[Skin diseases and hepatitis virus C infection]

Using a creative molecularbiologic technique in 1989 Choo and co-workers isolated a new virus of hepatitis C, an agent responsible for numerous cases of parenterally transmissible viral hepatitis. Hepatitis C virus is a RNA virus with unique genomic organisation. Six genotypes of hepatitis C virus have been identified, which differ in geographical distribution, tendency towards chronicity and sensitivity to antiviral therapy. Transmission occurs due to apparent and inapparent parenteral procedures (after transfusion, transplantation, transplacentally, during lactation, sexually or after accidental injury of medical staff). Mode of transmission through intact skin or mucosa has not been proved yet. Due to development of laboratory methods for detection of anti-hepatitis C virus antibodies and obligation for routine testing of blood donors for hepatitis C in majority of countries in the world, risk of post-transfusion hepatitis C is minimised to less than 1%. In 70% of patients the infection runs a chronic course, affecting numerous extrahepatic organ systems, including skin.

Mixed essential cryoglobulinemia is a disorder with deposition of circulating immune complexes in small and medium blood vessels. Clinical characteristics comprise palpable purpura on lower extremities, arthralgias and weakness. It might occur during autoimmune disorders, liver diseases and viral infections, among which hepatitis C infection has a central part. Mixed cryoglobulins can be detected in 35-54% of patients with hepatitis C and symptomatic vasculitis associated cryoglobulinemia, decreased C4 component of complement, positive rheumatoid factor and elevation of hepatic enzymes occurs in 10-21% of patients. Findings of anti-hepatic C virus antibodies and/or viral RNA in 96% of patients with mixed cryoglobulinemia can be considered as a definitive proof of etiopathogenetic association between hepatitis C infection and mixed cryoglobulinemia. Interferon alpha therapy is a first-choice therapy, although transient responses are frequent.

Hepatitis C infection has recently been recognised as an important precipitating factor of clinical porphyria cutanea tarda sympotomatology. Apart from high level of seropositivity among porphyria cutanea tarda patients (62-100%), association between these two entities hasn't been clearly revealed yet. The question whether hepatitis C infection is enough to be the only precipitating factor, or other hepatotoxic cofactors are necessary, still exits. Interferon therapy has been a meter of several studies, but no definite recommendations had been given about its administration in these cases.

About possible association between lichen planus and chronic liver diseases, and hepatitis C infection as well, suggest 35% prevalence of hepatic disorders in patients with lichen planus, and 9.8-23% of hepatitis C virus seropositivity. The clinical picture of lichen planus in hepatitis C virus infection is characterised by generalised skin lesions, with erosive involvement of oral mucous membrane, and by chronic course. Therapeutical efficiency of interferon is unpredictable, with possible improvement, cure or deterioration of lichen planus.

Other dermatological disorders (erythema nodosum, erythema multiforme, urticaria) may be direct consequences of hepatitis C infection, of other extrahepaic non-dermatological manifestations, or fortuitous reports.

Considering big pathogenetic potentials of hepatitis C virus with possible skin involvement, and proved association between cutaneous necrotising vasculitis with mixed essential cryoglobulinemia, porphyria cutanea tarda, lichen planus and chronic hepatitis C infection, all patients with these disorders should be tested for hepatitis C and all cases of hepatitis C should be searched for signs and symptoms of these skin diseases.