Regression of Gastric Lymphoma with Therapy for Helicobacter pylori Infection

  1. John F. Seymour, MB, BS, FRACP;
  2. Robert P. Anderson, MB, ChB, PhD, FRACP; and
  3. Prithi S. Bhathal, MB, BS, PhD, FRACP
  1. 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.

    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.

    Figure 1. Endoscopic view showing antral erythema and a raised 2-cm × 3-cm ulcer on the lesser curve in the proximal antrum with altered blood present ( ). Pretreatment biopsy specimen showing gastric surface epithelium coated with . The lumen also shows a group of lymphoma cells from the adjacent ulcer floor (hematoxylin and eosin stain; original magnification, x400). Pretreatment gastric biopsy specimen. High-power view of large-cell lymphoma expanding the lamina propria and separating gastric tubules. The lymphoma cells express the pan-B-cell marker CD20 (hematoxylin and eosin stain; original magnification, x400).
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      Figure 1. Endoscopic view showing antral erythema and a raised 2-cm × 3-cm ulcer on the lesser curve in the proximal antrum with altered blood present ( ). Pretreatment biopsy specimen showing gastric surface epithelium coated with . The lumen also shows a group of lymphoma cells from the adjacent ulcer floor (hematoxylin and eosin stain; original magnification, x400). Pretreatment gastric biopsy specimen. High-power view of large-cell lymphoma expanding the lamina propria and separating gastric tubules. The lymphoma cells express the pan-B-cell marker CD20 (hematoxylin and eosin stain; original magnification, x400). Top.arrowMiddle.Helicobacter pyloriBottom.

      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.

      John F. Seymour, MB, BS, FRACP

      Robert P. Anderson, MB, ChB, PhD, FRACP

      Prithi S. Bhathal, MB, BS, PhD, FRACP

      The Royal Melbourne Hospital Parkville 3050, Australia

      The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:

      •Include no more than 300 words of text, three authors, and five references

      •Type with double-spacing

      •Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.

      Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.

      Annals welcomes electronically submitted letters.

      References

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