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.
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http://dx.doi.org/10.1111/hel.12218 | DOI Listing |
Parasitol Int
January 2025
Department of Health Sciences, Unit of Clinical Microbiology, "Magna Græcia" University of Catanzaro "Mater Domini" Teaching Hospital, Catanzaro, Italy; Department of Health Sciences, Unit of Clinical Microbiology, "Magna Græcia" University of Catanzaro "Mater Domini" Teaching Hospital, Catanzaro, Italy. Electronic address:
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Supplementary General Sciences Department, Faculty of Oral and Dental Medicine, Future University in Egypt, Cairo 11835, Egypt.
Helicobacter pylori (H. pylori) is an extremely prevalent human pathogen globally that leads to severe illnesses. Sadly, the worldwide issue of H.
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Department of Oncological, Transplant and General Surgery, Faculty of Medicine, Medical University of Gdansk, 80-214 Gdansk, Poland.
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Department of Gastroenterology, Saiseikai Kanazawa Hospital, Ni-13-6 Akatsuchimachi, Kanazawa, Ishikawa, 920-0353, Japan.
Localized light chain amyloidosis is considered to be a plasmacytic B-cell lymphoproliferative disorder caused by antigenic induction. A hypothesis has been proposed that antigen-induced local plasmacytic B cells produce amyloidogenic proteins that are processed into amyloid fibrils in giant cells leading to amyloid fibril deposition. However, the inciting antigen exposure or immune response that signals plasmacytic B-cell infiltration, activation, and selection, is unknown.
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