الفهرس 
HELICOBACTER PYLORI HISTORYOnly 14 pages are availabe for public view
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Abstract
Introduction:
Helicobacter pylori infection is now recognized as a worldwide problem. H. pylori infection is the most common cause of chronic gastritis, and has been strongly linked to peptic ulcer disease and gastric cancer. H. pylori is estimated to infect one-half of the world’s population.
In addition to morphologic characterization, the organism can be biochemically characterized as catalase, oxidase, and urease positive. Urease appears to be vital for its survival and colonization; it is produced in abundance, making up more than 5 percent of the organism’s total protein weight. Bacterial urease activity is clinically important because it forms the basis for several invasive and noninvasive tests to diagnose infection.
Among microbial virulence factors identified so far, the H-pylori cytotoxin-associated gene A (cagA), its related pathogenicity island (cagPAI), vacuolating toxin A (VacA), and factors involved in adherence of H pylori to gastric epithelial cells, have been linked to enhanced pathogenicity of the bacterium. The immunoreactive 120–145 kDa protein CagA is encoded by cagA, which is found in 60–70% of H pylori strains in the industrialized world.( Suerbaum et al., 2002) cagA maps to the cagPAI, a gene cluster of 29 genes spanning 37 kb of genomic DNA. Some of the genes in the cagPAI region encode a type IV bacterial secretion apparatus, which can translocate cagA into host target cells. Phosphorylation of cagA may activate host signalling-pathways and subsequently influence host cellular functions, including proliferation, apoptosis, cytokine release, and cell motility. (6) In addition, several other cagPAI genes, such as cagG, cagH, cagI, cagL, and cagM, seem to be associated with particular epithelial cell responses relevant to H pylori pathogenicity.
Associations between H. pylori infection and a range of cardiovascular, respiratory, hepatobiliary, dermatological, neurological, autoimmune, allergic and haematological diseases, as well as growth and weight disorders and retardation, have been investigated. However, there is by no means consensus with regard to the findings of such studies, Mechanisms for an association of H. pylori with diabetes mellitus or insulin resistance or metabolic syndrome are unclear. Clinical diabetes might promote infection by lowering immunocompetence or altering gastric motility with autonomic neuropathy.
Aim:
We aim in this study to assess the correlation between helicobacter pylori infection and metabolic syndrome.
Methods:
This study includes 100 patients attended Ain Shams University Hospital Endoscopy Unit.
• The patients will be divided into two groups:
group A: includes 50 patients with positive H.pylori infection.
group B: includes 50 patients negative for H. pylori infection.
• Inclusion criteria: adults, males and females complaining of different upper GIT symptoms older than 18 years
• Exclusion criteria: Patients with viral hepatitis B or C infection.
All patients in this study will be subjected to:
1. Informed consent will be obtained from all the patients
2. Full history taking (history of diabetes or hypertention and drug history).
3. Complete physical examination included measurment of blood pressure and waist circumference).
4. Lab investigations including:
1. Fasting lipid profile (cholesterol-triglyceride-HDL-LDL).
2. Fasting blood sugar.
3. Hepatitis B surface antigen&Hepatitis C antibody.
4. Upper GIT endoscopy& biopsies.
5. Urease test to the biopsies taken.
6. Abdominal ultrasound.
Results:
This study included 100 patients have attended Ain Shams University Hospital Endoscopy Unit.
Table (1): Comparison between both groups as regards lipid profile.
P t H pylori –ve
N=50 Hpylori+ve
N=50 Variables
>0.05
NS 0.4 182+40 185+44 Cholesterol
>0.05
NS 0.7 44+12 43+11 HDL
>0.05
NS 0.6 112+34 115+36 LDL
>0.05
NS 0.9 132+60 145+63 TG
This table shows no statistically significant difference between both groups as regard different variables by using unpaired t-test. Comparing the two groups as regards serum cholesterol, HDL, LDL, and triglyceride, there were no statistically significant difference between the two groups (p>0.05).
Table (2): Comparison between both groups as regards metabolic syndrome.
P H pylori –ve
N=50 Hpylori+ve
N=50 Variables
<0.001
HS 37(74%) 18(36%) No
13(26%) 32(64%) Yes
This table shows that H-pylori positive group has higher percentage of metabolic syndrome, 64 % of the patients with H-pylori infection have metabolic syndrome in comparison to only 26% of the patients who have not H-pylori infection. And on the other hand 36% of the patients with H-pylori infection have not metabolic syndrome in comparison to 74% of the patients who have not H-pylori infection with statistically significant difference between both groups by using Fisher exact test.( P<0.001)
Table (18): Diagnostic performance of correlation between H-pylori infection and diagnosis of metabolic syndrome.
Variables %
Sensitivity 71.1%
Specificity 67%
Positive predictive value 64%
Negative predictive value 74%
Accuracy 69%
This table shows that the sensitivity of H-pylori infection as a predictor of metabolic syndrome is 71.1% and the specificity is 67% with over all accuracy as a predictor 69%.
Conclusion:
In this study Strong association between H-pylori and metabolic syndrome and cardiovascular disease has been demonstrated.