Vasculitis is the inflammation of blood vessels. It has many forms, easiest to detect as small vessel skin( cutaneous ) vasculitis.

IMMUNE COMPLEX MEDIATED VASCULITIS IN HEPATITIS B AND C INFECTIONS AND THE EFFECT OF ANTIVIRAL THERAPY.

Nityanand S; Holm G; Lefvert AK; Immunological Research Laboratory, Karolinska Hospital, Stockholm, Sweden. Clin Immunol Immunopathol, 1997 Mar, 82:3, 250-7

Case reports of seven patients with vasculitis and past or present viral hepatitis infection are presented, including studies on circulating immune complexes (CICs) and cryoglobulins by sucrose density gradient centrifugation or gel filtration, before and after antiviral therapy. Three patients had unusual vasculitic manifestations: coronary, large vessel, and muscle vasculitis, respectively. All the patients had high levels of CICs by the above methods, but only two had CICs by the C1q binding and conglutinin methods. The CICs/ cryoglobulins contained HBV and/or HCV antibodies, antigens, and genome. The concentration of hepatitis antibodies in immune complex form was severalfold higher than in the free form in serum. In one patient, the HBs antigen was present only in the CICs and in another, only hepatitis antibodies (no antigen/genome) were present in the serum or the cryoglobulins. With antiviral therapy, six patients went into long-lasting remissions. There was a temporal relationship between the regression of the vasculitic lesions and the decline in the levels of CICs/cryoglobulins.

CORRELATION OF LIVER AND SKIN HISTOPATHOLOGY WITH SEROLOGY IN A PATIENT WITH CUTANEOUS VASCULITIS AND HEPATITIS C INFECTION.

Ornstein MH; Phelps R; Kerr LD; Spiera H; Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029-6574. South Med J, 1994 Nov, 87:11, 1174-7

A strong body of evidence supports a viral etiology for many forms of vasculitis. Recent literature supports the association of the hepatitis C virus (HCV) with essential mixed cryoglobulinemia. We describe a case of cutaneous vasculitis associated with simultaneous active hepatic inflammation demonstrated by skin and liver biopsies. Immunofluorescence, hepatitis C serology, and study of the cryoprecipitate all confirmed HCV infection and deposition of immune complexes. Treatment with interferon alpha-2b was extremely effective as compared with prednisone and colchicine. This case provides further evidence that active hepatic infection with HCV may be a cause of cryoglobulinemia and cutaneous vasculitis. It also suggests that further studies of antiviral therapy for vasculitis should be explored.

CRYOGLOBULINEMIA AND CUTANEOUS LEUKOCYTOCLASTIC VASCULITIS WITH HEPATITIS C VIRUS INFECTION.

Buezo GF; García-Buey M; Rios-Buceta L; Borque MJ; Aragües M; Department of Dermatology, Universidad Autónoma, Madrid, Spain. Int J Dermatol, 1996 Feb, 35:2, 112-5

BACKGROUND: Mixed cryoglobulinemia (MC) is a systemic disorder, characterized by a typical clinical triad: purpura, weakness, and arthralgias, with visceral complications such as liver and renal involvement. The objective was to study the association between hepatitis C virus (HCV) infection and essential mixed cryoglobulinemia (EMC). PATIENTS AND METHODS: Markers of HCV infection in 11 patients with cryoglobulinemia were examined and hepatitis C virus (HCV) was detected in eight of them. These patients were included in a clinical and histologic study. Anti-HCV antibodies were determined by a second-generation enzyme-linked immunosorbent assay (ELISA-2) in sera and cryoprecipitates. Studies on HCV-RNA were performed by a two-stage polymerase chain reaction (PCR) in the serum. A control group, consisting of 28 patients with other cutaneous disorders, was studied for HCV infection using ELISA-2 and PCR. RESULTS: All patients had liver dysfunction, arthralgias, and purpura. Three patients had involvement of the peripheral nervous system, two had renal involvement, and one patient had Sjögren's syndrome. Cryocrits ranged from 3% to 20%. Six patients had type III cryoglobulinemia and the remaining two had type II. Markers for hepatitis B virus (HBV) were negative in all serum samples. Anti-HCV antibodies and HCV-RNA were positive in the serum of all the cases with MC. Anti-HCV antibodies were positive in all cases except for one of the cryoprecipitates tested. Four patients received recombinant interferon alfa. In two of them, serum aminotransferases became normal and cryoglobulins disappeared. CONCLUSIONS: The results strongly suggest that HCV infection is responsible for the cryoglobulinemia and vasculitis in patients with MC and that treatment with interferon alfa is presently the treatment of choice for such patients.

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