Anticardiolipin antibodies in chronic hepatitis C virus infection: is there an aetiopathogenetic link to antiphospholipid syndrome?

Chronic hepatitis c virus [HCV] has always been linked to extrahepatic autoimmune phenomena and found to be associated with various diseases known as extrahepatic manifestations of HCV. In addition, a variety of autoantibodies are detected in HCV patients. Recently HCV has been implicated as a cause of antiphospholipid syndrome [APS] which is usually defined by the association of clinical manifestations that comprise venous and/or arterial thrombosis, recurrent fetal losses, and thrombocytopenia, along with the presence of anticardiolipin [ACL] antibodies and/or lupus anticoagulant. Anticardiolipin antibodies can be induced by various infections diseases, however, they are not associated with thrombotic events as in the case of autoimmune diseases in which they are b2-glycoprotein I dependent and produce thrombotic events. To clarify whether an aetiopathogenesis exists between HCV and APS and meanwhile to study the prevalence, nature, and clinical significant of ACL auto antibodies in serum samples of HCV patients, the present study included one hundred and thirty subjects divided into three groups: a included 50 patients with chronic HCV infection, group b included 30 patients with APS [15 patients with primary and 15 with secondary type], and group c included 50 apparently normal age and sex-matched subjects taken as a control group. Clinical events as well as proper history of APS manifestations were recorded. The prevalence of ACL antibodies was detected by Elisa as well as its IgG and IgM isotypes, its B2-glycoprotein dependence was also evaluated. The present of cryoglobulins and other autontibodies as lupus anticoagulant [LA] and antinuclear antibodies [ANA] were determined as well, using indirect immunofkuorescence. HcVRNA and its viraemia titre were determined by RT-PCR and its quantitative testing. Our data showed that the prevalence of ACL antibodies in chronic HCV patients was found to be 42% which proved to be more than that in the normal controls [0%] but, its presence had no clinical significance. Our study clarified also that there is no significant association between a ACL antibodies and the presence of other auto antibodies or cryoglobulins in those patients. Furthermore, all HCV patients with positive ACL antibodies in our study were B-2 glycoprotein I independent. We concluded that the presence of ACL antibodies in chronic HCV patients seem to be an epiphenomenon and their presence has neither a clinical nor a laboratory significance in this category of patients. Thus, testing for HCV infection in APS patients or follow-up for the possibility of APS development in HCV patients might not be recommended. Thus, our study failed to implicate HCV as an aetiopathogeinc factor for APS