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  • Title: Genetic factors in the development of gastric precancerous lesions--a role of Helicobacter pylori ?
    Author: Jablonská M, Chlumská A.
    Journal: J Physiol Paris; 2001; 95(1-6):477-81. PubMed ID: 11595478.
    Abstract:
    UNLABELLED: Helicobacter pylori is believed to predispose to gastric cancer by inducing gastric precancerous alterations. There is a well known predisposition to gastric cancer and the risk of developing it is greater in relatives of patients with familial cases of this malignancy. The aim of this study was to determine the prevalence of gastric precancerous lesions (atrophy and intestinal metaplasia) and their association with Hp infection in first-degree relatives in patients with noncardia gastric cancer. METHODS: Hp status and gastric histology assessed by upper gastrointestinal endoscopy, biopsies from the antral and body region, the rapid urease test and staining for Hp, inflammation, activity, atrophy and intestinal metaplasia (prevalence and grading) were studied in 108 first-degree relatives of patients with noncardia gastric cancer and compared with 73 controls with mild non-ulcer dyspepsia who had no cancer relatives and were examined in the same way. RESULTS: subjects with and without cancer relatives had a similar prevalence of Hp infection (49 vs. 47%). Endoscopy revealed a few asymptomatic duodenal ulcers and small hiatus hernias in Hp positive subjects of both groups. Hp positive relatives of gastric cancer had a markedly higher prevalence of atrophy than those with Hp negativity without cancer relatives (29 vs. 9%) and those with Hp negativity and cancer relatives (29 vs. 3%. Prevalence of intestinal metaplasia was also higher in those with Hp positivity and cancer relatives than in those without cancer relatives (15 vs. 5% and was not present in Hp negative subjects with cancer relatives. Inflammation and activity showed similar scores in subjects with and without cancer relatives with higher scores in both Hp positive groups. The prevalence of precancerous lesions in the relatives of gastric cancer was nearly always confined to those with Hp positivity. One year after eradication the prevalence of atrophy in cancer relatives decreased from 29 to 14%; prevalence of intestinal metaplasia remained without substantial changes. Scores for inflammation and activity were also lower after eradication. CONCLUSIONS: First-degree relatives of patients with gastric cancer have an increased prevalence of gastric precancerous abnormalities which are strongly confined to those with Hp infection. Eradication of Hp in these subjects with cancer relatives reduces the prevalence of precancerous lesions (atrophy) and grades of inflammation and activity. In view of these results, eradication of Hp should be offered to such subjects.
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