Review article: the pathophysiology of thrombocytopenia in hepatitis C virus infection and chronic liver disease

摘要: Summary Background  The pathophystology of thrombocytopenia in patients with chronic liver disease resulting from hepatitis C virus (HCV) infection is complex and involves several complementary mechanisms that likely act concert. Aim  To summarize the available data on etiology disease. Results  In untreated C, both prevalence severity increase parallel extent disease, usually becoming clinically relevant when develop extensive fibrosis and/or cirrhosis. Pathogenetic include hypersptenism secondary to portal hypertension, bone marrow suppression either HCV itself or interferon treatment, aberrations immune system formation anti-platelet antibodies immune-complexes bind platelets facilitate their premature clearance, development immunologically-mediated extrahepatic manifestations including mixed cryoglobulinemia without associated joint, renal, cutaneous involvement, thrombopoietin (TPO) deficiency dysfunction. natural inverse relationship between TPO platelet levels not maintained; therefore, blood fail have clinical relevance predictive value assessing thrombocytopenic status a given patient. Conclusions  thrombocytopenisa multifactorial.