DETECTION OF IMMUNOGLOBULIN HEAVY-CHAIN GENE REARRANGEMENT BY POLYMERASE CHAIN-REACTION IN CHRONIC ACTIVE GASTRITIS ASSOCIATED WITH HELICOBACTER-PYLORI

Chronic active gastritis associated with Helicobacter pylori (CAG-Hp) has been linked to the pathogenesis of gastric B-cell lymphomas of muc osa-associated lymphoid tissue (MALT). To determine whether monoclonal lymphoid populations are present in CAG-Hp and histological predictor s of monoclonality exist, the authors examined 46 endoscopic biopsies from 41 patients with CAG-Hp, The authors scored gastric biopsies for the presence of lymphoepithelial lesions (LELs), intensity of lymphoid infiltrate, presence of lymphoid aggregates and germinal centers, coe xpression of CD43 (Leu 22) on B cells, and cytoplasmic immunoglobulin light chain restriction in formalin-fixed, paraffin-embedded tissues. DNA extracts from these routinely processed tissues were analyzed for immunoglobulin heavy chain (IgH) gene rearrangement by polymerase chai n reaction (PCR). Histological features, immunophenotype, gene rearran gement status, and clinical information were correlated. Six of the 46 biopsies (13%) from six of 41 patients (15%) showed a monoclonal PCR pattern. Monoclonal PCR patterns correlated with the presence of LELs (P < .015) but not with intensity of lymphoid infiltrate, presence of germinal centers, or presence of lymphoid aggregates, LELs correlated with germinal centers (P < .003) and intensity of infiltrate (P < .000 1). None of the cases showed cytoplasmic light chain restriction nor c oexpression of CD43 on B cells by immunohistochemistry. Clinical follo w-up was available in all six patients whose gastric biopsies had a mo noclonal PCR pattern (median, 58 months; range, 1 to 66 months) and 33 of the 35 patients with biopsies showing a polyclonal PCR pattern (me dian, 41 months; range 0.1 to 63 months), No patient developed gastric lymphoma. Monoclonality of lymphoid cells was detected by IgH PCR in 13% of patients with CAG-Hp. Although the authors cannot exclude the p ossibility that some patients with monoclonal gastric lymphoid infiltr ates may eventually develop overt lymphoma, no histological, immunophe notypic, nor clinical evidence of lymphoma was noted at presentation o r on clinical follow-up. Given the high incidence of CAG-Hp in the gen eral population and the relatively low incidence of gastric MALT lymph oma, clinicopathologic correlation is needed when interpreting tests f or clonality in this setting. The presence of clonal IgH gene rearrang ement in CAG-Hp, supports the hypothesis that H pylori is involved in the pathogenesis of low grade gastric B-cell MALT lymphomas. (C) 1996 by W.B. Saunders Company