Since the identification of hepatitis C virus (HCV) in 1989 as a causative agent for a number of the extrahepatic alterations related to HCV
infection an underlying immune mediated pathogenetic mechanism has been postulated. HCV-associated
thrombocytopenia may be considered complex and multifactorial in origin, since different mechanisms have been implicated in its pathophysiology. With respect to
autoimmune thrombocytopenia in chronic HCV
infection, the detection of specific
antibodies against
platelet glycoproteins have been reported only in a few studies, but no systematic study has been carried out. We examined the clinical, laboratory, and virological characteristics of a case series of 10 patients with
autoimmune thrombocytopenia (platelet count <150.0 x 10(9)/L) related to chronic HCV
infection. Cases, six males and four females, aged 57.1 +/- 12.6 years, presented high titers of
antibodies against
platelet glycoprotein (
GP) IIb/IIIa, GP Ia/IIa, and/or GP Ib/IX, and no other mechanism involved in the pathogenesis of HCV-associated
thrombocytopenia was identified. Furthermore, cases were not associated with particular HCV genotype. Complete platelet response was observed in two patients treated with pegylated
interferon plus
ribavirin, and partial platelet response was seen in two patients treated with
anti-D Ig and one patient treated with
corticosteroids. These findings indicate that an autoimmune mechanism may play a role in the pathogenesis of HCV-associated
thrombocytopenia in a proportion of these patients.