الفهرس 
Hepatitis C VirusOnly 14 pages are availabe for public view
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Abstract
Immune peripheral destruction of platelets was established by many studies. Higher levels of PAIgG antibodies were found in thrombocytopenic compared to non thrombocytopenic patients. On the other hand, fewer studies reported that PAIgG elevation was just a finding in hepatitis C patients with no association with thrombocytopenia and has no aetiologic role in HCV-associated thrombocytopenia. Impaired TPO production has been reported to have a role only late in the cirrhotic stage. However, it may be normal or even increased early in chronic active hepatitis. Direct role of hepatitis C virus is reported by many studies. Binding of HCV to glycoprotein VI (GPVI) on the platelet membrane leads to platelet activation with subsequent removal of platalets from circulation by reticuloendothelial system. Autoantibody-mediated suppression of megakaryopoiesis, infection of megakaryoblasts by HCV, Anti-TPO receptor antibodies and TPO receptor mutations are suggested points of research in the future. It is known that thrombocytopenia is a common side effect of interferon therapy and it is also well known as a manifestation of hypersplenism in patients with portal hypertension. Accelerated neutrophil apoptosis was suggested to be an aetiologic factor. Additionally, Serum factors secreted by the spleen was claimed to induce apoptosis. Cytokine dysregulation is also suggested by many studies as an aetiologic factor but further research is needed in this issue.