Hematologic Manifestations of Liver Disease

Abstract

The liver plays a key role in both protein biosynthesis and lipid metabolism. As a result, hepatic synthetic dysfunction can have adverse effects on both cellular and soluble components of blood. Anemia may occur due to the hemolysis of acanthocytes (spur cells), which is ultimately due to abnormal lipid composition of the red blood cell membrane. Thrombocytopenia may result from several different mechanisms. Cytopenias also may be a consequence of hypersplenism. The liver is the primary site for synthesis of most procoagulant and anticoagulant proteins. The coagulopathy of liver disease is therefore complex. Early in the course of liver disease, thrombocytopenia and a coagulopathy associated with a prothrombotic state are not uncommon, whereas with more advanced disease pancytopenia and coagulopathy associated with hemorrhage become manifest. Fresh frozen plasma and adjuncts to hemostasis may be used as temporizing measures in bleeding patients. However, definitive management of many of the defects due to fulminant hepatic failure requires liver transplantation.