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Morphologic and Histologic Changes in Gastric Adenomas After Helicobacter pylori Eradication: A Long‐Term Prospective Analysis
Author(s) -
Suzuki Sho,
Gotoda Takuji,
Suzuki Haruhisa,
Kono Shin,
Iwatsuka Kunio,
Kusano Chika,
Oda Ichiro,
Sekine Shigeki,
Moriyasu Fuminori
Publication year - 2015
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12218
Subject(s) - helicobacter pylori , medicine , prospective cohort study , term (time) , gastroenterology , helicobacter infections , physics , quantum mechanics
Background Helicobacter pylori infection causes gastric neoplasia via development of chronic atrophic gastritis and intestinal metaplasia. The effect of H. pylori eradication on pre‐existing gastric neoplasias is still controversial. The aim of this study was to use long‐term observation to clarify morphologic and histologic changes in gastric adenomas following H. pylori eradication. Materials and Methods Twenty‐seven patients with gastric adenomas (revised Vienna classification category 3 or 4.1) who underwent successful H. pylori eradication between April 1996 and December 1997 were followed up at regular intervals with endoscopic and histologic examination. The association between macroscopic and histologic regressions of the lesions and the following patient and lesion characteristics was assessed with univariate analysis: follow‐up period, age, sex, serum pepsinogen level, lesion size, lesion location, and histologic gastritis. Results The mean follow‐up period was 91.9 months (range 44–181 months). Twelve lesions (44.4%) showed macroscopic regression, of which 7 (25.9% of the total) also showed histologic regression, with the mean duration from H. pylori eradication to complete macroscopic and histologic regression being 19.9 months. The other 15 lesions (55.6%) remained stable macroscopically and histologically, of which 6 (22.2% of the total) progressed to malignancy during the follow‐up period. Univariate analysis revealed that female sex ( p = .005), smaller lesion size ( p = .025), higher baseline serum pepsinogen II level ( p = .041), and absence of intestinal metaplasia in the greater curvature of the corpus ( p = .026) were significantly associated with complete regression. Conclusions Helicobacter pylori eradication may induce regression in some gastric adenomas.