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Editor,—Radereret al (
) present an interesting case report of a patient with a mucosa associated lymphoid tissue (MALT) lymphoma of the stomach and descending colon. Their report adds to the growing literature of gastrointestinal MALT lymphomas that respond to antibiotic treatment. In addition to the numerous reports on antibiotic sensitive gastric lymphomas,1 those of the small intestine,2 salivary glands,3 4 nasal mucosa,5 and colon6 7 have recently been reported.
Although Helicobacter pylori is generally implicated as the inducing agent, this does not always appear to be the case. A related bacterium, H heilmannii, has also been found in association with gastric MALT lymphomas, including H pylori negative patients whose disease was still responsive to antibiotic treatment.8 Furthermore, other non-H pylori bacterial9 and protozoal10flora have been observed in gastric lymphomas specific to involved regions. In the report by Raderer et al, and in several of the others previously mentioned,3-7 H pylori was not identified in the extragastric lesions, leaving it open to speculation how H pylori may induce antigenic stimulation of these lymphomas. Moreover, in the report by Inoue and Chiba,7 not only was the rectal lesionH pylori negative but upper gastrointestinal endoscopy was normal. Their patient was seronegative forH pylori and had a negative rapid urease test, culture, and histological examination.
In light of this evidence, it seems that although H pylori may be the most common cause of many gastrointestinal MALT lymphomas, it is not the only causative organism. This is an important point to consider when confronted with patients diagnosed with H pylori negative MALT lymphomas.
Editor,—Hoption Cannet al again point out the fact thatHelicobacter pylori is not the sole cause of mucosa associated lymphoid tissue (MALT) lymphoma in some cases. They also suggest other, as yet undefined, bacterial/infectious causes in MALT lymphomas in extragastric sites in view of our case and the recent literature. While we believe this to be a valid point and agree with the already established notion of other contributing factors in addition to H pylori, we nevertheless advise that our findings should be interpreted with caution. In contrast with other cases reported in the literature and cited by the authors, our patient suffered from concurrent gastric and colonic MALT lymphoma and had evidence of H pylori infection. Thus one cannot rule out the fact that antigenic shedding ofH pylori from the stomach throughout the gastrointestinal tract or the presence of specific T cells alone was able to provide the colonic lesion with an antigenic drive needed for maintenance of the lymphoma. In this scenario, one would expect eradication of H pylori to lead to regression of the (still antigen and/or T cell dependent) lymphoma. The fact that various (apparently not H pylorirelated) intestinal as well as extraintestinal lesions regressed with antibiotic treatment is indeed highly suggestive of an underlying infectious process but does not necessarily constitute proof of this assumption, as direct antiproliferative mechanisms of various antibiotics, including clarithromycin, have been reported in different settings. Further investigations are needed before definite recommendations for (as yet empirical) antibiotic therapy in patients with extragastric MALT lymphomas can be given.
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