Prostate stem cell antigen gene TT genotype and development of intestinal metaplasia in Helicobacter pylori infection.

Uotani T1,2, Sugimoto M3, Ichikawa H4, Tanaka S1,2, Nagashima H5, Uchida T6, Graham DY1, Yamaoka Y1,2.

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Abstract

AIM:

Gastric cancer is etiologically related to interactions between Helicobacter pylori infection, environmental, and host factors. Gastric carcinoma is associated with a cascade of increasing atrophic gastric mucosal damage. Prostate stem cell antigen polymorphisms have been associated with an increased risk of gastric cancer. Here, we examined the interaction between prostate stem cell antigen polymorphisms and H. pylori in the progression of H. pylori gastritis.

METHODS:

Prostate stem cell antigen polymorphisms (TT, TC and CC) among H. pylori infected and uninfected Bhutanese were compared with the severity of H. pylori gastritis (neutrophils, monocytes, atrophy scores, H. pylori density, and the presence and extent of intestinal metaplasia) using the updated Sydney system.

RESULTS:

Biopsies from 339 patients were included. The proportion of biopsies with intestinal metaplasia was also significantly (P<0.05) greater among those with the TT genotype than with either the CT or CC genotype. Despite no significant differences in inflammation or H. pylori density scores, the scores for the premalignant condition, intestinal metaplasia in both the gastric corpus and antrum, among H. pylori infected with the TT genotype was significantly (P <0.05) greater than C allele carriers.

CONCLUSIONS:

Prostate stem cell antigen TT genotype was associated with more than a 3-fold increase in the prevalence and extent of gastric mucosal intestinal metaplasia compared to C allele carriers among H. pylori infected Bhutanese. This article is protected by copyright. All rights reserved.