Recent data suggest that hepatitis C viral (HCV) infection may induce a significant autoimmune reaction to platelets, but the mechanism is unknown. Many patients with chronic hepatitis C, in fact, have high levels of platelet-associated immunoglobulin G (PAIgG) and HCV-RNA is present in the platelets of 100% of those patients with thrombocytopenia and high PAIgG levels. Hepatitis C virus infection has been associated with the development of thrombocytopenic purpura, sometimes triggered during interferon (IFN) therapy. In such cases, the treatment of the underlying disease is a difficult problem to solve. We report the case of a patient with chronic hepatitis C, who developed life-threatening thrombocytopenic purpura after a prolonged course of IFN-alpha2b over a 4-year period. Treatment with anti-immunoglobulin gammaglobulin (Polyglobin; Química Farmaceutica Bayer, Barcelona, Spain) had a transient effect on the platelet count, but prolonged therapy with prednisone was necessary for definitive relief of the haematological complication. Two years later, the patient was treated with combined therapy, including ribavirin (1200 mg/day) and IFN-alpha2b (5 mU, t.i.w.) for 12 months. This therapy induced a sustained response, both biochemical and virological, without haematological complications. This observation suggests that ribavirin may be of benefit in the treatment of immune-mediated thrombocytopenia in patients with chronic hepatitis C, preventing the harmful effect of IFN-alpha but also allowing both drugs to be combined so as to increase the probability of sustained remission of the liver disease.

In 30-50% of patients with portal thrombosis, no underlying etiology is found. The recent reports of new hereditary clotting defects are contributing to the understanding of this problem, but they only justify a small number of idiopathic cases. Instead, anticoagulant protein C resistance, caused by a mutation in the V factor gene, appears to be at least 10 times more common than any of the other known inherited deficiencies of anticoagulant proteins. In spite of that, extensive thrombosis of portomesenteric or hepatic venous circulation has been rarely described in this hereditary clotting defect. We report a typical case of familial and recidivant deep vein thrombosis in a young man heterozygous for the factor V Leiden mutation (Arg506-Gln), who developed an acute portal and mesenteric vein thrombosis. The patient was discharged with an oral anticoagulant treatment and remains asymptomatic 2 years later. In conclusion, the high prevalence of the factor V Leiden in young and aged patients with idiopathic vein thrombosis and the case here described makes it obligatory to consider this disorder in patients with portal and/or mesenteric vein thrombosis, especially in those without evident etiology.