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Editor,—We read with great interest the article by Kawahara et al(Gut1999;45:20–23) reporting the increase of antibody titres to HGC-27 cells in Helicobacter pylori positive patients with mucosa associated lymphoid tissue (MALT) lymphoma when compared with titres in patients with other gastroduodenal diseases and in healthy subjects. Previously, other authors1 showed that antigenic mimicry betweenH pylori and the host mucosa may induce autoimmune responses which lead to the development of the disease.
Recently, we have diagnosed a few cases of synchronous gastric adenocarcinoma and low grade MALT lymphoma (unpublished data). Although the development of simultaneous primary gastric lymphoma and carcinoma is a rare event, in view of Kawahara et al's data we think that the occurrence of both pathologies could be underestimated. In fact, the gastric glandular epithelium present inside a MALT lymphoma might be susceptible to neoplastic transformation, owing to either the presence of common oncogenic factors or to the induction of immune responses to host components. The latter mechanism may lead to tissue injury of an autoimmune nature. The possibility of coexisting MALT lymphoma and gastric adenocarcinoma should be kept in mind, especially in patients infected withH pylori as an aetiopathogenic role for this bacterium in both diseases has been postulated.
H pylori plays a key role in the natural history of gastric MALT lymphoma and represents an example of antigen mediated tissue stimulation and lymphoproliferation, with possible subsequent lymphomagenesis. We agree with Kawaharaet al that undefined bacterial components or the host immune response to the bacterial infection could promote autoimmune responses to host antigen in certain subjects. Further studies are needed to clarify the role of antibodies to Hsp60 and HGC-27, but it is possible hypothesise that other as yet unidentified antibodies may also be involved.
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