Chronic and acute liver diseases may be accompanied by substantial changes in primary hemostasis. Thrombocytopenia develops as a consequence of defective platelet production, increased consumption, and/or increased splenic sequestration. In addition, ill-defined platelet function defects may further impair primary hemostasis. However, defects in platelet number and function appear (partly) compensated for by increased levels of von Willebrand factor (VWF) and decreased circulating ADAMTS13. Consequently, patients with liver diseases may have a relatively well-functioning primary hemostatic system, which does not necessarily necessitate prophylactic transfusion of platelet concentrates, for example, prior to invasive procedures. Thrombopoietin receptor agonists are able to increase the platelet count, but normalization of the platelet count in patients with cirrhosis may lead to a thrombotic risk due to the high plasma levels of von Willebrand factor. The platelet count is a reasonable diagnostic and prognostic tool in patients with liver diseases. Platelets also have functions unrelated to cessation of bleeding in the context of liver disease. By incompletely understood mechanisms, platelets contribute to regeneration of the liver, for example, following a partial hepatectomy. In animal models of chronic or acute liver failure, platelets have been shown to exert both detrimental and beneficial effects. Whether platelets can both stimulate and inhibit progression of liver disease depending on the exact clinical context requires further study.
|Title of host publication||Platelets in Thrombotic and Non-Thrombotic Disorders|
|Subtitle of host publication||Pathophysiology, Pharmacology and Therapeutics: an Update|
|Editors||Paolo Gresele, Neal S. Kleiman, José A. Lopez, Clive P. Page|
|Number of pages||1402|
|Publication status||Published - 2017|