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Letters |1 August 1997

Regression of Gastric Lymphoma with Therapy for Helicobacter pylori Infection

John F. Seymour, MB, BS, FRACP; Robert P. Anderson, MB, ChB, PhD, FRACP; Prithi S. Bhathal, MB, BS, PhD, FRACP

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  • The Royal Melbourne Hospital; Parkville 3050, Australia
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TO THE EDITOR:
The normal stomach has no resident lymphoid tissue, but Helicobacter pylori infection elicits lymphocytic infiltration [1]. Infrequently, a clone of mature B lymphocytes then arises, the proliferation of which depends on factors produced by benign T lymphocytes in the presence of H. pylori[2]. These factors include tumor necrosis factor-α, interleukin-6, interleukin-1β, and interleukin-10 [3]. Eradication of H. pylori usually induces durable regression of these low-grade mucosa-associated lymphoid tissue (MALT) lymphomas [4], suggesting that although they are unequivocally clonal, they remain dependent on T-cell-derived stimulation. Although often thought to arise from low-grade MALT lymphoma through clonal evolution [5], gastric large-cell lymphomas are not thought to be dependent on such T-cell-derived stimuli, even when associated with H. pylori.
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Seymour JF, Anderson RP, Bhathal PS. Regression of Gastric Lymphoma with Therapy for Helicobacter pylori Infection. Ann Intern Med. ;127:247. doi: 10.7326/0003-4819-127-3-199708010-00026

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Published: Ann Intern Med. 1997;127(3):247.

DOI: 10.7326/0003-4819-127-3-199708010-00026

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Print ISSN: 0003-4819 | Online ISSN: 1539-3704

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