Helicobacter pylori infection in patients with gastric involvement by adult T-Cell leukemia/lymphoma

BACKGROUND. Gastrointestinal involvement is seen frequently in patients with adult T-cell leukemia/lymphoma (ATLL). The authors previously showed a relatively low prevalence of Helicobacter pylori infection in individuals with human T-cell lymphotropic virus I (HTLV-1) infection, including patients with ATLL; however, the correlation between H. pylori infection and ATLL gastric involvement has not been investigated. METHODS. The authors studied 71 patients with ATLL. Gastric involvement was confirmed by endoscopy and biopsy. H. pylori infection was detected by serology, rapid urease test, and immuno histo chemistry on biopsy samples. The expression of adhesion molecules on ATLL cells or their ligands on the vasculature in gastric mucosa was analyzed immunohistochemically. The expression of mucosal addressin cell adhesion molecule I (MAdCAM-1) was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. RESULTS. Gastric involvement was detected in 21 patients (30%), including 8 patients with acute clinical subtype ATLL and 13 patients with lymphoma type ATLL. The prevalence of H. pylori infection was 86% (18 of 21 patients) in the patients with gastric involvement but only 38% (19 of 50 patients) in the patients without such involvement (P < 0.001). The expression of lymphocyte function-associated antigen I (LFA-1) and its ligand, intercellular adhesion molecule 1 (ICAM-1), was most frequent on ATLL cells infiltrating the stomach and was enhanced substantially on vascular endothelium in 1:1, pylori-infected gastric mucosa. Human mucosal lymphocyte antigen I also was expressed on infiltrating ATLL cells in the stomach. The expression of MAdCAM-1 mRNA assessed by RT-PCR also was seen selectively in H, pylori-infected patients. CONCLUSIONS. ATLL cells infiltrate gastric tissues infected with H. pylori, probably through the interaction of adhesion molecules on these cells and their ligands on the vasculature, i.e., through the LFA-1/ICAM-1 pathway. (C) 2002 American Cancer Society.