We read with great interest the article entitled “Hepatitis C and Risk of Lymphoma: Results of The European Multicenter Case-Control Study EPILYMPH” by Nieters et al1 in the December 2006 issue of Gastroenterology. The study demonstrates that hepatitis C virus (HCV) RNA-positive individuals have a 2-fold increased risk for B-cell non-Hodgkin lymphoma (B-NHL) and a greater than 3-fold elevated risk for diffuse large B-cell lymphoma (DLBCL), supporting a model that chronic HCV replication contributes to lymphomagenesis. These results are in line with our previous findings indicating that HCV infection increases the risk for lymphomas originating from germinal or post-germinal center cells such as DLBCL, mucosa-associated lymphoid tissue lymphoma, and lymphoplasmocitoid lymphomas2 and with the notion that chronic antigen stimulation sustained by HCV is the likely mechanism that drives the HCV-driven B-cell lymphomagenesis. [3], [4] and [5] In keeping with Nieters et al, we also suggested that HCV infection could be involved in the pathogenesis of Helicobacter pylori–negative marginal zone lymphomas.6

B-Cell lymphomas associated with HCV infection

SANSONNO, Domenico Ettore;
2007-01-01

Abstract

We read with great interest the article entitled “Hepatitis C and Risk of Lymphoma: Results of The European Multicenter Case-Control Study EPILYMPH” by Nieters et al1 in the December 2006 issue of Gastroenterology. The study demonstrates that hepatitis C virus (HCV) RNA-positive individuals have a 2-fold increased risk for B-cell non-Hodgkin lymphoma (B-NHL) and a greater than 3-fold elevated risk for diffuse large B-cell lymphoma (DLBCL), supporting a model that chronic HCV replication contributes to lymphomagenesis. These results are in line with our previous findings indicating that HCV infection increases the risk for lymphomas originating from germinal or post-germinal center cells such as DLBCL, mucosa-associated lymphoid tissue lymphoma, and lymphoplasmocitoid lymphomas2 and with the notion that chronic antigen stimulation sustained by HCV is the likely mechanism that drives the HCV-driven B-cell lymphomagenesis. [3], [4] and [5] In keeping with Nieters et al, we also suggested that HCV infection could be involved in the pathogenesis of Helicobacter pylori–negative marginal zone lymphomas.6
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/23139
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