Complete regression of primary gastric plasmacytoma following Helicobacter pylori eradication.

Abstract

Dear Editor, Papadaki and coworkers [1] describe a case of gastric plasmacytoma responding to eradication of Helicobacter pylori (HP). As the authors have pointed out, the clinical features of the case, along with the prompt response of the tumour to HP eradication, show a striking analogy to gastric MALT lymphoma. In view of this, they propose HP as a potential causative agent in the development of gastric plasmacytoma. In our opinion, a note of caution should nevertheless be added when interpreting their findings. According to the literature [2], extraosseous plasmacytoma is predominantly found in the upper respiratory tract, but has also been reported to occur in the gastrointestinal tract including the stomach. The MALT lymphoma concept, however, begs the question whether gastric plasmacytoma as a real tumour entity does indeed exist. The postulated cell of origin of MALT lymphoma is the marginal zone B cell, which corresponds to a post germinal-centre B cell with rearranged and mutated immunoglobulin heavy and light chain genes [3]. These cells apparently display the capacity to differentiate into plasma cells, and most early antibody-secreting cells are thought to originate from marginal zone B-cell precursors [4]. In fact, MALT lymphomas often include high numbers of plasma cells, a phenomenon termed plasmacytic differentiation [3]. This feature is found in up to 30% of patients with MALT lymphoma [5], and is especially prominent in a rare type of MALT lymphoma termed immunoproliferative small intestinal disease (IPSID). Plasmacytic differentiation may also explain cases initially described as extramedullary plasmacytoma within classical MALT organs such as the GI tract, which might in fact be MALT lymphomas where plasma cells are effacing any trace of the classical histological features. The fact that the case presented by Papadaki and coworkers was responsive to HP eradication further underscores the hypothesis that this tumour might in fact have been a gastric MALT lymphoma showing extreme plasmacytic differentiation. If this assumption is correct, the finding of responsiveness to HP eradication is not unexpected, as a high percentage of HP-associated gastric MALT lymphomas restricted to the stomach regress following antibiotic therapy. Taken together, the data presented add further support to our view that gastric plasmacytomas should be regarded as MALT lymphomas with extreme plasmacytic differentiation, especially when associated with HP and responding to antibiotic therapy.