H. pylori infection-negative gastric cancer

Abstract

Helicobacter pylori (H. pylori) infection is considered to be the main etiological factor of gastric carcinogenesis. H. pylori infection induces superficial gastritis, which progresses to atrophic gastritis with loss of acid secretion and then to dysplasia and cancer. As H. pylori are eliminated once they have caused gastric atrophy and intestinal metaplasia after longtime colonization, the possibility of false-negative results of conventional H. pylori tests could increase in gastric cancer with severe gastric atrophy. The incidence of H. pylori infection-negative gastric cancer (HPIN-GC) varied among studies according to the definition of H. pylori-negative infection. When combination of multiple methods (histologic examination, rapid urease test, urea breath test, H. pylori culturing, anti-H. pylori antibody, and polymerase chain reaction assay for H. pylori) are used and past H. pylori infection ruled out by the presence of atrophic change, HPIN-GC is compromised about 2-5 % of gastric cancer. The cardia location is common in HPIN-GC. The more advanced pathologic T stage and N stage in HPIN-GC have been reported in some studies. Many previous studies reported that negative H. pylori infection was an independent poor prognostic factor, but recent researches found no significant difference in prognosis between H. pylori-positive and H. pylori-negative cancer.