The Islamic University-Gaza Deanship of Graduate Studies Biological Sciences Master Program Medical Technology Facutly of Science Risk Factors Associated with Helicobacter pylori Infection in Gaza, Palestine By Rana M. Abu-Mugesieb Supervisor Dr. Abdelraouf A. Elmanama Dr. Mofeed M. Mokhallalati Submitted in Partial Fulfillment for the Master Degree of Science in Biological Science-Medical Technology June 2007
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The Islamic University-Gaza
Deanship of Graduate Studies
Biological Sciences Master Program
Medical Technology
Facutly of Science
Risk Factors Associated with Helicobacter pylori Infection in
Gaza, Palestine
By
Rana M. Abu-Mugesieb
Supervisor
Dr. Abdelraouf A. Elmanama Dr. Mofeed M. Mokhallalati
Submitted in Partial Fulfillment for the Master Degree of Science in
Biological Science-Medical Technology
June 2007
i
Declaration
“I herby declare that this submission is my own work and that, to the best of
my knowledge and belief, it contains no material previously published or
written by another nor material which to a substantial extent has been
accepted for the award of any other higher degree or diploma of the
university or other institute of higher learning, except where due
or stored in retrieval system, without prior permission of the author.
ii
Abstract
Background: Helicobacter pylori (H. pylori) infection is usually acquired inearly childhood. H. pylori infection is associated with several uppergastrointestinal disorders. Local data on the epidemiology of the infection arescarce in Palestine. The purpose of this study is to measure the rate and toexplore the associated factors among the population living in Gaza strip.
Method: This study included eighty nine randomly selected participants fromnon-hospitalized patients. Age, sex, socioeconomic status and other potentialrisk factors were assessed using a structured interview. Ultra Rapid UreaseTest was performed on biopsy specimens followed by histology examinedwith Methylene blue stain, HpSAg test to detect antigen in stool specimenand Hp IgM antibody was measured in blood using ELISA technique.
Results: The study subjects comprised of 89 participants. Age rangedbetween 13-77 years, with mean age 37.03, (37.1%) were females and(62.9%) were males. The rate of H. pylori infection was (48.3%). There werevariations between the different tests. URUT was easily performed, reliableand non-expensive test; HpSAg test was non invasive, simple and could beused for the diagnosis of H. pylori infection, histology by using methyleneblue stain and serology by detection IgM antibody in blood. In crude analysis,the rate was associated with type of drinking water during childhood with Pvalue =0.018. H. pylori infection showed no significant correlation with age,sex, weight, marital status, smoking, education level, coffee drinking, oralhygiene, socioeconomic status including number of persons living in theaccommodation, number of persons in each room, income, type ofaccommodation, contact with animals, travelling abroad, consumption ofdrugs and antibiotics. Tea drinking proved to be a protective factor against H.pylori infection.
Conclusion: The results of this work supported the hypothesis that H. pyloriacquisition occurs early in childhood and persist through out life. In addition,H. pylori infection appears to be multifactorial. Tea proved to have aprotective effect against H. pylori infection.
Keywords: H. pylori, URUT, HpSAg, ELISA, Biopsy specimen,socioeconomic status, Gaza.
iii
باللغة العربیةمستخلص
Helicobacter)(العدوى ببكتیریا :تمھید pyloriھذه ، ما تكتسب في الطفولة المبكرة عادًة
ال یوجد .العدوى یصاحبھا مجموعة من األمراض في الجزء العلوي من الجھاز الھضمي
ن ھذه الغرض م.معلومات وبائیة عن ھذه البكتریا واألمراض التي قد تصاحبھا في فلسطین
.الدراسة تحدید عوامل الخطر التي قد تزید من اإلصابة بھذه البكتیریا
ض عشوائیا من عدة مستشفیات في قطاع 89في ھذه الدراسة تم اختیار :البحثطریقة مری
تاریخھ المرضي باإلضافة لعدة ، نظام حیاتھ، عمربالتتعلق كل مریض خضع لعدة أسئلة .غزة
IgM عینات من كل مریض عینة دم لفحص 3تم أخذ .صاديأسئلة تشمل الوضع االقت
antibodyعینة براز لفحص ، في الدمAntigenوعینة خزعة من المعدة أخذت بواسطة
Methyleneوفحص نسیجي باستخدام صبغة URUTمختص بجھاز المنظار للقیام بفحص
Blue.
-13مرضى تتراوح ما بین مریض كانت أعمار ال89 في ھذه الدراسة التي شملت :النتائج
الرجال كانت نسبةبینما%37.1نسبة النساء كانت . سنة37 سنة ومعدل العمر 77
.Hنسبة انتشار ، 62.9% pylori)48.3(% ،من .ھناك اختالف ما بین الفحوصات األربع
اء أھم النتائج في ھذه الدراسة وجود عالقة مھمة بین اإلصابة بھذه البكتیریا ومصادر شرب الم
نوع ، لم یكن ھناك أي عالقة مھمة ما بین اإلصابة بالبكتیریا والعمر.في مرحلة الطفولة
التدخین ، أنواع األدویة التي یستخدمھا، عدد أفراد عائلتھ، الوضع االقتصادي للمریض، الجنس
كعامل حمایة من من أھم النتائج في ھذه الدراسة وجد أن شرب الشاي یعمل .و شرب القھوة
.تیریاالبك
.H(النتائج من ھذه الدراسة أثبتت أن اإلصابة ببكتریا :االستنتاج pylori( تكون في مرحلة
كما استنتج من ھذه الدراسة فائدة .الطفولة مرتبطة بعوامل خطر مثل مصادر شرب الماء
.لبكتیریاابھذهلالصابةالشاي كمضاد
iv
Dedication
This thesis is dedicated to my father Dr. Mohammed, my Mother and my
brothers, Ahmed, Sameh and my sister Sawsan who supported me all
the way since the beginning of my study and always encouraged me to
pursue my ambitions and my goals.
Finally, this thesis is dedicated to all those who believe in the richness of
learning.
v
Acknowledgment
First I would like to thank Allah for helping me to finish this thesis.
I would in particular like to thank:
Dr. Abdelraouf A. Elmanama and Dr. Mofeed M. Mokhallalati my
supervisors, for sharing their skills in the world of research and always
making time in their busy schedule when needed. I have been especially
fascinated by, and learnt from, their remarkable ability to always move
forward.
I also would like to thank Dr. Ahmed Shahwan, Dr. Mohamed Adwan, Dr.
Abdul-latif Alhaj, Dr. Mohammed Abu-humied, Dr. Abdul-Aziz Alfarra, Dr.
Eiad Al-jabri, Dr. Yousef Moa’amer, Dr. Samir Al-Ghazali , Dr. Majed
Hassona at Gaza hospitals for their cooperation. Kamal Huliel, Nahed Al-
Halabi, Rehab Al-Najar and Yaser for facilitating sample collection and their
advising during my work.
Thanks to Al-Amal lab supervisor; Yaser Hamdona and Mohamed for
helping and allowing me to perform some of my laboratory work in their lab.
Computer engineer Mahmood Al-azbat who helped me in my work on SPSS
software.
Thanks to the Deanship of science and research at the Islamic University-
Gaza for their support and generosity through its grants to the faculty
members in the University.
Thanks to the laboratory staff of the Islamic University-Gaza for allowing
me open access to the laboratory and facilities. Lastly but not least I would
like to thank my friends and family for all the help and support and for
keeping me aware of the fact that there is life out- side of work.
vi
Table of Contents
Items Page
Declaration iAbstractArabic Abstract
iiiii
Dedication ivAcknowledgment vTable of contents ixList of tables xList of figures xiList of abbreviation xii
Chapter I Introduction 1
1.1 Overview 11.2 Statement of the problem 41.3 Objective 41.4 Significance 5
Chapter II Literature Review 6
2.1 The Microorganism 62.1.1 History of the microorganism 62.1.2 General aspects of H. pylori microbiology and infection 7
2.1.2.1 H. pylori characteristics 72.1.2.2 Bacterial infection 82.1.2.3 Structures 9
A. Flagella 9B. Outer membrane proteins 10C. Lipopolysaccharide 11D. The genome 11
2.1.2.4 Biodiversity 12A. Habitat diversity 12B. Genetic diversity and species diversity 13
2.1.2.5 Virulence factor 14A. The cag PAI and Vac A 14B. Adhesion 16C. H. pylori enzymes 20
2.1.3 Gastric helicobacter species2.1.4 Taxonomy of H. pylori
2021
2.2 Epidemiology of H. pylori Infection 222.2.1 Prevalence of H. pylori infection 222.2.2 Incidence of H. pylori infection 232.2.3 Risk factor for H. pylori infection 23
2.2.3.1 The family 242.2.3.2 Environmental and behavioural factor 25
vii
2.2.3.3 Host and bacterial factor 262.2.4 Transmission of H. pylori infection 28
2.2.4.1 Fecal oral and gastro-oral routs 282.2.4.2 Oral-oral rout 292.2.4.3 Environmental source: water and food 302.2.4.4 Animal reservoir 312.2.4.5 Intra familial transmission 32
2.3 Clinical Manifestation of H. pylori Infection 332.3.1 Natural course of H. pylori infection 332.3.2 Gastritis 342.3.3 Peptic ulcer disease 342.3.4 Gastric cancer 342.3.5 Other H. pylori associated condition 352.3.6 Extra gastric manifestation of H. pylori in children 36
2.4 Diagnostic Tests for Detection of H. pylori Infection 392.4.1 Biopsy-based test 392.4.2 Tests based on detection of specific anti H. pylori antibodies 402.4.3 Urea breath test 422.4.4 Test based on detection of bacterial antigen or bacterial DNA
in feces42
2.5 Treatment of H. pylori Infection 432.5.1 Indication of treatment 432.5.2 Combined antibacterial regimens against H. pylori infection 452.5.3 Factor influencing treatment results 462.5.4 Alternative for treatment of H. pylori infection 472.5.5 Recurrence of H. pylori infection after eradication 482.5.6 Prevention of H. pylori associated disease 49
Chapter III Materials and Methods 52
3.1 Material and Reagents 523.2 Permission and Ethical Consideration 533.3 Patients 533.4 Sample Size 533.5 Sample Collection 53
3.5.1 Gastric biopsy 533.5.2 Blood sample for serological evaluation 553.5.3 Stool sample for antigen detection 55
3.6 Sample Processing 553.6.1 Blood sample 55
3.6.1.1 Principle of the ELISA test 55
viii
3.6.1.2 Assay procedure 563.6.1.3 Calculation of result 56
3.6.3 Stool sample 583.6.3.1 Kit components 583.6.3.2 Pre assay control and operations 583.6.3.3 Assay procedure (Quantitative Assay ) 603.6.3.4 Calculation of result 60
3.7 Questionnaire 603.8 Analysis of Data 61
Chapter IV Results 62
4.1 Study Sample Description 624.2 Ultra Rapid Urease Test 634.3 Gastric biopsies Stained with Methylene Blue 634.4 H. pylori Serum IgM 644.5 H. pylori Antigen Detection From Stool 644.6 True Positive for H. pylori Infection. 654.7 Statistical Analysis of H. pylori Tests Results (Chi square) 664.8 H. pylori Infection among the Study Sample 694.9 Risk Factors For H. pylori Infection. 69
4.9.1 Personal variables 704.9.2 Life style variables 714.9.3 Drug history 734.9.4 Antibiotics intake during the last month 734.9.5 Socioeconomic status 74
Chapter V Discussion 76
5.1 H. pylori tests 775.1.1 Evaluation of H. pylori Tests5.1.2 The rate of H. pylori infection
7780
5.2 Risk Factors Associated with H. pylori infection 805.2.1 Age 805.2.2 Sex 815.2.3 Weight 815.2.4 Marital status 825.2.5 Smoking 825.2.6 Coffee drinking 835.2.7 Tea drinking 835.2.8 Type of drinking water 845.2.9 Oral hygiene 855.2.10 Antibiotic consumption 865.2.11 Drugs consumption 865.2.12 Education 87
ix
5.2.13 Income 885.2.14 Number of persons in the accommodation 885.2.15 Type of accommodation 89
Chapter VI Conclusion and Recommendations 90
References 92
Appendices 111
Appendix A: Questionnaire form in English 112Appendix B: Questionnaire form in Arabic 114
x
List of tables
Table (2.1)…………………………………………………………………………………….Human and land animal gastric Helicobacter
21
Table (4.1)…………………………………………………………………………………….Age and sex distribution of the study sample
62
Table (4.2)…………………………………………………………………………………….Distribution of positive and negative results in each of the four tests used
65
Table (4.3)…………………………………………………………………………………….True H. pylori positive
65
Table (4.4)…………………………………………………………………………………….Chi square test for statistical differences between the results of Methyleneblue stain and URUT
66
Table (4.5) ……………………………………………………………………………………Chi square test for statistical differences between the results ofMethylene blue stain and IgM in serum
66
Table (4.6)……………………………………………………............................................Chi square test for statistical differences between the results ofMethylene blue stain and HpSAg
67
Table (4.7) ……………………………………………………………………………………Chi square test for statistical differences between the results of URUTand HpSAg
67
Table (4.8) ……………………………………………………………………………………Chi square test for statistical differences between the results of IgM andURUT
67
Table (4.9) ……………………………………………………………………………………Chi square test for statistical differences between the results of IgM andHpSAg
68
Table (4.10)…………………………………………………………………………………..Pearson correlation between the different H. pylori tests
68
Table (4.11)…………………………………………………………………………………..Age distribution of H. pylori positive subjects
Table (4.16)…………………………………………………………………………………..Effects of socioeconomic status
75
xi
List of Figure
Figure (2.1)…………………………………………………………………………………...H. pylori; The curved bacillus with unipolar flagella is visualized by ascanning electron microscope and depicted in a schematic drawing
8
Figure (2.2)…………………………………………………………………………………...Adhesion of Helicobacter pylori to gastric epithelial cells induces amultitude of changes to the host cell, the most common of which areshown in the diagram
17
Figure (3.1)…………………………………………………………………………………...Olympus Video trolley tv-z CLE-10 machine
Figure (3.3)…………………………………………………………………………………...Schematic presentation of the HpSAg detection procedures
59
Figure (4.1)…………………………………………………………………………………...Ultra rapid urease test
63
Figure (4.2)…………………………………………………………………………………...Methylene blue stained gastric biopsies showing the helical bacilli
64
xii
List of abbreviation
ALeb Blood group A derivative of Lewis b.BabA Blood group antigen binding A adhesion.BabB Blood group antigen binding B adhesionBE Barrett’s EsophagusBIC Bovine Immune ColostrumBLeb blood group B derivative of Lewis b.Cag A Cytotoxin-Associated GeneCag A Cytotoxin –Associated Protein.cag-PAI cag-Pathogenicity Island.CFU Colony Forming UnitCGA Cultured gastric adenocarcinomaDU Duodenal UlcerELISA Enzyme-linked immunosorbent assayESPCG European Society of Primary Care GastroenterologyG-C ratio Guanine-Cytosine ratioGERD Gastroesophageal Reflux DiseaseGI Gastrointestinal tractHpSAg Helicobacter pylori Stool Antigen detection kitH. pylori Helicobacter pyloriHLA-DQA1 Human Leukocyte Antigen LocusHP-NAP H. pylori Neutrophil-Activating ProteinIARCIgM, A,G
International Agency for Research on CancerImmunoglobulin M, A, G
ICAM Intercellular Adhesion MoleculeIL InterleukinLe b, x, y Lewis blood group antigen b, x and y.LPS LipopolysaccharideLT Labile ToxinMALT Mucosa Associated Lymphoid TissueMB Methylene BlueNADPH Nicotinamide Adenine Dinucleotide PhosphateNASPGN North American Society for Pediatric GastroenterologyNF_B Nuclear Factor_B.NIHNIS
National Institute of HealthNew Israel Shekel
NSAIDS Non Steroidal Anti Inflammatory DrugsOMP Outer Membrane ProteinsPAI Pathogenicity IslandPCR Polymerase Chain ReactionPMNs Polymorphic Nucleated CellsPPI Proton Pump Inhibitor
enzyme conjugate, substrate, stop solution, transfer pipettes, strip holder,
strip sealer and wooden stick applicators.
3.6.3.2 Pre assay controls and operations
1) Stool sample was prepared as described in figure 3.3, which illustrate the
instructions for the proper use of H. pylori Ag extraction kit.
2) The liquid components were checked by the naked-eye for visible particles
or aggregates (to eliminate the possibility of contamination). The
chromogen/substrate was checked for color (colorless or pale blue) by
aspirating a small volume of it with a sterile transparent plastic pipette. All
other components were checked according to the manufacturer
recommendations.
3) The content of the 20x concentrated wash solution was diluted with the
proper diluent.
4) The calibrator set were dissolved.
5) All the other components were allowed to reach room temperature (about
1 hr) and then mixed by vortex.
6) The ELISA incubator was set at 37 oC.
7) The ELISA reader was turned on at least 20 minutes before reading.
59
Instruction for use
Open the collection device andintroduce the extraction brush deeplyinto the specimen. Rotate the brush 3-4times in order to collect the rightamount of sample (about 0.2 g).
Transfer the brush into a test tube.Add 1ml Extraction Buffer and then mixon vortex for 1 min in order to dissolvethe sample in solution.
Discard the brush and insert the filterpiston into the tube. Push the pistondown to the bottom in order to release asoluble filtered material with thePasteur pipette.
.
Figure (3.3): Schematic presentation of the HpSAg detection procedure
1
2
3
Extractionbrush
1
Collection deviceand sample
2
Test tube andextraction buffer
Vortex
3
Filtered sample
Well
Filtering piston
Pasteur pipette
60
3.6.3.3 Assay procedure (Quantitative Assay)
1) The required number of strips was placed in the plastic holder and the
wells for calibrator and samples were carefully labelled. A1 + B1 wells were
left empty for blanking purposes.
2) One hundred µL Calibrators was pipetted in duplicate into the calibrator
wells.
3) With the Pasteur pipette supplied, 3 drops of the extracted stool sample
were aspirated and dispensed into the sample well.
4) Then 100 µl enzymatic conjugate were dispensed in all wells, except for
A1 + B1, used for blanking operations.
5) Following the addition of the conjugate, the color of the samples has
turned from brown to pale reddish and the microplate was incubated for 120
min at 37 oC.
6) When the first incubation is over, the microplate was washed 5 times.
7) Two hundreds µl chromogen/substrate were added into all wells including
A1+B1. The microplate was incubated protected from light at room
temperature (18-24 oC) for 20 min.
8) Sulphuric acid (100 µl) were pipetted into all the wells to stop the
enzymatic reaction, using the same pipetting sequence as in step 7.
9) The color intensity of the solution was measured in each well, using 450
nm filters and at 620-630nm filters.
3.6.3.4 Calculation of result
For qualitative reading
The test results were calculated by means of cut-off value determined from
the OD450nm value of the (CAL0) and the OD450nm of the CAL0.1 µg/ml
with the following formula: Cut-off = (CAL0+CAL0.1) / 2
3.7 Questionnaire
An interview questionnaire was used to collect data from eligible patients.
The independent variables included in the questionnaire were; gender,
61
weight, height, age, civil state, tea and coffee drinking, smoking, type of food
ingested (meat, fish, vegetables, othres), type of water drinking during
childhood and adulthood (filtered, municipality or well water), garbage
collection in the neighbourhood, indicators of socioeconomic status:
educational level, family income, type of accommodation (house, flat, villa),
water supply (well, municipality), sewage system, number of rooms and
number of persons residing in each dwelling, contact with animal, travelling
abroad, consuming antibiotics, consuming drugs and dental complain (See
annex for the Arabic questionnaire).
3.8 Analysis of Data
Data generated from the study was tabulated as Microsoft Excel sheets and
uploaded to Statistical Package for Social Sciences (SPSS version 11).
Cross tabulation of variables were generated. Chi square was used to detect
statistically significant correlation among variables.
Chapter IVResults
62
Chapter IV
Results
4.1 Study Sample Description
This study was conducted during the period from September 2006 to March
2007. During the study period, 122 patients undergoing upper gastrointestinal
endoscopy were interviewed and they answered several questions regarding
personal information and their life style. A serum, gastric biopsy and stool
specimens were collected. Among them only 89 patients provided the three
specimen types.
Those patients are non-hospitalized patients from different hospitals across
Gaza strip. Approximately 10% from patients were from Al-shifa hospital,
45% from Balsam-hospital, 30% from the European-hospital and 15% from
the Al-karamah-hospital. The following table is a concise description of the
study sample.
Table (4.1): Age and sex distribution of the study sample
Sex
Male FemaleTotal
Age group
No. % No. % No. %
13-20 1 16.7 5 83.3 6 6.8
21-35 37 78.7 10 21.3 47 52.8
36-50 11 50 11 50 22 24.7
Over 51 8 57.1 6 42.9 14 15.7
Total 56 62.9 33 37.1 89 100
The study population age ranged between 13-77 years, with mean age
37.03. (37.1%) are females and (62.9%) are males. Males constituted about
two third of the age group 21-35 years.
63
4.2 Ultra Rapid Urease Test
The test which was performed on biopsy collected from patients during upper
gastroscopy proved to be rapid and simple. The following table (4.2) shows
the results of rapid urease test which indicate 32.6% positivity. Figure (4.1)
shows positive (pink to red) and a negative (yellow to orange) URUT.
Figure (4.1): Ultra rapid urease test (left positive; right negative).
4.3 Gastric biopsies Stained with Methylene Blue
Although simple to perform and does not require special equipment, the
reading and interpreting of results was somewhat tedious and requires time.
From the 86 biopsies stained with Methylene blue, 40 showed H. pylori
constituting 46.5% (table 4.2). Three samples were lost during the course of
this work. Figure 4.2 illustrates a positive Methylene blue stained smear for
H. pylori.
64
Figure (4.2): Methylene blue stained gastric biopsies showing the helical
bacilli
4.4 H. pylori Serum IgM
The result of H. pylori Serum IgM performed using ELISA Kit is listed in table
(4.2). According to the manufacturer recommendations of interpreting
absorbances of serum samples, 40 (44.9%) of the samples were considered
positive.
4.5 H. pylori antigen Detection From Stool
H. pylori antigen detection from stool is receiving attention from service
laboratories as well as from researchers. According to the manufacturer
recommendation of interpreting absorbances of the extracted stool samples,
32 (36%) were considered positive (table 4.2).
65
Table (4.2): Distribution of positive and negative results in each of the four
tests used1URUT 2MB stain 3HpSAg 4IgM
H. pyloriNo. % No. % No. % No. %
Negative 60 67.4 46 51.7 57 64.0 49 55.1
Positive 26 32.6 40 46.5 32 36.0 40 44.9
Total 89 100 86 96.6 89 100 89 1001URUT; Ultra Rapid Urease Test, 2 MB; Methelyene Blue stain, 3 HpSAg; H. pylori Stool
antigen and 4 IgM; H. pylori Immunoglobuline M
From the table one can notice the variation between the four tests, the
highest positivity for H. pylori was in the IgM test and methylene blue 44.9%
followed by HpSAg test 36.0% and the lowest positivity was in urease test
32.6%.
4.6 True Positive For H. pylori Infection.
As indicated in table (4.2), there are variations in the percentage of positive
results for the four employed tests. A true positive was assumed if URUT
and/or Methylene blue tests were positive (table 4.3) (189). All the
subsequent correlations between possible risk factors and H. pylori infection
were done with the true positive.
Table (4.3): True H. pylori positive
H. pylori Frequency Percent
Negative 46 51.7
Positive 43 48.3
Total 89 100.0
66
4.7 Statistical Analysis of H. pylori Tests Results (Chi square)
In table (4.4), (4.5) and (4.6) there were statistically significant differences
between MB and URUT, IgM and HpSAg test with P value<0.01. As shown in
table (4.4) the agreement in positive result between MB and URUT test was
92.9%. In table (4.5) the difference between IgM test and MB were significant
with P value<0.01. The agreement were 69.2% in positive result. In table
(4.6) the agreement between MB and HpSAg test were 96.8% in positive
result and in table (4.7) the agreement between URUT and HpSAg test were
89.7% in positive result, URUT and HpSAg gave statistical significant
differences with P=0.01. In table (4.8) the difference between IgM and URUT
was not significant (P=0.415), but the difference between HpSAg and IgM
that showed in table (4.9) was significant with P=0.034 and the agreement
between the positive result 47.5%.
Table (4.4): Chi square test for statistical differences between the results of
Methylene blue stain and URUT
MB test
Negative PositiveUltra rapid urease
testNo % No. %
P
value
Negative 44 75.9 14 24.1
positive 2 7.1 26 92.9<0.01
Total 46.0 53.5 40 46.5
Table (4.5): Chi square test for statistical differences between the results of
Methylene blue stain and IgM in serum
MB test
Negative PositiveIgM in serum
No % No. %
P
value
Negative 34 72.3 13 27.7
positive 12 30.8 27 69.2
Total 46 53.5 40 46.5
<0.01
67
Table (4.6): Chi square test for statistical differences between the results of
Methylene blue stain and HpSAg
MB test
Negative PositiveHpSAg
No % No. %
P
value
Negative 45.0 81.8 10.0 18.2
positive 1.0 3.2 30.0 96.8
Total 46.0 53.5 40.0 46.5
<0.01
Table (4.7): Chi square test for statistical differences between the results of
URUT and HpSAg
HpSAg
Negative PositiveURUT
No. % No. %
P
value
Negative 54.0 90.0 6.0 10.0
positive 3.0 10.3 26.0 89.7
Total 57.0 64.0 32.0 36.0
<0.01
Table (4.8): Chi square test for statistical differences between the results of
IgM and URUT
Ultra rapid urease test
Negative PositiveIgM in serum test
No % No. %
P value
Negative 34 69.4 15 30.6
positive 26 65.0 14 35.0
Total 60 67.4 29 32.6
0.415
68
Table (4.9): Chi square test for statistical differences between the results of
IgM and HpSAg
HpSAg
Negative PositiveIgM in serum test
No % No. %
P value
Negative 36 73.5 13 26.5
positive 21 52.5 19 47.5
Total 57 64.0 36 36.0
0.034
Table (4.10): Pearson correlation between the different H. pylori tests.
hygiene status, socioeconomic status include, education level, income, type
of accommodation, number of persons living in the accommodation, number
of persons in each room, type of water, the sewage system, contact with
animals, traveling abroad and drug consumption could not be considered as
a risk factor of H. pylori infection as demonstrated by the results of this study.
8. The statistical analysis of data obtained from this work demonstrated a
significance protective property of tea against H. pylori infection with a
significant P value.
9. Our results support the hypothesis that H. pylori infections in developing
countries is predominantly acquired during childhood.
6.2 Recommendations
1. As a result of our study we recommend that further investigation to detect
the possible sources of H. pylori infection especially drinking water
2. We recommend using urease test at the physician office as a simple, one
minute test.
3. More than one biopsy during gastroscopy is recommended to increase the
sensitivity of tests depending on the activity of the bacterium (URUT and
MB).
4. We recommend that tea leaves should be tested for their effect on H.
pylori both in vivo and vitro.
92
References
(1) Suporn T., Supujchara N., Aruchalean T., Kanit A., Paneeya P., et al,2006- A Rapid Serologic Test and Immunoblotting for the Detection ofHelicobacter pylori Infection in Children. J Trop Pediatr. 52(4):267-287
(2) Marshall B., 2001 - Helicobacter pylori physiology and genetics. Onehundred years of discovery and rediscovery of Helicobacter pylori and itsassociation with peptic ulcer disease. Mobley H., Mendz G., and HazellS.,(eds): ASM Press.: 19-24
(3) Marshall B., Warren J., 1984- Unidentified curved bacilli in the stomachof patients with gastritis and peptic ulceration. Lancet. 1(8390): 1311-1315.
(4) Goodwin C., Armstrong J., Chilvers T., Peters M., Collins D., et al,1989 - Transfer of Campylobacter pylori and Campylobacter mustelae toHelicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobactermustelae comb. nov., respectively. Int J Syst Bacteriol. 39(4): 397-405.
(5) Goodwin C., Worsley B.,1993- Microbiology of Helicobacter pylori.Gastroenterol. Clin North Am. 22(11) :5-19.
(6) Van Zwet A., Thijs J., Roosendaal R., et al,1996- Review: Practicaldiagnosis of Helicobacter pylori infection. Eur J Gastroenterol Hepatol. 8(5):501-507.
(7) Hu L., Mobley H., 1993-Expression of catalytically active recombinantHelicobacter pylori urease at wild type levels in Escherichia coli. InfectImmun. 61(6):2569-2569.
(8) Chun D., Shun N., Shi H., Jia Y., 2000- Seroepidemiology ofHelicobacter pylori infection among asymptomatic Chinese children. World J.Gastroenterol. 6(5) :759-761.
(11) Danesh J., Collins R., Peto R., 1997-Chronic infections and coronaryheart disease: is there a link?. Lancet. 350 ( 9075):430-436
(12) Germán R., Guadalupe A., Geny F., 2001- Helicobacter pylori: Recentadvances in the study of its pathogenicity and prevention. Salud pública deméxico. 43(3):237-247
93
(13) Torres J., Perez-Perez G., Goodman K., Atherton J., Gold B., et al ,2000- A comprehensive review of the natural history of Helicobacter pyloriinfection in children. Arch Med Res.31(5 ):431-469
(14) Lacy B., semore J., 2001- Helicobacter pylori: ulcers and more: thebeginning of an era. J Nutr. 131(27) :89-93
(15) Gold B., 2001- Helicobacter pylori infection in children. Curr ProblPediatr Adolesc Health Care. 31(8):247-266
(16) Brown L., 2000- Helicobacter pylori: epidemiology and routes oftransmission. Epidemiol Rev.22(2) :83-97
(17) Zmira S., Haim S., Yaron N., Gabriel D., Douglas J., et al, 2002-Resistance of Helicobacter pylori isolated in Israel to metronidazole,clarithromycin, tetracycline, amoxicillin and cefixime. J. Antimicrob.Chemother.49(6) :1023-1026.
(18) Abdollah B., Robert W., Remon A., Yongdai K., Malla R., et al, 2000-Seroepidemiology of Helicobacter pylori infection in a population of Egyptianchildren. Inter. J. Epidemiol. 29(5) :928-932.
(19) Ina S., Jose B., Ari S., Neiva C., Camila S., et al, 2005- Prevalence ofHelicobacter pylori infection and associated factors among adults in SouthernBrazil: a population-based cross-sectional Study. BMC Public Health. 5(118):1-10.
(20) Yi-Hui L., Hong G., Peng-Bin Z., Xiao-Yan Z., Si-Ping D., 2004-Clinical value of Helicobacter pylori stool antigen test, ImmunoCard STATHpSA, for detecting H pylori infection. World J Gastroenterol. 10(6) :913-914
(21) Agence d’évaluation des technologies et des modes d’interventionen santé ( AETMIS). 2005- The 13C-Urea Breath Test for Detection ofHelicobacter pylori: Potential Applications in Québec. Report prepared byLonny Erickson (AETMIS 05- 05). Montréal: AETMIS.
(22) Athanasios M., Eva P., Kurt S, Margit W., Manfred L., et al, 1998-Detection of Helicobacter pylori in Stool Specimens by PCR and AntigenEnzyme Immunoassay. J. Clin. Microbiol. 36(9): 2772–2774.
(23) Hoffman J., David R., 2001- Treatment of Helicobacter pylori. CurrOpin Gastroenterol. 17 (1):30–34
(24) Broutet N., Tchamgoue S., Pereira E., Lamouliatte H., Salamon R.,et al, 2003- Risk factors for failure of Helicobacter pylori therapy—results ofan individual data analysis of 2751 patients. Aliment Pharmacol Ther.17(1):99–109.
94
(25) Roosendaal R., Kuipers E., Buitenwerf J., Uffelen C., Meuwissen S.,et al. 1997- Helicobacter pylori and the birth cohort effect: Evidence of acontinuous decrease of infection rates in childhood. Am J Gastroenterol. 92(9):1480-1482.
(26) Czinn S., Cai A., Nedrud J., 1993-Protection of germ-free mice frominfection by Helicobacter felis after active oral or passive IgA immunization.Vaccine. 11(6) :637-642.
(27) Negrini R., Poiesi C., Savio A., Paterlini A., Buffoli F., et al. 1994-Molecular mimicry of gastric antigen by Helicobacter pylori: A role in thepathogenesis of atrophic gastritis? Am J Gastroenterol. (89): 1329.
(28) Sebastian S., Pierre M., 2002- Helicobacter pylori Infection. The NewEngland J. medic. 347(15):1175-1186.
(29) Bellack N., Koehoorn M., MacNab Y., Morshed M., 2006- Aconceptual model of water's role as a reservoir in Helicobacter pyloritransmission: a review of the evidence. Epidemiol Infect. 134(3) : 439-449
(30) Kusters J., Vanvilet A., Kuipers E., 2006- Pathogenesis of Helicobacterpylori infection. CMR. 19(3) : 449-490
(31) Gueneau P.,Loiseaux-De G., 2002- Helicobacter: molecular phylogenyand the origin of gastric colonization in the genus. Infect Genet Evol.1(3):215-223
(32) Owen R., 1998- Helicobacter--species classification and identification.Br Med Bull. 54(1): 17-30.
(33) Fox J., 2002- The non-H pylori helicobacters: their expanding role ingastrointestinal and systemic diseases. Gut. 50(2): 273-283
(34) Enroth H., K. Wreiber, et al. 1999- In vitro aging of Helicobacter pylori:changes in mor- phology, intracellular composition and surface properties.Helicobacter. 4(1): 7-16.
(35) Solnick J., K. Chang, et al. 2003- Natural acquisition of Helicobacterpylori infection in newborn rhesus macaques. J. C.M. 41(12), 5511-5516
(36) Andersen L., Dorland A., Karacan H., Colding H., Nilsson H., et al,2000- Possible clinical importance of the transformation of Helicobacter pyloriinto coccoid forms. Scand J Gastroenterol. 35 (9): 897-903.
(37) Kivi M., Johansson A., Reilly M., Tindberg Y., 2005- Helicobacterpylori status in family members as risk factors for infection in children.Epidemiol. & Infect. 133 (4): 645-652.
95
(38) Testerman T., McGee D., Mobley H., 2001- Helicobacter pyloriphysio logy and genetics. Adherence and colonization. (eds): ASM Press,Washington, D.C. USA.: 381-417.
(39) Mahdavi J., Sondén B., Hurtig M., Olfat F., Forsberg L., et. Al, 2002-Helicobacter pylori SabA adhesin in persistent infection and chronicinflammation. Sci. 297 (5581): 573-578.
(40) Yamaoka Y., Kita M., Kodama T., Imamura S., Ohno T., et al, 2002-Helicobacter pylori infection in mice: Role of outer membrane proteins incolonization and inflammation. Gastroenterol. 123 (6): 1992-2004.
(41) Blaser M., Berg D., 2001- Helicobacter pylori genetic diversity andrisk of human disease. J Clin Invest. 107 (7): 767-773.
(42) Terry K., Williams S., Connolly L., Ottemann K., 2005- Chemotaxisplays multiple roles during Helicobacter pylori animal infection. InfectImmun. 73 (2): 803-811.
(43) Zambon C., Navaglia F., Basso D., Rugge M., Plebani M., 2003-Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically incausing intestinal metaplasia. J Clin Pathol 56 (4): 287-291.
(44) Taylor D., Rasko D., Sherburne R., Ho C., Jewell L., 1998- Lackof correlation between Lewis antigen expression by Helicobacter pylori andgastric epithelial cells in infected patients. Gastroenterol. 115(5): 1113-1122.
(46) Deitsch K., Moxon E., Wellems T., 1997- Shared themes of antigenicsvariation and virulence in bacteria, protozoa, and fungal infections. MicrobiolMol Biol Rev. 61(1): 281-293
(47) Boneca I., de Reuse H., Epinat J., Pupin M., Labigne A., et al, 2003- Arevised annotation and comparative analysis of Helicobacter pylorigenomes. Nucl. Acid. Res. 31(6): 1704-1714.
(48) Cover T., Berg D., Blaser M., Mobley H., 2001- Principles of BacterialPathogenesis, chapter 11; H. pylori patho. :509-558.
(49) Nilsson C., Sillén A., Eriksson L., Strand M., Enroth H., et al,2003- Correlation between cag pathogenicity island composition andHelicobacter pylori-associated gastroduodenal disease. Infect Immun.71(11): 6573-6581.
(51) Ilver D., Arnqvist A., Ogren J., Frick I., Kersulyte D., et al, 1998-Helicobacter pylori adhesin binding fucosylated histo-blood group antigensrevealed by retagging. Sci. 279 (5349):373- 377.
(52) Soto G., Hultgren S., 1999- Bacterial adhesins: common themes andvariations in architecture and assembly. J.B. 181 (4):1059-1071.
(53) Odenbreit S., Puls J., Sedlmaier B., Gerland E., Fischer W., et al,2000- Translocation of Helicobacter pylori CagA into gastric epithelial cells bytype IV secretion. Sci. 287 (5457):1497-1500.
(54) Kim N., Marcus E., Wen Y., Weeks D., Scott D., et al, 2004- Genes ofHelicobacter pylori Regulated by Attachment to AGS Cells. I.A.I. 72(4) :2358-2368.
(55) Park Y., Richard J.,1998- Contact-dependent protein secretion inPorphyromonas gingivalis. Infect. Immun. 66 (10):4777-4782.
(56) Segal E., Cha J., Lo J., Falkow S., Tompkins L., 1999- Altered states:involvement of phosphorylated CagA in the induction of host cellular growthchanges by Helicobacter pylori. Proc. Natl. Acad. Sci. USA. 96 (25):14559-14564.
(57) Madrid J., Ballesta J., Castells M., Hernandez F., 1990-Glycoconjugate distribution in the human fundic mucosa revealed by lectin-and glycoprotein-gold cytochemistry. Histochem. 95 (2):179-187.
(58) Ebert M., Schandl L., Malfertheiner P., 2002- Helicobacter pyloriinfection and molecular changes in gastric carcinogenesis. J. Gastroenterol.13 (1): 45-49.
(59) McCormick B., Parkos C., Colgan S., Carnes D., Madara J., 1998-Apical secretion of a pathogen-elicited epithelial chemoattractant activity inresponse to surface colonization of intestinal epithelia by Salmonellatyphimurium. J. Immunol. 160 (1):455-466.
(60) Slattery M., Dong C., 2003- Neutrophils influence melanoma adhesionand migration under flow conditions. Int. J. Cancer. 106 (5):713-722.
(61) Blaser M., 1996- The bacteria behind ulcers. Sci. Am. 274 (2):104-107.
(62) Satin B., Del Giudice G., Della Bianca V., Dusi S., Laudanna C., etal, 2000- The neutrophil-activating protein (HP-NAP) of Helicobacter pylori isa protective antigen and a major virulence factor. J. Exp. Med. 191 (9):1467-1476.
97
(63) Kwok T., Backert S., Schwarz H., Berger J., Meyer T., 2002- Specificentry of Helicobacter pylori into cultured gastric epithelial cells via a zipper-like mechanism. Infect. Immun. 70 (4):2108-2120.
(64) Telford J., Covacci A., Rappuoli R., Chiara P., 1997- Immunobiologyof Helicobacter pylori infection. Curr. Opin. Immunol. 9 (4):498-503.
(65) Allen L., 2001- The role of the neutrophil and phagocytosis in infectioncaused by Helicobacter pylori. Curr Opin Infect Dis. 14 (3): 273-277.
(66) Allen L., Schlesinger L., Kang B., 2000- Virulent strains ofHelicobacter pylori demonstrate delayed phagocytosis and stimulatehomotypic phagosome fusion in macrophages. J Exp Med. 191 (1):115-128.
(67) Weeks D., Eskandari S., Scott D., Sachs G., 2000- A H+-gated ureachannel: the link between Helicobacter pylori urease and gastric colonization.Sci. 287 (5452):482–485.
(68) Solnick J., Schauer D., 2001- Emergence of diverse Helicobacterspecies in the pathogenesis of gastric and enterohepatic diseases. ClinMicrobiol Rev. 14 (1):59-97.
(69) Parsonnet J., 1998- Helicobacter pylori: the size of the problem.Gut.;43 (1):6–9.
(70) Murray L., McCrum E., Evans A.,Bamford K., 1997- Epidemiology ofHelicobacter pylori infection among 4742 randomly selected subjects fromNorthern Ireland. Int J Epidemiol. 26(1) :880–887.
(71) Reshetnikov O., Denisova D., Zavyalova L., Haiva V., GranbergC., 2003- Helicobacter pylori seropositivity among adolescents inNovosibirsk, Russia: prevalence and associated factors. J PediatrGastroenterol Nutr. 36 (1):72–76
(72) Bergenzaun P., Kristinsson KG., Thjodleifsson B., SigvaldadottirE., Mölstad S., et al., 1996- Seroprevalence of Helicobacter pylori in southSweden and Iceland. Scand J Gastroenterol. 31(12):1157–1161
(73) Malaty H., Graham D., Isaksson I., Engstrand L., Pedersen N.,1998- Co-twin study of the effect of environment and dietary elements onacquisition of Helicobacter pylori infection. Am J Epidemiol. 148 (8):793–797
(74) Malaty H., Evans D., Evans D., Jr., Graham D., 1992- Helicobacterpylori in Hispanics: Comparison with blacks and whites of similar age andsocioeconomic class. Gastroenterol. 103 (3): 813-816.
98
(75) Malaty H., El-Kasabany A., Graham D., Miller C., Reddy S., et al,2002- Age at acquisition of Helicobacter pylori infection: A follow-up studyfrom infancy to adulthood. Lancet. 359 (9310): 931-935.
(76) Rupnow M., Shachter R., Owens D., Parsonnet J., 2000- A dynamictransmission model for predicting trends in Helicobacter pylori and associateddiseases in the United States. Emerg Infect Dis. 6 (3): 228-237.
(77) Oona M., Utt M., Nilsson I., Uibo O., Vorobjova T., et al, 2004-Helicobacter pylori infection in children in Estonia: decreasingseroprevalence during the 11-year period of profoundsocioeconomicchanges. Helicobacter. 9(3) :233–241
(78) de Oliveira A., Rocha G., Queiroz D., de Moura S., Rabello A.,1999a- Seroconversion for Helicobacter pylori in adults from Brazil. Trans RSoc Trop Med Hyg. 93 (3) :261–263
(79) Rocha G., Rocha A., Silva L., Santos A., Bocewicz A., et al, 2003-Transmission of Helicobacter pylori infection in families of preschool-agedchildren from Minas Gerais, Brazil. Trop Med Int Health. 8 (11) : 987-991
(80) Lambert J., Lin S., Sievert W., Nicholson L., Schembri M., et al,1995-High prevalence of Helicobacter pylori antibodies in aninstitutionalized population: Evidence for person-to-person transmission.AmJ Gastroenterol. 90 (12) : 2167-2171.
(81) Tindberg Y., Bengtsson C., Granath F., Blennow M., Nyrén O., eta l , 2001b- Helicobacter pylori infection in Swedish school children: Lack ofevidence of child-to-child transmission outside the family. Gastroenterol.121 (2) : 310-316.
(82) Tsai C., Perry S., Sanchez L., Parsonnet J., 2005- Helicobacter pyloriinfection in different generations of hispanics in the San Francisco bayarea. Am J Epidemiol. 162 (4) : 351-357.
(83) Woodward M., Morrison C., McColl K., 2000- An investigation intofactors associated with Helicobacter pylori infection. J Clin Epidemiol. 53 (2) :175-181.
(84) Brenner H., Rothenbacher D., Bode G., Dieudonne P., Adler G.,1999- Active infection with Helicobacter pylori in healthy couples. EpidemiolInfect. 122 (1) : 91-95
(85) Mendall M., Goggin P., Molineaux N., Levy J., Toosy T., et al, 1992-Childhood living conditions and Helicobacter pylori seropositivity in adult life.Lancet. 339 (8798) : 896-897
99
(86) Brown L., Thomas T., Ma J., Chang Y., You W., et al, 2002-Helicobacter pylori infection in rural China: Demographic, lifestyle andenvironmental factors. Int J Epidemiol 31.(3) : 638-645
(87) Glynn M., Friedman C., Gold B., Khanna B., Hutwagner L., et al,2002- Seroincidence of Helicobacter pylori infection in a cohort of ruralBolivian children: Acquisition and analysis of possible risk factors. Clin InfectDis. 35 (9) : 1059-1065
(88) Goodman K., Correa P., Tengana Aux H., Ramirez H., DeLany J.,et al 1996- Helicobacter pylori infection in the Colombian Andes: Apopulation-based study of transmission pathways. Am J Epidemiol. 144 (3) :290-299
(89) Kuepper-Nybelen J., Thefeld W., Rothenbacher D., Brenner H., 2005-Patterns of alcohol consumption and Helicobacter pylori infection: Results of apopulation-based study from Germany among 6545 adults. Aliment PharmacolTher. 21 (1): 57-64.
(90) Aspholm-Hurtig M., Dailide G., Lahmann M., Kalia A., Ilver D., et al,2004- Functional adaptation of BabA, the H. pylori ABO blood group antigenbinding adhesin. Sci. 305 (5683): 519-522.
(91) Rothenbacher D., Weyermann M., Bode G., Kulaksiz M., Stahl B.,et al, 2004- Role of Lewis A and Lewis B blood group antigens inHelicobacter pylori infection. Helicobacter. 9 (4): 324-329.
(92) Magnusson P., Enroth H., Eriksson I., Held M., Nyrén O., et al, 2001-Gastric cancer and human leukocyte antigen: Distinct DQ and DR allelesare associated with development of gastric cancer and infection byHelicobacter pylori. Cancer Res. 61 (6): 2684-2689
(93) Hartland S., Newton J., Griffin S., Donaldson P., 2004- A functionalpolymorphism in the interleukin-1 receptor-1 gene is associated withincreased risk of Helicobacter pylori infection but not with gastric cancer. DigDis Sci. 49 (9): 1545-1550.
(94) Björkholm B., Guruge J., Karlsson M., O'Donnell D., Engstrand L.,et al, 2004- Gnotobiotic transgenic mice reveal that transmission ofHelicobacter pylori is facilitated by loss of acid-producing parietal cells indonors and recipients. Microbes Infect. 6 (2): 213-220.
(95) Salama N., Shepherd B., Falkow S., 2004- Global transposonmutagenesis and essential gene analysis of Helicobacter pylori. JBacteriol. 186 (23): 7926- 7935
(96) Perez-Perez G., Salomaa A., Kosunen T., Daverman B., RautelinH., et al, 2002- Evidence that cagA+ Helicobacter pylori strains are
100
disappearing more rapidly than cagA- strains. Gut. 50 (1): 295- 298.
(97) Parsonnet J, Shmuely H, Haggerty T., 1999- Fecal and oralshedding of Helicobacter pylori from healthy infected adults. JAMA. 282(23):2240–2245
(98) Song Q., Spahr A., Schmid R., Adler G., Bode G., 2000a-Helicobacter pylori in the oral cavity: high prevalence and great DNA diversity.Dig Dis Sci. 45.(11):2162–2167
(99) Adams B., Bates T., Oliver J., 2003- Survival of Helicobacter pylori in anatural freshwater environment. Appl Environ Microbiol. 69 (12):7462–7466
(100) Krumbiegel P., Lehmann I., Alfreider A., Fritz G., Boeckler D., etal., 2004- Helicobacter pylori determination in non-municipal drinking waterand epidemio- logical findings. Isotopes Environ Health Stud. 40 (1):75–80.
(101) She F., Su D., Lin J., Zhou L., 2001- Virulence and potentialpathogenicity of coccoid Helicobacter pylori induced by antibiotics. World JGastroenterol.7 (2):254–258
(102) Rodrigues M., Queiroz D., Bezerra Filho J., Pontes.K, RodriguesR., et al, 2004- Prevalence of Helicobacter pylori infection in children from anurban community in north-east Brazil and risk factors for infection. Eur JGastroenterol Hepatol. 16 (2):201–205.
(103) Rothenbacher D., Winkler M., Gonser T., Adler G., Brenner H.,2002b- Role of infected parents in transmission of Helicobacter pylori to theirchildren. Pediatr Infect Dis J. 21 (7):674–679
(104) Malaty H., Kumagai T., Tanaka E., Ota H., Kiyosawa K., et al.,2000- Evidence from a nine-year birth cohort study in Japan of transmissionpathways of Helicobacter pylori infection. J Clin Microbiol. 38 (5) :1971–1973
(105) Maaroos H., Vorobjova T., Sipponen P., Tammur R., Uibo R., etal., 1999- An 18- year follow-up study of chronic gastritis and Helicobacterpylori association of CagA positivity with development of atrophy and activityof gastritis. Scand J Gastroenterol. 34 (9):864–869.
(106) NIH Consensus Conference, 1994- Helicobacter pylori in pepticulcer disease. NIH consensus development panel on Helicobacter pylori inpeptic ulcer disease. JAMA. 272 (1): 65-69.
(107) Rothenbacher D., Brenner H., 2003- Burden of Helicobacter pyloriand H. pylori-related diseases in developed countries: Recent developmentsand future implications. Microbes Infect. 5 (8): 693-703
101
(108) Correa P., Piazuelo M., Camargo M., 2004- The future of gastriccancer prevention. Gast. Cancer. 7 (1): 9-16.
(109) Uemura N., Okamoto S., Yamamoto S., Matsumura N., YamaguchiS., et al, 2001- Helicobacter pylori infection and the development of gastriccancer. N Engl J Med. 345 (11): 784-789.
(110) El-Omar E., Carrington M., Chow W., McColl K., Bream J., et al,2000- Interleukin-1 polymorphisms associated with increased risk of gastriccancer. Natur. 404 (6776): 398-402.
(111) Farinha P., Gascoyne R., 2005- Helicobacter pylori and MALTlymphoma. Gastroenterol. 128 (6): 1579-1605
(112) Malfertheiner P., Peitz U., 2005- The interplay between Helicobacterpylori, gastro-oesophageal reflux disease, and intestinal metaplasia. Gut 54.(1): 13-20
(114) Russo-Mancuso G., Branciforte F., Licciardello M., La Spina M.,2003- Iron deficiency anemia as the only sign of infection with Helicobacterpylori: a report of 9 pediatric cases. Int J Hematol. 78(5):429–431
(115) Ciacci C., Sabbatini F., Cavallaro R., Castiglione F., Di Bella S., etal, 2004- Helicobacter pylori impairs iron absorption in infected individuals.Dig Liver Dis. 36(7):455–460
(116) Björksten B., Sepp E., Julge K., Voor T., Mikelsaar M., 2001- Allergydevelopment and the intestinal microflora during the first year of life. J AllergyClin Immunol. 108(4):516–520
(117) Matysiak-Budnik T., van Niel G., Mégraud F., Mayo K., BevilacquaC., et al., 2003- Gastric Helicobacter infection inhibits development of oraltolerance to food antigens in mice. Infect Immun. 71(9):5219–5224.
(118) Passaro D., Taylor D., Meza R., Cabrera L., Gilman R., et al, 2001-Acute Helicobacter pylori infection is followed by an increase in diarrhealdisease among Peruvian children. Pediatric. 108(5):87.
(119) Perry S., Sanchez L., Yang S., Haggerty T., Hurst P., et al, 2004-Helicobacter pyloriand risk of gastroenteritis. J Infect Dis. 90.(2):303–310
102
(120) Spechler S., 2002- Barrett's esophagus and esophagealadenocarcinoma: pathogenesis, diagnosis, and therapy. Med. Clin. North.Am. 86 (6):1423-1445.
(121) Ackermark P., Kuipers E., Wolf C., Breumelhof R., Seldenrijk C., etal, 2003- Colonization with cagA-positive Helicobacter pylori strains inintestinal metaplasia of the esophagus and the esophagogastric junction.Am. J. Gastroenterol. 98 (8):1719-1724.
(122) Labenz J., Blum A., Bayerdörffer E., et al., 1997- OccuringHelicobacter pylori infection in patients with duodenal ulcer may provokereflux esophagitis. Gastroenterol. 112 (5) :1442-1447.
(123) Vicari J., Peek R., Falk G., et al., 1998- The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophagealreflux disease. Gastroenterol. 115 (1):50-57
(124) Gasbarrini A., Marignani M., Tartaglione R., et al., 1998- Regressionof autoimmune thrombocytopenia after eradication of Helicobacter pylori.Lancet. 352 (1) : 878
(125) Dixon M., Genta R., Yardley J., Correa P., 1996- Classification andgrading of gastritis. The updated Sydney System. International Workshop onthe Histopathology of Gastritis, Houston. Am J Surg Pathol. 20 (10):1161–1181.
(126) Rotimi O., Cairns A., Gray S., Moayyedi P., Dixon M., 2000-Histological identification of Helicobacter pylori: comparison of stainingmethods. J Clin Pathol. 53(10):756–759.
(127) Chen X., van der Hulst R., Bruno M., van der Ende A., Xiao S., etal., 1999- Interobserver variation in the histopathological scoring ofHelicobacter pylori related gastritis. J Clin Pathol. 52 (8) :612–5.
(128) Zullo A., Hassan C., Lorenzetti R., Winn S., Morini S., 2003- Aclinical practice viewpoint: to culture or not to culture Helicobacter pylori?.Dig Liver Dis. 35(5):357–361.
(129) Malfertheiner P., Enrique Dominguez-Munoz J., Heckenmüller H.,Neubrand M., Fischer H., et al, 1996- Modified rapid urease test fordetection of Helicobacter pylori infection. Eur J Gastroenterol Hepatol. 8(1):53–6
(130) Weiss J., Mecca J., da Silva E., Gassner D., 1994- Comparison ofPCR and other diagnostic techniques for detection of Helicobacter pyloriinfection in dyspeptic patients. J Clin Microbiol. 32 (7) :1663–1668.
103
(131) Menard A., Santos A., Mégraud F., Oleastro M., 2002- PCR-restrictionfragment length polymorphism can also detect point mutation A2142C in the23S rRNA gene, associated with Helicobacter pylori resistance toclarithromycin. Antimicrob Agents Chemother. 46 (4) :1156–1157.
(132) Gold B., Khanna B., Huang L., Lee C., Banatvala N., 1997-Helicobacter pylori acquisition in infancy after decline of maternal passiveimmunity. Pediatr Res. 41 (5) :641–646.
(133) Kindermann A., Konstantopoulos N., Lehn N., Demmelmair H.,Koletzko S., 2001- Evaluation of two commercial enzyme immunoassays,testing immunoglobulin G (IgG) and IgA responses, for diagnosis ofHelicobacter pylori infection in children. J Clin Microbiol. 39 (10) :3591–3596
(134) Sobala G., Crabtree J., Dixon M., Schorah C., Taylor J., et al,1991- Acute Helicobacter pylori infection: clinical features, local andsystemic immune response, gastric mucosal histology, and gastric juiceascorbic acid concentrations. Gut. 32 (11) :1415–1418
(135) Cutler A., Prasad V., Santogade P., 1998a- Four-year trends inHelicobacter pylori IgG serology following successful eradication. Am J Med.105 (1):18–20
(136) Bergey B., Marchildon P., Peacock J., Mégraud F., 2003- What isthe role of serology in assessing Helicobacter pylori eradication?. AlimentPharmacol Ther. 18 (6) :635–639.
(137) Cutler A., 1998b- Accuracy and economics of Helicobacter pyloridiagnosis.Yale J Biol Med. 71 (2) :75–79.
(138) Hoang T., Wheeldon T., Bengtsson C., Phung D., Sörberg M., etal, 2004- Enzyme-linked immunosorbent assay for Helicobacter pylori needsadjustment for the population investigated. J Clin Microbiol. 42 (2) :627–630.
(139) Rocha G., Oliveira A., Queiroz D., Carvalho A., Nogueira A., 2000-Immunoblot analysis of humoral immune response to Helicobacter pylori inchildren with and without duodenal ulcer. J Clin Microbiol. 38 (5) :1777–1781.
(140) Vaira D., Vakil N., 2001- Blood, urine, stool, breath, money, andHelicobacter pylori. Gut. 48 (3) :287–289.
(141) Kabir S., 2003- Review article: clinic-based testing for Helicobacterpylori infection by enzyme immunoassay of faeces, urine and saliva. AlimentPharmacol Ther. 17 (11):1345–1354.
(142) Malfertheiner P., Mégraud F., O'Morain C., Hungin A., Jones R.,et al, 2002- European Helicobacter pylori Study Group (EHPSG). Currentconcepts in the management of Helicobacter pylori infection – the Maastricht
(143) Laine L., Estrada R., Trujillo M., Knigge K., Fennerty M.,1998-Effect of proton-pump inhibitor therapy on diagnostic testing for Helicobacterpylori. Ann Intern Med. 129 (7) :547–550
(144) Vaira D., Malfertheiner P., Mégraud F., Axon A., 1999- Diagnosis ofHelicobacter pylori infection by HpSA test. European Helicobacter pyloriHpSA Study Group. Lancet. 354 (9191):1732.
(145) Makristathis A., Barousch W., Pasching E., Binder C., KudernaC., et al, 2000- Two enzyme immunoassays and PCR for detection ofHelicobacter pylori in stool specimens from pediatric patients before andafter eradication therapy. J Clin Microbiol. 38 (10) :3710–3714
(146) Gisbert J., Pajares J., 2004a- Stool antigen test for the diagnosis ofHelicobacter pylori infection: a systematic review. Helicobacter. 9 (4) :347–368
(147) Casswall T., Nilsson H., Bergström M., Aleljung P., WadströmT., et al., 1999- Evaluation of serology, 13C-urea breath test, andpolymerase chain reaction of stool samples to detect Helicobacter pylori inBangladeshi children. J Pediatr Gastroenterol Nutr. 28 (1) :31-36
(148) Fontana C., Favaro M., Pietroiusti A., Pistoia E., Galante A., et al,2003- Detection of clarithromycin-resistant Helicobacter pylori in stoolsamples. J Clin Microbiol. 41 (8) :3636–3640.
(149) Hojo M., Miwa H., Ohkusa T., Ohkura R., Kurosawa A., et al, 2002-Alteration of histological gastritis after cure of Helicobacter pylori infection.Aliment Pharmacol Ther. 16 (11) :1923–1932
(150) Wotherspoon A., Doglioni C., Diss T., Pan L., Moschini A., et al.,1993- Regression of primary low-grade B-cell gastric lymphoma of mucosa-associated lymphoid tissue type after eradication of Helicobacter pylori.Lancet. 342 (8871) :575–577.
(151) Wong B., Lam S., Wong W., Chen J., Zheng T., et al, 2004- ChinaGastric Cancer Study Group. Helicobacter pylori eradication to preventgastric cancer in a high-risk region of China: a randomized controlled trial.JAMA. 291 (2) :187–194
(152) Wu J., Chan F., Ching J., Leung W., Hui Y., Leong R., et al.,2004- Effect of Helicobacter pylori eradication on treatment of gastro-oesophageal reflux disease: a double blind, placebo controlled, randomisedtrial. Gut. 53 (2) :174–179.
105
(153) Rubin G., Meineche-Schmidt., Roberts A., Childs S., de Wit N.,1999- The management of Helicobacter pylori infection in primary care. Eur JGen Pract. 5 (1) :98–104.
(154) Gold B., Colletti R., Abbott M., Czinn S., Elitsur Y., et al, 2000-North American Society for Pediatric Gastroenterology and Nutrition.Helicobacter pylori infection in children: recommendations for diagnosis andtreatment. J Pediatr Gastroenterol Nutr. 31 (5) :490–497
(155) Drumm B.,Koletzko S.,Oderda G., 2000- Helicobacter pylori infectionin children: a consensus statement. European Paediatric Task Force onHelicobacter pylori. J Pediatr Gastroenterol Nutr. 30 (2) :207–213
(156) Laheij R., Rossum L., Jansen J., Straatman H., Verbeek A., 1999-Evaluation of treatment regimens to cure Helicobacter pylori infection – ameta-analysis. Aliment Pharma- col Ther. 13 (7) :857–864.
(157) Tindberg Y., Casswall T., Blennow M., Bengtsson C., GranströmM., et al, 2004- Helicobacter pylori eradication in children and adolescentsby a once daily 6-day treatment with or without a proton pump inhibitor in adouble-blind randomized trial. Aliment Pharmacol Ther. 20 (3) :295–302.
(158) Sherman P., Hassall E., Hunt R., Fallone C., Veldhuyzen VanZanten S., et al, 1999- Canadian Helicobacter Study Group ConsensusConference on the approach to Helicobacter pylori infection in children andadolescents. Can J Gastroenterol. 13 (7) :553–559
(160) Mégraud F. 2004- Basis for the management of drug-resistantHelicobacter pylori infection. Drugs. 64 (17) :1893–1904
(161) Mégraud F., Lehn N., Lind T., Bayerdorffer E., O'Morain C., etal., 1999- Antimicrobial susceptibility testing of Helicobacter pylori in a largemulticenter trial: the MACH 2 study. Antimicrob Agents Chemother. 43 (11):2747–2752
(162) Wheeldon T., Granström M., Hoang T., Phuncarg D., Nilsson L.,et al, 2004- The importance of the level of metronidazole resistance for thesuccess of Helicobacter pylori eradication. Aliment Pharmacol Ther. 19 (12):1315–1312
(163) Lambert J., Midolo P., 1997- The actions of bismuth in thetreatment of Helicobacter pylori infection. Aliment Pharmacol Ther. 11(1):27–33.
106
(164) Wermeille J.,Cunningham M., Dederding J., Girard L., Baumann R.,et al., 2002- Failure of Helicobacter pylori eradication: is poor compliance themain cause?. Gastroenterol Clin Biol. 26 (3) :216–219
(165) Fennerty M., Lieberman D., Vakil N., Magaret N., Faigel D., et al,1999- Effectiveness of Helicobacter pylori therapies in a clinical practicesetting. Arch Intern Med. 159 (14) :1562–1566
(166) Hamilton-Miller J., 2003- The role of probiotics in the treatment andprevention of Helicobacter pylori infection. Int J Antimicrob Agents. 22 (4):360–366
(167) Annuk H., Hirmo S., Türi E., Mikelsaar M., Arak E., et al, 1999-Effect on cell surface hydrophobicity and susceptibility of Helicobacterpylori to medicinal plant extracts. FEMS Microbiol Lett. 172 (1) :41–45
(168) Di Mario F., Aragona G., Dal Bo N., Cavestro G., Cavallaro L., etal., 2003- Use of bovine lactoferrin for Helicobacter pylori eradication. DigLiver Dis. 35 (10) :706– 710
(172) Marnila P., Rokka S., Rehnberg-Laiho L., Kärkkäinen P.,Kosunen T., et al., 2003- Prevention and suppression of Helicobacter felisinfection in mice using colostral preparation with specific antibodies.Helicobacter. 8 (3) :192–201.
(174) Leal-Herrera Y., Torres J., Monath T., Ramos I., Gomez A., etal, 2003-High rates of recurrence and of transient reinfections of Helicobacter pylori ina population with high prevalence of infection. Am J Gastroenterol. 98 (11):2395–2402
(175) Seo M., Okada M., Shirotani T., Nishimura H., Maeda K., et al.,2002b- Recurrence of Helicobacter pylori infection and the long-termoutcome of peptic ulcer after successful eradication in Japan. J ClinGastroenterol. 34 (2) :129–134
107
(176) Knippig C., Arand F., Leodolter A., Nilius M., Bayerdorffer E., etal., 2002- Prevalence of H. pylori-infection in family members of H. pyloripositive and its influence on the reinfection rate after successful eradicationtherapy: a two-year follow-up. Z Gastroenterol. 40 (6) :383–387
(177) Soto G., Bautista C., Roth D., Gilman R., Velapatino B., et al., 2003-Helicobacter pylori reinfection is common in Peruvian adults after antibioticeradication therapy. J Infect Dis. 188 (9) :1263–1275
(178) Mitchell H., Hu P., Chi Y., Chen M., Li Y., Hazell S., 1998- A low rate ofreinfection following effective therapy against Helicobacter pylori in adeveloping nation (China). Gastroenterol. 114 (2) :256–261
(179) Rowland M., Kumar D., Daly L., O'Connor P., Vaughan D., et al,1999- Low rates of Helicobacter pylori reinfection in children. Gastroenterol.117 (2) :336–341
(180) Farrell S., Milliken I., Doherty G., Murphy J., Wootton S., et al.,2004- Total family unit Helicobacter pylori eradication and pediatric re-infection rates. Helicobacter. 9 (4) :285–288
(181) Kuipers E., Nelis G., Klinkenberg-Knol E., Snel P., Goldfain D., etal, 2004- Cure of Helicobacter pylori infection in patients with refluxoesophagitis treated with long term omeprazole reverses gastritis withoutexacerbation of reflux disease: Results of a randomised controlled trial. Gut.53 (1) : 12-20.
(182) Ruggiero P., Peppoloni S., Rappuoli R., Del Giudice G., 2003- Thequest for a vaccine against Helicobacter pylori: How to move from mouse toman?. Microbes Infect.5 (8): 749-756.
(183) Talley N., Silverstein M., Agreus L., Nyren O., Sonnenberg A., etal, 1998- AGA Technical review: evaluation of dyspepsia. Gastroenterol.114(3) : 582-595.
(184) Patel P., Khulusi S., Mendall M., Lloyd R., Jazrawi R., et al., 1995-Prospective screening of dyspeptic patients by Helicobacter pylori serology.Lancet. 346(8986) : 1315-1318.
(185) Ofman J., Etchason J., Fullerton S., Kahn K., Soll A., 1997-Management strategies for Helicobacter pylori - seropositive patients withdyspepsia: clinical and economic consequences. Annals of Internal Medicine;126(4) : 280-291.
(186) Destura R., Labio E., Barrett L,, Alcantara C., Gloria V., et al, 2004-Laboratory diagnosis and susceptibility profile of Helicobacter pylori infection
108
in the Philippines. Annals of Clinical Microbiology and Antimicrobials. 16(3):25.
(187) Misra S., Misra V., Dwivedi M., singh P., Bhargava V., et al, 1999-Evaluation of the one minute ultra rapid urease test diagnosing helicobacterpylori. Postgrad. Med. J. 75 (881):154-156
(188) Porsch-Özcürümez M., Doppl W., Hardt P., Schnell-Kretschmer H.,Tuncay M., et al, 2003- Impact of migration on helicobacter pyloriseroprevalence in the offspring of Turkish immigrants in Germany) - TheTurk. J. of Pediatr. 45(3): 203-208
(189) Ogata S., Kawakami E., Reis F., 2002 –Evaluation of invasivemethod to diagnosis Helicobacter pylori infection in children and adolescentswith dyspepsia invasive method to diagnose Hp infection. Medicina, RibeirãoPreto, 35(1) : 24-29.
(191) Soll A., 1996- Consensus conference. Medical treatment of pepticulcer disease.Practice guidelines. Practice Parameters Committee of theAmerican College of Gastroenterology. Jama. 275(8):622-629
(192) de Oliveira A., Rocha G., Queiroz D., Barbosa M., Silva S., 1999-prevalence of H.pylori infection in a population from the rural area ofaracua,MG,Brazil. Revista de Microbiologia., 30(1) :59-61.
(193) Imrie C., FRACP, Rowland M., Billy Bourke M., Brendan DrummM., 2001- Is Helicobacter pylori Infection in Childhood a Risk Factor forGastric Cancer?. Pediatrics. 107(2): 373-380
(194) Lehmann F., Drewe J., Terracciano L., Stuber R., Frei R., et al,1999- Comparison of stool immunoassay with standard methods fordetecting Helicobacter pylori infection. BMJ. 319(7222);1409
(195) Vaira D., Holton J., Menegatti M., Ricci C., Gattal L., et al, 2000-Invasive and non-invasive tests for Helicobacter pylori infection. AlimentPharmacol Ther, 14(3) :13-22.
(196) Thijs J., Vanzewit A., Thijs W., Oey H., Karrenbild A., et al, 1996-Diagnostic tests for Helicobacter pylori: A prospective evaluation of theiraccuracy, without selecting a single test as the gold standard. Am JGastroenterol. 91(10) :2125-2129,.
(197) Falsafi T., Valizadeh N., Sepehr S., Mehri Najafi., 2005- Applicationof a Stool Antigen Test To Evaluate the Incidence of Helicobacter pylori
109
Infection in Children and Adolescents from Tehran, Iran. Clinic. and diag.laborat immun. 12(9) : 1094–1097
(199) Caravalho A., Queiroz D., Mendes E., Rocha G., Penna F., 1991-Diagnosis and distribution of Helicobacter pylori in the gastric mucosa ofsymptomatic children. Braz J Med Biol Res 24(2) :163-166,.
(200) Wong B., Wong W., Wang W., Tang V., Young J., et al, 2001- Anevaluation of invasive and non-invasive tests for the diagnosis ofHelicobacter pylori infection in Chinese. Aliment Pharmacol Ther. 15(4) :505-511,.
(201) Dickey W, Kenny B., McConnell J., 1996- Effect of proton pumpinhibitors on the detection of Helicobacter pylori in gastric biopsies. AlimentPharmacol Ther, 10(3):289-293.
(202) Lam S., Talley N, 1998- Consensus conference on the managementof Helicobacter pylori infection. J Gastroenterol Hepatol, 13(1):1-12
(203) Logan R., Walker M., Misiewicz J., Gummett P., Karim Q., et al,1995- Changes in the intragastric distribution of Helicobacter pylori duringtreatment with omeprazole. Gut, 36(1):12-6.
(204) Leung W., et al, 1998- False-negative biopsy urease test in bleedingulcers is due to buffering effects of blood. Am J Gastroenterol. 93(10): 1914–1918
(205) Gisbert J., et al, 2006- Accuracy of Helicobacter pylori diagnostictests in patients with bleeding peptic ulcer: a systematic review and meta-analysis. Am J Gastroenterol 101(4) : 848–863
(206) Chow D., Sung J., 2007- Is the prevalence of idiopathic ulcers reallyon the increase? Nature Clinical Practice Gastroenterology & Hepatology.4(4) : 176-177
(207) Gunaid A., Hassan N., Murray-Lyon I., 2003- Prevalence and riskfactors for Helicobacter pylori infection among Yemeni dyspeptic patients.Saud. Med. J. 24(5) :512-517
(208) Almadi M., Aljebreen A., Tounesi F., Abdo A., 2007- Helicobacterpylori prevalence among medical students in a high endemic area. Saud.Med. J. 28(6) :896-898
(209) Rodrigues M., Queiroz D., Rodrigues R., Rocha A., Braga Neto M.,et al, 2005- Helicobacter pylori infection in adults from a poor urban
110
community in northeastern Brazil: demographic, lifestyle and environmentalfactors. Braz J Infect Dis 9(5):405-410
(210) Graham D., Malaty H., Dolores G., et al, 1991- Epidemiology ofHelicobacter pylori in an Asymptomatic Population in the United States.Effect of Age, Race and Socioeconomic Status. Gastroenterol; 100(6):1495-1501.
(211) Sathar M., Gouws E., Simjeea E., Mayat A., 1997-Seroepidemiological study of H. pylori infection in South African. Trans R SocTrop Med Hyg; 91(4):393-395
(212) Sood M., Joshi S., Akobeng A., Mitchell J., Thomas G., 2005-Growth in children with Helicobacter pylori infection and dyspepsia. Archiv. ofDisea in Child. 90(10):1025-1028
(213) Bakka A.,,Salih B., 2002-. Prevalence of Helicobacter pylori infectionin asymptomatic subjects in Libya. Diagn Microbiol Infect Dis. 43(4):265-268.
(214) Tomb J., White O., Kerlavage A., Clayton R., Sutton G., et al., 1997-The complete genome sequence of the gastric pathogen Helicobacter pylori.Nature. 388(6642):539-47
(215) Endoh K, Leung F., 1994- Effects of smoking and nicotine on thegastric mucosa: A review of clinical and experimental evidence.Gastroenterol. 107(3):864-878.
(216) El-Barrawy M., Morad M., Gaber M., 1997-Role of Helicobacter pyloriin the genesis of gastric ulcerations among smokers and nonsmokers. East.Medit. Health J. 3(2): 316-321.
(217) Brenner H., Rothenbacher D., Bode G., Adler G.,1997- Relation ofsmoking and alcohol and coffee consumption to active Helicobacter pyloriinfection: cross sectional study. BMJ. 315(7121):1489-1492.
(218) Mabe K., Yamada M., Oguni I., Takahashi T., 1999- In Vitro and InVivo Activities of Tea Catechins against Helicobacter pylori. Antimicrob.Agent. and Chemother.. 43(7):1788-1791.
(219) Rolle-Kampczyk U., Fritz G., Diez U., Lehmann I., Richter M., et al,2004- Contaminated well water: a risk factor for Helicobacter pylori infectionInt J Hyg Environ Health. 207(4):363-368
(220) Peach H., Pearce D., Farish S., 1997- Helicobacter pylori infection inan Australian regional city: prevalence and risk factors MJA. 167(6):310-313.
(221) Megraud F., 1997- How should Helicobacter pylori infection bediagnosed? Gastroenterol. 113 (6): 93-98.
111
(222) Rothenbacher D., Bode G., Adler G., Brenner H., 1997- Use ofcommonly prescribed antibiotics is not associated with prevalence ofHelicobacter pylori infection in adults. Scand J Gastroenterol. 32(11):1096-1099.
(223) McCallion W., Murray L., Bailie A., et al., 1997- Helicobacter pyloriinfection in children: relation with current household living conditions. Gut.39(1) :18-21.
(224) Fox J., Batchelde M., Marini R., et al., 1995- Helicobacter pyloriinduced gastritis in the domestic cats. Infect. Immun. 63(7):2674-81.
(225) Fiedorek S., Malaty H., MP., Dolores L. Evans P., et al, 1991-Factors Influencing the Epidemiology of Helicobacter pylori Infection inChildren. Pediatrics. 88(3). 578-582
Appendices
112
Islamic university – Gaza
Medical Technology
Department
غزة–الجامعة اإلسالمیة
قسم التحالیل الطبیة
The aim of this questionnaire is to determine the risk factor associated with H.pylori
infection.
All personal information will be confidential
Thanks for your corporation ……
Sample number…………….. Patients name……………….
1-Age……………
2- Sex ………… Male Female
3-Weight …………..
4-Martial Status…… Married Single Divorced
5-Do you smoke? Yes No
................6-How many cigarettes per day?
7- Do you drink tea? Yes No
8- How many cups of tea do you drink per day?………………
9-Do you drink coffee? Yes No
10- How many cups of coffee do you drink per day? ……..11- What type of water did you drink during childhood?
Municipality or well water Filtered
12-What type of water did you drink during adulthood ?
Municipality or well water Filtered
13-Have you any dental complains?
No Yes
113
14-What is your education level?
University High school Intermediate school Less
15-What is your family income?………………….
16-What is the socio-economics level of your neighborhood?
Good Fair Poor
17-Is there a garbage collecting system in your area?
Yes No
18-What is the type of your accommodation?
Villa House Flat
19-How many rooms are in your accommodation? ……….
20-How many members are in your family? …………….
21-How many persons are living in each room?...........
22-What’s the source of water in your house?
Municipality Wells
23- Evaluation of sewage system in your house
Good Fair Poor
24- Do you take drugs? Yes
25- Did you take any antibiotics in the last month? Yes
26- Have you any animals in your house? Yes
27- Did you ever travel abroad?
Yes No
No
No
No
Medical Tests
1-(Ultra Rapid Urease Test)…………..
2-(Methylene Blue stains)……………….
3-(IgM in serum)…………..
4-(HpSAg)………………
114
Islamic university – Gaza
Medical Technology
Department
غزة–الجامعة اإلسالمیة
قسم التحالیل الطبیة
.Hیھدف ھذا االستبیان إلى معرفة عوامل الخطر المرتبطة ببكتیریا pylori المسببة للقرحة المعدة :
......كل البیانات ستبقى قید السریة التامة
جاز ھذه الدراسة نرجو مساعدتكم في أن
شاكرین لكم حسن تعاونكم
................. اسم المریض.....................العینةرقم
.......................... العمر -1
الجنس -2 أنثى ذكر
.......................... الوزن-3
مطلق أو منفصل أعزب متزوج
ال نعم
الحالة االجتماعیة -4
ھل تدخن السجائر أو الشیشة؟-5
………………….. 6 إذا كنت تدخن فكم مرة بالیوم؟-
ال ال نعم
.......................
ال نعم
........................
7ھل تشرب الشاي؟-
من إذا كنت تشرب الشاي كم كوبا -8
الشاي تشرب في الیوم؟
ھل تشرب القھوة؟-9كم فنجان في،القھوة إذا كنت تشرب -10
الیوم تشرب؟تشربھ في ما ھو نوع الماء الذي كنت-11 من اآلبارأو بلدیة مفلتر
الطفولة؟
ما ھو نوع الماء الذي كنت تشربھ حالیا؟12 أو من اآلبار بلدیة مفلتر
من مشاكل صحیة في أسنانك؟ھل تعاني13 نعم ال
حصلت علیھ؟ ھو مستوى التعلیم الذي 14 دون ذالك متوسط ثانوي جامعي
115
..................... ما ھو الدخل المادي للعائلة؟15
الحي الذي تسكن بھ كیف تصنفھ؟16 دون ذالك متوسط جید
ھل یتم جمع القمامة باستمرار؟17 ال نعم
ما ھو نوع السكن؟18 شقةوسط سكن مت فیال
..................... ما ھو عدد الغرف في المنزل؟19
................... كم عدد أفراد العائلة ؟20
.................... كم فرد یسكن كل غرفة؟21
ما ھو مصدر الماء في المنزل؟22 میاه البلدیة میاه اآلبار
كیف ھو نظام الصرف الصحي لدیكم؟23 دون ذالك متوسط جید