title: Review article: the pathophysiology of thrombocytopenia in hepatitis C virus infection and chronic liver disease.
abstract: 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 in concert.
  
  
  OBJECTIVE
  To summarize the available data on the etiology of thrombocytopenia in patients with chronic liver disease.
  
  
  RESULTS
  In patients with untreated hepatitis C, both prevalence and severity of thrombocytopenia increase in parallel with the extent of disease, usually becoming clinically relevant when patients develop extensive fibrosis and/or cirrhosis. Pathogenetic mechanisms include hypersptenism secondary to portal hypertension, bone marrow suppression resulting from either HCV itself or interferon treatment, aberrations of the immune system resulting in the formation of anti-platelet antibodies and/or immune-complexes that bind to platelets and facilitate their premature clearance, development of immunologically-mediated extrahepatic manifestations including mixed cryoglobulinemia with or without associated joint, renal, or cutaneous involvement, and thrombopoietin (TPO) deficiency secondary to liver dysfunction. In chronic liver disease, the natural inverse relationship between TPO and platelet levels is not maintained; therefore, blood TPO levels fail to have clinical relevance or predictive value in assessing the thrombocytopenic status of a given patient.
  
  
  CONCLUSIONS
  The development of thrombocytopenisa in patients with chronic liver disease is complex and multifactorial.
authors.affiliation: Division of Hematology and Medical Oncology, Weill Medical College of Cornell University, New York, NY 10021, USA. babette@med.cornell.edu
authors.forename: B B
authors.initials: BB
authors.lastname: Weksler
mesh_terms: D000998:Antiviral Agents / Q000009:adverse effects*; D001792:Blood Platelets / Q000378:metabolism; D002908:Chronic Disease; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects; D008107:Liver Diseases / Q000150:complications*; D010346:Patient Care Management; D011092:Polyethylene Glycols / Q000009:adverse effects; D011994:Recombinant Proteins; D013154:Spleen / Q000378:metabolism*; D013223:Statistics as Topic; D013921:Thrombocytopenia / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy
chemical_list: D000998:Antiviral Agents; D007074:Immunoglobulin G; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; C100416:peginterferon alfa-2a