Severity of atrophic gastritis related to antiparietal cell antibody and gastric carcinogenesis, including p53 mutations

Abstract

Infection with Helicobacter pylori (Hp) has been linked to atrophic gastritis, an inflammatory precursor of non-cardia gastric carcinoma. Mutations in the p53 gene are one of the most frequent genetic alterations in gastric carcinoma. In a subgroup of atrophic gastritis, antiparietal cell antibody (APCA) has been detected. This study was aimed to clarify the role of APCA in the progression of atrophic gastritis and gastric carcinogenesis, and to determine the relationship of the severity of atrophic gastritis to gastric carcinoma and to p53 mutations. In 494 control subjects and 284 gastric carcinoma patients, serum APCA was evaluated and all subjects and patients were classified into four groups using serologic markers (anti-Hp IgG antibody and pepsinogen (PG) test: positive; PG I < 70 microg/L and PG I/II ratio < 3.0) as follows: A, HP- PG-; B, HP+ PG-; C, HP+ PG+ and D, HP- PG+. p53 mutations were analyzed in 174 of 284 patients. Antiparietal cell antibody seropositivity increased from group B to D, however, no difference in its positivity was found between controls and patients. The incidence of gastric carcinoma increased from A to D, especially the intestinal subtype. The frequency of p53 gene mutations was higher in PG+ than in PG- gastric carcinoma. Antiparietal cell antibody seropositivity is involved in the progression of a subgroup of atrophic gastritis, but not associated with gastric carcinogenesis. Severe atrophic gastritis is associated with susceptibility to gastric carcinoma, especially the intestinal subtype, and p53 mutations.