医学
肠化生
幽门螺杆菌
胃肠病学
内科学
胃窦
胃炎
胃
吉姆萨染色
组织学
病理
摘要
BACKGROUND: We aimed to evaluate Helicobacter pylori eradication impact on the gastric carcinogenesis cascade following the evolution of intestinal metaplasia (IM) in gastric antrum after Helicobacter pylori (HP) eradication. METHODS: We followed yearly for a 5 year period after bacterial eradication, 69 HP positive patients with gastric or duodenal ulcers who showed antral gastric intestinal metaplasia at histology at time 0. All patients, eradicated by OAC triple short-term therapy and assessed both performing 13C-UBT 1 month after eradication and by Giemsa stain, persisted HP negative during follow-up. Upper endoscopy with 6 biopsies from gastric antrum at least 2 cm away from pylorus, was repeated every year in each patient involved in the study, in order to evaluate IM evolution and HP eradication persistence. During the follow-up histological specimens were examinated from the same pathologist and IM differentiated as complete (type I), incomplete (type II) or incomplete solphomucin-positive (type III). Statistical analysis between different groups after each year was performed by chi2 method. RESULTS: At time 0.48 cases out of 69 (69.7%) presented type I IM, 14 cases (20.2%) type II IM and 7 cases (10%) type III IM. IM presence in histological specimens after 1, 2, 3, 4 and 5 years from HP eradication were evaluated and statistical analysis between the 3 IM groups after each control showed a significant regression after HP eradication in type I versus III IM (p<0.001), mostly 2 and 3 years after HP eradication, but no significance in type I versus II IM (p=0.284) neither in type II versus III IM (p=0.981) also after 5 years. CONCLUSIONS: HP eradication permits complete intestinal metaplasia regression in gastric antrum 2 or 3 years after antibiotic treatment. Otherwise incomplete IM in gastric antrum, both type II and III, is not significantly modified after bacterial eradication.
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