Helicobacter pylori associated gastric pathology in patients with type II diabetes mellitus and its relationship with gastric emptying: The Ankara study
N. Guvener et al., Helicobacter pylori associated gastric pathology in patients with type II diabetes mellitus and its relationship with gastric emptying: The Ankara study, EXP CL E D, 107(3), 1999, pp. 172-176
Citations number
16
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
Helicobacter pylori (HP) is the most common cause of nonerosive nonspecific
gastritis. Gastric and duadenal ulcer both are found to be associated with
HP infection. Another consequence of HP infection is that it may progress
to chronic atrophic gastritis which is a well recognized risk factor for ad
enocarcinoma of the stomach. So by extension. HP infection can be accepted
as a risk factor for gastric cancer. From this aspect, identification of ri
sk groups is increasingly important. It is well-known that patients with di
abetes mellitus are mon pr-one to infection. Besides this, presence of gast
roparesis diabeticorum may lead to bacterial overgrowth in the upper gastro
intestinal (GI) tract.
The present crossectional study was planned to study the presence of HP inf
ection in diabetic patients with alterations in upper GI motility and to co
mpare the results with healthy control group.
Group I consisted of 51 patients with type II diabetes mellitus las defined
by National Data Group criteria) without any dyspeptic symptoms. Twenty-fi
ve age-matched healthy people served as a control in group II. Radionuclide
-labelled solid meals were used to calculate gastric emptying time (GET). A
ccording to the results, patients in group I were divided into two groups.
Patients with prolonged GET were grouped as group IA. while group IB consis
ted of patients with normal or shortened GET. Presence of HP gastritis is d
etermined by histopathologic examination of endoscopic biopsy specimen.
The results showed that the prevalence of I-IP gastritis in group I and II
were 80.4% and 56% respectively and the difference was significant statisti
cally (p: 0.03. In group IA, the prevalence of HP infection was estimated t
o be 88.2%, while in group IB it was 76.5% but the difference was not signi
ficant (p: 0.31). We have not found any correlation between HbA1c levels an
d the presence of HP infection in both group IA and IB (p values 0.26 and 0
.15 respectively).
We conclude that the prevalence of MP gastritis is higher in asymptomatic d
iabetic patients compared with healthy people. But there is no association
between the alterations in GET and the presence of HP gastritis as indicate
d by our results. So prolonged GET may not be:regarded as a specific pathog
enic mechanism or a cause of HP infection in NIDDM patients.