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1 August 1997 | Volume 127 Issue 3 | Page 247
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-
A 73-year-old woman presented with generalized lymphadenopathy, recurrent epigastric pain, and weight loss. Panendoscopy done 5 years earlier had shown chronic gastritis with biopsy-proven H. pylori infection; now, this procedure revealed a malignant ulcer (Figure 1 on page 247, top), with B-cell diffuse large-cell lymphoma and H. pylori-associated chronic active gastritis confirmed on biopsy (Figure 1, middle and bottom). No low-grade MALT lymphoma was seen in the current, or previous, specimens. The patient received 14 days of therapy with omeprazole, ampicillin, and metronidazole with maintenance ranitidine, but she declined cytotoxic chemotherapy. Repeated panendoscopy done 8 weeks later showed complete healing of the ulcer with no residual lymphoma on biopsy, although light colonization of H. pylori and mild chronic gastritis persisted. No regression of the peripheral lymphadenopathy was seen. LETTER
Regression of Gastric Lymphoma with Therapy for Helicobacter pylori Infection
TO THE EDITOR: 
, interleukin-6, interleukin-1ß, 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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In this patient, regression of gastric large-cell lymphoma in response to H. pylori eradication, albeit incomplete, establishes that some aggressive lymphomas may remain dependent on immunoregulatory factors. Although we do not suggest that anti H. pylori therapy should replace conventional treatment, bacterial eradication should be considered as a component of therapy for gastric large-cell lymphoma.
Author and Article Information
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 Top Author & Article Info References |
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References
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1. Stolte M, Eidt S. Lymphoid follicles in the antral mucosa: immune response to Campylobacter pylori. J Clin Pathol. 1989; 42:1269-71.
2. Hussell T, Isaacson P, Crabtree JE, Spencer J. The response of cells from low-grade B-cell gastric lymphomas of mucosa-associated lymphoid tissue to Helicobacter pylori. Lancet. 1993; 342:571-4.
3. Blasser MJ, Parsonnet J. Parasitism by the "slow" bacterium Helicobacter pylori leads to altered gastric homeostasis and neoplasia. J. Clin Invest. 1994; 94:4-8.
4. Roggero E, Zucca E, Pinotti G, Pascarella A, Capella C, Savio A, et al. Eradication of Helicobacter pylori infection in primary low-grade gastric lymphoma of mucosa-associated lymphoid tissue. Ann Intern Med. 1995; 122:767-9.
5. Chan JK, Ng CS, Isaacson PG. Relationship between high-grade lymphoma and low-grade B-cell mucosa-associated lymphoid tissue lymphoma (MALToma) of the stomach. Am J Pathol. 1990; 136:1153 64.
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