title: A past history of gastric ulcers and Helicobacter pylori infection increase the risk of gastric malignant lymphoma.
abstract: Helicobacter pylori (H. pylori) is a causative agent for peptic ulcers as well as some types of gastric lymphoma; however, the relationship between a peptic ulcer history in combination with H. pylori infection and the risk of gastric lymphoma has not been fully evaluated. To examine this point, we conducted a case-control study with 645 patients histologically diagnosed as having malignant lymphomas and 3225 non-cancer controls. Plasma H. pylori IgG status was assessed for subgroups for which blood samples were available (116 cases and 114 controls). An association with a history of gastric, but not duodenal ulcers was found for gastric lymphoma [odds ratio (OR) = 5.41, 95% confidence interval (CI): 3.12-9.39]. In the examination according to histological subtype, the OR was high for both gastric mucous-associated lymphoid tissue (MALT) lymphoma (OR = 5.54, 95% CI: 2.56-12.01) and diffuse large B-cell lymphoma (DLBCL) (OR = 7.23, 95% CI: 2.62-19.90). In the analysis of H. pylori antibody, the risk of total gastric lymphoma was associated with H. pylori infection (OR = 5.34, 95% CI: 1.42-20.05). A high prevalence of H. pylori infection was also found for both gastric MALT lymphoma (8 out of 10: 80.0%) and DLBCL (8 out of 9: 88.9%). Further, in subgroup analysis of subjects with H. pylori infection, gastric ulcer history, but not duodenal ulcer history was associated with the risk of gastric lymphoma (OR = 4.15, 95% CI: 1.02-16.89). In conclusion, we found a positive association with a past history of gastric ulcer and H. pylori infection for gastric lymphoma, while duodenal ulcer history was no association. These results suggested the risk of gastric lymphoma increased by interaction between H. pylori infection and gastric ulcer history. Further studies are warranted.
authors.affiliation: Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Keitaro
authors.initials: K
authors.lastname: Matsuo
authors.forename: Hidemi
authors.initials: H
authors.lastname: Ito
authors.forename: Kaoru
authors.initials: K
authors.lastname: Hirose
authors.forename: Kenji
authors.initials: K
authors.lastname: Wakai
authors.forename: Toshiko
authors.initials: T
authors.lastname: Saito
authors.forename: Shigeki
authors.initials: S
authors.lastname: Sato
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Morishima
authors.forename: Shigeo
authors.initials: S
authors.lastname: Nakamura
authors.forename: Ryuzo
authors.initials: R
authors.lastname: Ueda
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tajima
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D004381:Duodenal Ulcer / Q000150:complications; D005260:Female; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D006801:Humans; D008223:Lymphoma / Q000150:complications* / Q000382:microbiology; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000150:complications* / Q000382:microbiology; D013276:Stomach Ulcer / Q000150:complications / Q000382:microbiology*