33 Background: Atrophic gastritis and intestinal metaplasia are sequential consequences of chronic H. pylori infection. H. pylori infection is a well-known risk factor for gastric adenocarcinoma and MALT lymphoma of stomach. Atrophic gastritis and intestinal metaplasia increase the risk of gastric adenocarcinoma development. The relationship between gastric MALT lymphoma and atrophic gastritis-intestinal metaplasia has not been on the spot of interest. We investigated the clinical characteristics of gastric MALT lymphoma and co-presence of atrophic gastritis and intestinal metaplasia. Methods: Study was conducted by review of electronic medical record of patients who were diagnosed with gastric MALT lymphoma at an academic institute, the Yeouido St. Mary's Hospital, Seoul, Korea, from January 2001 to March 2018. Results: A total of 51 subjects were enrolled consecutively during the study period and analyzed retrospectively. The mean age was 57.5-year-old. The male to female ratio was 1.04 (26/25). On histologic examination, background atrophic gastritis was accompanied in 64.7% (33/51). Serum pepsinogen I, II and gastrin level, as serological marker for atrophy, were evaluated in 21 subjects. Thirteen out of 21 (61.9%) were compatible with serological atrophic gastritis (pepsinogen I / II ratio of less than three or pepsinogen I < 70 ng/mL). Conclusions: Prevalence of background mucosal atrophy or intestinal metaplasia was around 60% in patients with gastric MALT lymphoma. This is comparable to that of general population and lower than that of patients with gastric adenocarcinoma. Even though age can be a confounding factor, this result suggests different carcinogenic pathway of gastric MALT lymphoma from adenocarcinoma.
Gastric adenocarcinoma at stage IV with complete remission after neoadjuvant therapy concurrent with adenosquamous carcinoma of the ampulla of Vater: a case report and literature review
