TY - CHAP M1 - Book, Section TI - Hemostatic Dysfunction Related to Liver Diseases A1 - Lichtman, Marshall A. A1 - Kaushansky, Kenneth A1 - Prchal, Josef T. A1 - Levi, Marcel M. A1 - Burns, Linda J. A1 - Linch, David C. Y1 - 2022 N1 - T2 - Williams Manual of Hematology, 10e AB - Loss of hepatic parenchymal cells leads to decreased plasma levels of all plasma coagulation factors except factor VIII and von Willebrand factor, which are produced primarily by endothelial cells.Thrombocytopenia occurs frequently and is usually a result of splenic sequestration (see Chaps. 26 and 74) but may also be caused by an autoimmune mechanism, disseminated intravascular coagulation (DIC) (see Chap. 86), folic acid deficiency, and decreased platelet production due to thrombopoietin (TPO) deficiency. Platelet dysfunction also contributes to the hemostatic abnormalities.Enhanced fibrinolysis is common and appears to be caused by complex pathogenetic mechanisms, including release and impaired clearance of plasminogen activators.Dysfibrinogenemia is relatively frequently found in patients with chronic liver disease.Patients with chronic liver disease may develop a consumption coagulopathy—in its most extreme form, DIC (see Chap 86).Studies employing sophisticated coagulation tests have shown that due to a rebalancing of the coagulation system in patients with chronic liver failure, thrombin generation is basically normal in the majority of patients, whereas some patients may have a prothrombotic phenotype. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - hemonc.mhmedical.com/content.aspx?aid=1189336597 ER -