One of the extrahepatic manifestations of HCV infection outlined in the review by Gumber and Chopra [1] is the link between HCV infection and essential mixed cryoglobulinemia and the speculation that the former is an etiologic agent of the latter. We and other researchers agree that HCV may be an important etiologic agent of monoclonal gammopathies. Accordingly, we report an interesting case that we recently encountered.

A 47-year-old woman was admitted to the renal service at our institution because of progressive deterioration of renal function, which necessitated hemodialysis. Our hematology service was consulted for work-up of thrombocytopenia. At another institution, the patient had previously received a diagnosis of hepatitis C (by radioimmunoblot assay), type II cryoglobulinemia, proliferative glomerulonephritis (biopsy-proven), and acute renal failure. The patient had never had arthralgias or the Raynaud syndrome. She received a course of interferon- therapy on two occasions (total duration, 6 to 8 months), and renal function improved.

One year later, after the patient had been admitted to our institution, HCV RNA was still detectable by polymerase chain reaction despite the previous antiviral therapy. The cryocrit was 3.9%, and serum protein electrophoresis showed low levels of total protein, albumin, and ß and fractions. These laboratory values are consistent with renal loss. Immunofixation electrophoresis of the serum and washed cryoprecipitate showed an IgM, monoclonal protein. Examination of bone marrow aspirate and biopsy specimens, obtained to evaluate thrombocytopenia, showed adequate numbers of megakaryocytes and numerous atypical lymphoid aggregates composed of small round lymphoid cells. Immunophenotypic analysis of the bone marrow (by flow cytometry) showed a 1% monoclonal () B-cell population. Because a scan of the liver and spleen showed hepatosplenomegaly, the thrombocytopenia was believed to be secondary to sequestration. Our observation and others in the European literature [2-4] suggest that chronic HCV antigenic stimulation may have a role in the cause of monoclonal gammopathies [5]. The finding of atypical lymphoid aggregates in the bone marrow also suggests that monoclonality in some patients may be the result of an immunoproliferative disorder driven by HCV-related oncogenesis.