Anti‐Helicobacter pylori therapy in localized gastric mucosa‐associated lymphoid tissue lymphoma: A prospective, nationwide, multicenter study in Japan

Abstract

Background Helicobacter pylori eradication therapy was approved in Japan for the first‐line, standard treatment of H. pylori‐positive gastric mucosa‐associated lymphoid tissue (MALT) lymphoma. Although several retrospective studies or small‐scale single‐center studies have been reported, a prospective, large‐scale, nationwide, multicenter study has not been reported from Japan.Materials and MethodsWe conducted a prospective, nationwide, multicenter study to evaluate the clinical efficacy of rabeprazole‐based triple H. pylori eradication therapy for patients with localized gastric MALT lymphoma in practice‐based clinical trial. A total of 108 H. pylori‐positive patients with stage I/II 1 gastric MALT lymphoma underwent H. pylori eradication therapy. The primary endpoints were complete remission (CR) rate and the rate of transfer to secondary treatment. The secondary endpoints were CR maintenance duration and overall survival (OS).Results CR of lymphoma was achieved in 84 of 97 patients (86.6%), during the period 2.0‐44.7 months (median, 5.3 months) after starting H. pylori eradication treatment. CR was maintained in 77 of 81 patients (95.1%) for 0.4‐53.2 months (median, 33.1 months). Secondary treatments (radiotherapy, rituximab, or gastrectomy) for gastric MALT lymphoma were needed in 10 of the 97 patients (10.31%). During follow‐up, OS rate was 96.9% (94/97) and the causes of 3 deaths were not related to lymphoma.ConclusionsRabeprazole‐based H. pylori eradication therapy demonstrated a high CR rate, long CR maintenance, and a good OS for patients with localized gastric MALT lymphoma in this prospective, practice‐based, multicenter study.

Exploring the impact of Helicobacter pylori on gut microbiome composition

“…It triggers pathogenesis by creating reactive oxygen species and modulating host-inflammatory responses. This pathogen is known to cause diseases of the upper gastrointestinal tract such as peptic ulcer, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma [2, 3]. Further, recent studies have linked H .…”

Management ofHelicobacter pyloriinfection: the Maastricht VI/Florence consensus report

“…ESMO guidelines67 support waiting 3–6 months after eradication to assess regression in H. pylori -negative patients before starting other treatment—usually radiation for localised disease, chemotherapy for more advanced cases. ESMO guidelines have now extended this recommendation for H. pylori eradication to all cases of gastric marginal zone B-cell lymphoma (the preferred WHO term), regardless of stage67 due to the occasional response even in some cases of disseminated disease 65 66 70–72. Unlike the association of Cag-carriage and VacAs1/m1/i1 type with gastric adenocarcinoma, no specific H. pylori gene products are linked to lymphoma development 73…”

Microbiome and cancer

“…Helicobacter pylori H. pylori is an established carcinogen with an age-standardized incidence rate of 8.7 cases per 100,000 individuals per year (de Martel et al, 2020) and is detectable in over half of the world's population (Hooi et al, 2017). Overall, H. pylori contributes to peptic ulcers, gastric cancers, and mucosa-associated lymphoid tissue (MALT) lymphomas (Cover and Blaser, 2009;Sugizaki et al, 2018) via its interferences in the Wnt/b-catenin pathways regulating cellular turnover and apoptosis. H. pylori can indirectly influence the development of cancer as outlined by the Correa pathway (Correa et al, 1975;Correa and Piazuelo, 2012) via a chronic inflammatory response mediated by the recruitment of polymorphonuclear neutrophils and invasion of mononuclear lymphocytes, stimulating a predominantly Th1type response by proinflammatory signaling through interleukin (IL)-1B, tumor necrosis factor (TNF)a, and interferon (IFN)g (Bagheri et al, 2018;Guiney et al, 2003;Hafsi et al, 2004).…”