Enzymatic estimation
2.Estimation of Total Triglycerides
Method: GPO - DAP method
3.Estimation of HDL cholesterol
Principle: Enzymatic estimation
APPENDIX-II D
PROFORMA APPLICATION FOR ETHICS COMMITTEE APPROVAL
SECTION A
A
Title of the study
“STUDY OF LIPID PROFILE IN
TYPE-2 DM IN A.I.M.S, RURAL SETUP- A COMPARATIVE STUDY”
B
Principle investigator
(Name and Designation)
Dr. MITHUN SOMAIAH
P.G. (GENERAL MEDICINE),
ADICHUNCHUNAGIRI INSTITUTE OF
MEDICAL SCIENCES.B.G NAGARA,
MANDYA DISTRICT -571448
C
Co-investigator
(Name and Designation)
Dr.SHASHIKANTHA.
Professor
Department of GENERAL MEDICINE
AIMS, B.G. Nagara-571448
D
Name of the Collaborating
Department/Institutions
DEPT OF BIOCHEMISTRY
e
Whether permission has been obtained from the heads of the
collaborating departments & Institution
YES
Section – B
Summary of the Project
APPENDIX – I
Section – C
Objectives of the study
APPENDIX – I
Section – D
Methodology
APPENDIX – II
A
Where the proposed study will be undertaken
DEPARTMENT OF GENERAL MEDICINE.,
S.A.H. & R.C., B.G.NAGARA
B
Duration of the Project
24 MONTHS
C
Nature of the subjects:
Does the study involve adult patients?
Does the study involve Children?
Does the study involve normal volunteers?
Does the study involve Psychiatric patients?
Does the study involve pregnant women?
YES
NO
NO
NO
NO
D
If the study involves health volunteers
I. Will they be institute students?
II. Will they be institute employees?
III. Will they be Paid?
IV. If they are to be paid, how much per session?
NO
NO
NO
NO
E
Is the study a part of multi central trial?
NO
F
If yes, who is the coordinator?
(Name and Designation)
Has the trail been approved by the ethics Committee of the other
centers?
If the study involves the use of drugs please indicate
whether.
I. The drug is marketed in India for the indication in which it
will be used in the study.
II. The drug is marketed in India but not for the indication in
which it will be used in the study
III. The drug is only used for experimental use in humans.
IV. Clearance of the drugs controller of India has been obtained
for:
· Use of the drug in healthy volunteers
· Use of the drug in-patients for a new indication.
· Phase one and two clinical trials
· Experimental use in-patients and healthy volunteers.
NA
NA
-
NA
NA
NA
NA
NA
G
How do you propose to obtain the drug to be used in the
study?
· Gift from a drug company
· Hospital supplies
· Patients will be asked to purchase
· Other sources (Explain)
NA
H
Funding (If any) for the project please state
· None
· Amount
· Source
· To whom payable
NO
I
Does any agency have a vested interest in the out come of the
Project?
NO
J
Will data relating to subjects /controls be stored in a
computer?
NO
K
Will the data analysis be done by
· The researcher?
· The funding agent
YES
NO
L
Will technical / nursing help be required form the staff of
hospital.
If yes, will it interfere with their duties?
Will you recruit other staff for the duration of the study?
If Yes give details of
I. Designation
II. Qualification
III. Number
IV. Duration of Employment
NO
NO
NO
NA
M
Will informed consent be taken? If yes
Will it be written informed consent:
Will it be oral consent? Will it be taken from the subject
themselves?
Will it be from the legal guardian? If no, give reason:
YES, INFORMED CONSENT WILL BE TAKEN FROM THE SUBJECT
THEMSELVES
N
Describe design, Methodology and techniques
APPENDIX II
Ethical clearance has been accorded.
Chairman,
P.G Training Cum-Research Institute,
A.I.M.S., B.G.Nagara.
Date :
PS : NA – Not Applicable
APPENDIX-III
8. LIST OF REFERENCES
1. Chaturvedi, N., John H. Fuller and Marja- Ritta Taskinen
2001:
"Differing associations of lipid and lipoprotein disturbances
with the macrovascular and micro vascular complications of type 2
diabetes". Diabetes Care, 24(12): 2071-2076.
2. Mazzone, T., 2000: "Current concepts and controversies in the
pathogenesis,prevention nd of the macrovascular treatment
complications of diabetes. J Lab. Clin. Med., 135: 437-443.
3 Bagdade, J.D., et al 1967:"Diabetic lipemia. A form of
acquired fat induced lipemia". N. Engl. J Med.,276: 427-433.
4. Nikkila, E.A. and Hormila, P., 1978: "Serum lipids and
lipoproteins in insulin-treated diabetes.Demonstration ofincreased
HDL concentrations". Diabetes, 27: 1078-1086.
5. CHANCE GW,; ALBUTT EC,; EDKINS SM . Serum lipids and
lipoproteins in untreated diabetics. Lancet. 1969;1:1126-8.
MedlineWeb of Science. 4. BILLIMORIA JD,; ISAACS AJ, ... CHASE HP,;
GLASGLOW AM d. 1976;130:1113-7
www.annals.org/content/95/4/426.refs
6. Blood Lipids and Human Atherosclerosis
JOHN W. GOFMAN M.D., PH.D.1; HARDIN B. JONES PH.D.1; FRANK T.
LINDGREN B.S.1; THOMAS P. LYON M.D.1; HAROLD A. ELLIOTT B.S.1;
BEVERLY STRISOWER B.S.1; , Ultracentrifugal Laboratory Group1
..From the Donner Laboratory, Division of Medical Physics and the
Radiation Laboratory, University of California, Berkeley 4,
California.
7. Plasma triglyceride level is a risk factor for cardiovascular
disease independent of high-density lipoprotein cholesterol level:
a meta-analysis of population-based prospective studies by John E.
Hokanson
8. Sharma (1970) and Jain (1980) observed increase in the levels
of serum total lipids,in type 2 DM .... Sharma D, Bansal BC,
Prakash C. Serum lipid studies in thin insulin dependent diabetics
... Ganda OP, Hayes EJ, Soledner Js, et al.
www.rssdi.org/1995_jan-mar/original_article3.pdf
9. Nerurkar SV, Retnam VJ, Taskar SP, Bhandarkar SD. Lipid
composition of plasma lipoproteins in treated diabetics. J Postgrad
Med 1983;29:201
Nerurkar SV, Retnam VJ, Taskar SP, Bhandarkar SD. Lipid
composition of plasma lipoproteins in treated diabetics. J Postgrad
Med [serial online] 1983 [cited 2010 Nov 15];29:201. Available
from: http://www.jpgmonline.com/text.asp?1983/29/4/201/5511
10. Brunzell, J.D., et al 1982:"Chylomicronemia syndrome". Med.
Clin. .North Am., 66: 455-468.
11.. American Diabetes Association 1987 :"Nutritional
recommendations and for individuals with diabetes mellitus".
Diabetes Care, 10:126-132
12. JM Olefsky, JW Farquhar… - The American Journal of …, 1974 -
ElsevierWe have previously proposed a sequential hypothesis to help
explain the genesis of endogenous hypertriglyceridemia in man. This
scheme states that insulin resistance → hyperinsulinemia→ increased
very low density lipoprotein (VLDL)-triglyceride (TG) production
rate
NEWER ARTICLES
1. IMPACT OF DURATION OF TYPE 2 DIABETES
MELLITUS ON LIPID PROFILE-
This cross-sectional study was conducted at Khyber Medical
College Peshawar from
February 2009 to July 2009
Riffat Sultana, Department of Physiology, Khyber Medical
College, Peshawar, Pakistan.
2. A Study on Lipid Profile Levels of Diabetics and Non-
Diabetics Among Naini Region of Allahabad, India
Sapna Smith,
Alok M Lall
Division of Biochemistry, Allahabad Agricultural
Institute-Deemed University, Allahabad UP India
211007
3. Vascular Structural and Functional Changes in Type 2 Diabetes
Mellitus
Evidence for the Roles of Abnormal Myogenic Responsiveness and
Dyslipidemia
Ian Schofield, MRCP; Rayaz Malik, PhD, MRCP; Ashley Izzard, PhD;
Clare Austin, PhD; Anthony Heagerty, MD, FRCP From the
Cardiovascular Research Group, Department of Medicine, Manchester
Royal Infirmary, Manchester, UK
4. Alterations in high-density lipoprotein metabolism and
reverse cholesterol transport in insulin resistance and type 2
diabetes mellitus: role of lipolytic enzymes, lecithin:cholesterol
acyltransferase and lipid transfeR proteins.(S. E. Borggreve,†, R.
De Vries,†, R. P. F. Dullaar)
Article first published online: 25 NOV 2003
5. Lipids and Lipoproteins in Patients With Type 2 Diabetes
Ronald M. Krauss, MD
6. Proatherogenic Role of Elevated CE Transfer From HDL to VLDL1
and Dense LDL in Type-2 Diabetes -: Impact of the Degree of
Triglyceridemia
Maryse Guérin; Wilfried Le Goff; Taous S. Lassel; Arie Van Tol;
George Steiner; M. John Chapman, Erasmus University, Rotterdam,
Netherlands (A.V.T.); and the Toronto Hospital, Toronto, Ontario,
Canada (G.S.). )
ABBREVIATIONS
TG -Triglyceride
TC -Total Cholesterol
VLDLc -Very Low Density Lipoprotein Cholesterol
HDLc -High Density Lipoprotein Cholesterol
LDLc -Low Density Lipoprotein Cholesterol
CAD -Coronary Artery Disease