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Journal Article
B-cell lymphomas involving the skin associated with hepatitis C virus infection.
International Journal of Dermatology 2002 September
BACKGROUND: A role for hepatitis C virus (HCV) infection has been suggested in the pathogenesis of non-Hodgkin lymphomas (NHL).
AIM: To evaluate the characteristics of cutaneous lymphomas occurring in HCV-infected patients, and to investigate the hypothesis of a direct infection of malignant cells.
METHODS: Three patients showing a positive serology for HCV and a cutaneous lymphoma were studied. Analysis of HCV replication was performed using reverse transcriptase-polymerase chain reaction. The presence of HCV RNA was also assessed in biopsies from lesional skin and in a lymph node in one case. Genotype characterization was carried out on the basis of LiPA genotyping assays using viral genomic amplification products.
RESULTS: Cutaneous NHL occurred in patients with chronic and replicative HCV infection, and exhibited a B-cell phenotype (one diffuse large B-cell lymphoma, one follicular lymphoma, and one marginal zone B-cell lymphoma). All patients were male; two of them were former intravenous drug abusers, while the HCV contamination route was unknown in the third. The search for HCV RNA in the skin and in lymph nodes yielded negative results. HCV genotypes were 1b in two cases and 3a in one case.
CONCLUSION: These results show that a subset of B-cell cutaneous NHL is associated with a replicative HCV infection and suggest that HCV is not involved in lymphomagenesis through a direct infection of malignant cells. The ability of HCV to trigger a chronic B-cell lymphoproliferation could represent another mechanism, while a fortuitous association cannot be excluded.
AIM: To evaluate the characteristics of cutaneous lymphomas occurring in HCV-infected patients, and to investigate the hypothesis of a direct infection of malignant cells.
METHODS: Three patients showing a positive serology for HCV and a cutaneous lymphoma were studied. Analysis of HCV replication was performed using reverse transcriptase-polymerase chain reaction. The presence of HCV RNA was also assessed in biopsies from lesional skin and in a lymph node in one case. Genotype characterization was carried out on the basis of LiPA genotyping assays using viral genomic amplification products.
RESULTS: Cutaneous NHL occurred in patients with chronic and replicative HCV infection, and exhibited a B-cell phenotype (one diffuse large B-cell lymphoma, one follicular lymphoma, and one marginal zone B-cell lymphoma). All patients were male; two of them were former intravenous drug abusers, while the HCV contamination route was unknown in the third. The search for HCV RNA in the skin and in lymph nodes yielded negative results. HCV genotypes were 1b in two cases and 3a in one case.
CONCLUSION: These results show that a subset of B-cell cutaneous NHL is associated with a replicative HCV infection and suggest that HCV is not involved in lymphomagenesis through a direct infection of malignant cells. The ability of HCV to trigger a chronic B-cell lymphoproliferation could represent another mechanism, while a fortuitous association cannot be excluded.
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