Abstract
A 66-year-old man presented with skin lesions that had developed 4 days previously. He had a history of membranoproliferative glomerulonephritis and chronic hepatitis virus infection, but he refused treatment. Physical examination revealed cutaneous lesions (Figure A). Cryoglobulins were present. His serum C3 level was normal and his CH50 and C4 levels were decreased. An increase of polyclonal immunoglobulin G was present. A skin biopsy examination showed leukocytoclastic vasculitis. The patient refused hepatitis treatment and a prednisone treatment was started. After a 6-month follow-up evaluation, the patient had no evidence of cutaneous vasculitis and he receives no steroids. The etiopathogenesis of leukocytoclastic vasculitis is not very well known.1Albrecht Schirren C. Zachoval R. Shirren C.G. et al.A role for chronic hepatitis C virus infection in a patient with cutaneous vasculitis, cryoglobulinemia, and chronic liver disease.Dig Dis Sci. 1995; 40: 1221-1225Crossref PubMed Scopus (31) Google Scholar, 2Hamid S. Ponciano D.C. Lee M.L. Urticarial vasculitis caused by hepatitis C virus infection: response to interferon alfa therapy.J Am Acad Derm. 1998; 39: 278-280Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar Some investigators think that leukocytoclastic vasculitis is caused by deposition of immune complexes in postcapillary venules, probably cryoglobulins that destroy the vessel’s wall.2Hamid S. Ponciano D.C. Lee M.L. Urticarial vasculitis caused by hepatitis C virus infection: response to interferon alfa therapy.J Am Acad Derm. 1998; 39: 278-280Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar However, other investigators have shown that hepatitis C virus is present in the vessel walls.3Durand J.M. Kaplanski G. Richard M.A. et al.Cutaneous vasculitis in patient infected with hepatitis C virus Detection of hepatitis C virus RNA in the skin by polymerase chain reaction.Br J Dermatol. 1993; 128: 359-360Crossref PubMed Scopus (36) Google Scholar In this case, we think that leukocytoclastic vasculitis probably was produced by immune complexes and not by hepatitis C virus.
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