Abstract

In chronic hepatitis C virus (HCV) infection there is high prevalence of numerous extrahepatic manifestations. Peripheral neuropathy (PN), in the form of symmetric polyneuropathy, asymmetric polyneuropathy, and multineuropathy, may be associated also with HCV infection and is usually related to mixed cryoglobulinemia (CG). However, some HCV+ patients with PN without CG were recently reported, suggesting a possible direct role of HCV in the pathogenesis of PN. From January 2000 to December 2002 we studied 50 HCV+ patients: 21 with symptomatic CG and 29 with chronic HCV without symptomatic CG (23 without CG, 5 with asymptomatic CG). Particular care was taken to exclude other possible causes of PN. Patients without symptomatic CG were examined before starting combined therapy with interferon‐alpha and ribavirin, if needed. Fifteen patients with symptomatic CG had axonal sensorimotor polyneuropathy, 6 axonal sensorimotor multineuropathy or asymmetric polyneuropathy. Six HCV+ patients had other causes of PN (1 CIDP, 2 diabetes, 1 CIDP and diabetes, 1 alcoholism, 1 paraneoplastic with anti‐Hu antibodies). No HCV+ patients without (symptomatic) CG or other possible causes of PN showed clinical and electrophysiological evidence of PN. Our study casts doubts on the existence of a PN directly caused by HCV and suggests that finding a PN in a HCV+ patient without CG should prompt to search for a different cause of PN.

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