Lymphoid proliferations and lymphomas associated with gastric metaplasia, dysplasia, and carcinoma

Gastric carcinomas are invariably accompanied by lymphoid proliferations. W e studied their features in 22 resected gastric carcinomas in which the lym phoid proliferations ranged from reactive lymphoid follicles to mucosa-asso ciated lymphoid tissue (MALT) lymphomas. In most cases, the collections of lymphocytes were abundant, which is remarkable considering the lack of lymp hoid tissue in the normal stomach. They were not haphazardly located but in direct contact with the metaplastic, dysplastic, and neoplastic epithelial cells, in positions suggestive of defense barriers. They consisted of newl y formed lymphoid follicles with reactive germinal centers sometimes high u p in the superficial mucosa, collections of plasma cells beneath the surfac e epithelium, and large aggregates of B cells above and below the musculari s mucosae as well as abundant T cells. The latter, both CD4+ and CD8+, were seen within metaplastic epithelial cells as well as within carcinomatous g lands that were partially destroyed, resembling apparent neoplastic lympho- epithelial lesions (LEL). In three cases, the B cells infiltrating the gast ric muscular layers represented MALT-lymphomas adjacent to gastric carcinom as, as confirmed by polymerase chain reaction (PCR) analysis in two cases. In a case of lymphoepithelioma-like carcinoma, the excessive lymphoid cells were predominantly of T-CD8+ type. In this case, EBV identified by EBV-enc oded RNA and latent membrane protein was present in large amounts. Helicoba cter pylori was seen in only six cases in areas of chronic gastritis that w ere distant from carcinoma. H pylori was not present in the areas of metapl asia, dysplasia, or carcinoma. It appears that the lymphoid proliferations accompanying these gastric changes do not arise in response to the pathogen ic agent H pylori, which caused the persistent infection leading to them ye t is no longer present, but rather in response to the existence of the abno rmal epithelial cells. Thus the lymphoid proliferations consistently associ ated with gastric metaplasia, dysplasia, and neoplasia may be regarded as i mmune reactions to the long-term cellular changes triggered by the initial chronic gastritis. On rare occasions, the exaggerated lymphoid proliferatio ns may reach the end of the spectrum, resulting in MALT lymphomas coexisten t with gastric carcinomas. Copyright (C) 1999 by W.B. Saunders Company.