Lymphoid aggregates in gastric biopsies: relationship to other mucosal lesions.
The purpose of this study is to estimate the prevalence of lymphocyte aggregates (precursor of MALT lymphomas) in gastric mucosal biopsies and to associate gastric lymphoid tissue with the age of patients, Helicobacter-associated gastritis and other gastric mucosal pathology. A consecutive series of gastric mucosal samples from 150 children and 256 adults were assessed for the presence of lymphoid aggregates as well as morphological characteristics, Helicobacter pylori status, signs of gastritis, mucosal atrophy and lymphoepithelial lesions. Fifteen selected samples with prominent lymphoid aggregates and 10 controls were examined immunohistochemically for the immunoglobulins A, G, M, lymphocytes B and T, clonality of B cell population, atypical lymphocytes and Epstein-Barr virus (EBV) antigen. There was an increase of H. pylori infection and mucosal lymphoid aggregates (MALT) rates in parallel with the increasing age of patients noted in the histological assessment of the mucosal samples. A close association of lymphoid aggregates with H. pylori infection and prominent active gastritis was found, but in adults with chronic non-active, particularly atrophic gastritis this association became weaker. No morphological and immunohistochemical signs of MALT lymphoma were present. Lymphoid aggregates in children were larger, with follicles, but less numerous and tended to be located in the intermediate and deeper parts of the gastric mucosa. Immunohistochemical studies showed an increase of IgA, IgM and lymphocytes T in the deeper part of the lamina propria in H. pylori-associated gastritis and lymphocyte T accumulation in the periphery of the lymphoid follicles. No evidence of monoclonality, CD31 positive lymphocytes or EBV antigen was detected. Lymphoid aggregates are related, but not exclusively, to H. pylori infection. Their detection rates achieve a peak in young adults with H. pylori infection. Lymphocytic aggregates are also present in chronic atrophic gastritis without H. pylori infection and may relate to autoimmune inflammatory response to other factors.
Jaśkiewicz
K
K
Department of Pathology, University Medical School, Gdańsk, Poland. kaz@amedec.amg.gda.pl
Kobierska
G
G
D000293:Adolescent; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D002449:Cell Aggregation; D002648:Child; D005753:Gastric Mucosa / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D005756:Gastritis / Q000150:complications / Q000276:immunology / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000276:immunology / Q000473:pathology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006801:Humans; D007136:Immunoglobulins / Q000378:metabolism; D008221:Lymphoid Tissue / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D018442:Lymphoma, B-Cell, Marginal Zone / Q000209:etiology / Q000276:immunology / Q000473:pathology; D008875:Middle Aged; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
D007136:Immunoglobulins