GASTRIC INFECTION BY HELICOBACTER-PYLORI AND ANTRAL GASTRITIS IN HYPERGLYCEMIC OBESE AND IN DIABETIC SUBJECTS

Citation
G. Perdichizzi et al., GASTRIC INFECTION BY HELICOBACTER-PYLORI AND ANTRAL GASTRITIS IN HYPERGLYCEMIC OBESE AND IN DIABETIC SUBJECTS, The New microbiologica, 19(2), 1996, pp. 149-154
Citations number
23
Categorie Soggetti
Microbiology
Journal title
The New microbiologica
ISSN journal
11217138 → ACNP
Volume
19
Issue
2
Year of publication
1996
Pages
149 - 154
Database
ISI
SICI code
1121-7138(1996)19:2<149:GIBHAA>2.0.ZU;2-D
Abstract
The aim of this work was to ascertain if diabetes and obesity can affe ct gastric colonization by Helicobacter pylori. 59 hospitalized subjec ts with dyspepsia and endoscopic antral gastritis were selected. They were divided into three groups: I) 13 patients with normal body weight and without diseases other than gastritis (control group); II) 15 pat ients with essential obesity of whom 10 had impaired glucose tolerance (IGT); III) 31 patients with type II diabetes mellitus, of whom 14 we re obese. Three gastric biopsies were obtained from each patient for h istologic examination and H. pylori detection by means of rapid urea t est, culture and histological evidence of Helicobacter-Like Organisms (HLO). Age, sex, blood glucose, cholesterol, triglycerides, HDL-choles terol, basal gastrine, duration of illness, body weight were statistic ally analysed. Differences between the three groups were not statistic ally significant. There was a higher prevalence of H. pylori infection both in obese and in diabetic patients with respect to control subjec ts. Prevalence became still higher in obese patients with impaired glu cose tolerance. Among the three tests used for the detection of H. pyl ori, culture and rapid urea were reliable and specific, while the hist ologic test was highly sensitive but barely specific. Our data suggest that both obesity and type II diabetes may be associated with an incr eased incidence of H. pylori colonization. This could be related to th e reduced gastric motility observed in both pathologies and chemical c hanges in gastric mucosa following non-enzymatic glycosylation process es.