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PubMed

Doi

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Journal

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Issn Print

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Brief description/objective

Chronic infection with hepatitis C virus (HCV) may be complicated by the development of systemic vasculitis. Vasculitis is either caused by mixed cryoglobulinemia or a non-cryoglobulinemic vasculitis resembling polyarteritis nodosa (PAN). Antiviral treatment with interferon-alpha (IFN) and subsequent clearing of HCV mostly leads to improvement of vasculitic symptoms, but vasculitis may also be exacerbated and even cases of new onset of vasculitis may occur. Exacerbations of both cryoglobulinemic and PAN-type vasculitis in chronic HCV infection have been described under treatment with IFN. The most common symptom is vasculitic neuropathy. However, peripheral neuropathy in a HCV-infected patient treated with IFN may also be caused by direct neurotoxic or antiangiogenic effects of IFN itself, often requiring a nerve biopsy to establish the exact diagnosis. The clinical course of vasculitic complications of IFN treatment is variable and ranges from regression of symptoms despite continuation of IFN treatment to fatal exacerbations despite termination of IFN treatment and additional immunosuppressive therapy. In most cases of IFN-induced vasculitis, immunosuppressive therapy with corticosteroids has been employed, leading to improvement of symptoms. We report the case of a patient with chronic HCV infection who first developed cryoglobulinemic vasculitis after initiation of therapy with the polyethylene glycol (PEG)-conjugated form of IFN (PEG-IFN) and discuss it in the context of the relevant literature. First onset of cryoglobulinemic vasculitis after initiation of IFN therapy has not been described so far.