Lower Risk of Gastric Atrophy and Intestinal Metaplasia in Patients with MALT Lymphoma despite Helicobacter pylori Infection
10.7704/kjhugr.2019.19.2.115
- Author:
Sang Min LEE
1
;
Dae Young CHEUNG
;
Joon Ki MOON
;
Jin Il KIM
;
Soo Heon PARK
;
Jae Kwang KIM
Author Information
1. Department of Internal Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea. adagio@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Gastritis, atrophic;
Helicobacter pylori;
Intestinal metaplasia;
Lymphoma;
Stomach
- MeSH:
Adenocarcinoma;
Atrophy;
Electronic Health Records;
Gastrins;
Gastritis, Atrophic;
Helicobacter pylori;
Helicobacter;
Humans;
Korea;
Lymphoid Tissue;
Lymphoma;
Lymphoma, B-Cell, Marginal Zone;
Metaplasia;
Pepsinogen A;
Prevalence;
Retrospective Studies;
Seoul;
Stomach
- From:The Korean Journal of Helicobacter and Upper Gastrointestinal Research
2019;19(2):115-119
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Atrophic gastritis and intestinal metaplasia are sequential consequences of chronic Helicobacter pylori (H. pylori) infection. These conditions are well known to increase the risk of gastric adenocarcinoma development. Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is also a malignant consequence of H. pylori infection, but the relationship between gastric MALT lymphoma and atrophic gastritis-intestinal metaplasia has not been a focus of interest. We investigated the clinical characteristics of atrophic gastritis and intestinal metaplasia in patients with gastric MALT lymphoma. MATERIALS AND METHODS: A study was conducted by reviewing the electronic medical records of patients diagnosed as having gastric MALT lymphoma at an academic institute, the Yeouido St. Mary's Hospital, Seoul, Korea, between January 2001 and December 2018. RESULTS: Fifty-eight subjects were enrolled consecutively during the study period and analyzed retrospectively. The patients' mean age was 56.9 years old. The male-to-female ratio was 1.15 (31/27). On histological examination, background atrophic gastritis and intestinal metaplasia were detected in 26.8% (15/58) of cases. Serum pepsinogen I, II and gastrin levels, as serological markers of atrophy, were evaluated in 28 subjects. Three (5.2%) of the 28 cases were compatible with serological atrophic gastritis (pepsinogen I/II ratio of <3 and pepsinogen I level of <70 ng/mL). CONCLUSIONS: In patients with gastric MALT lymphoma, the prevalence of background mucosal atrophy or intestinal metaplasia was 26.8% on histological examination and 5.2% on serological analyses. These rates are lower than those in patients with gastric adenocarcinoma. This result suggests a different carcinogenic pathway of gastric MALT lymphoma from that of adenocarcinoma.
