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
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.