Markus Peck‐Radosavljevic1
1Department of Gastroenterology and Hepatology, University of Vienna Medical School, Vienna, Austria
Tóm tắt
Moderate thrombocytopenia
is a frequent finding in cirrhosis of the liver and well
tolerated in most instances. The pathophysiology of thrombocytopenia
in liver disease has long been associated with the concept
of hypersplenism, where portal hypertension was thought to cause
pooling and sequestration of all corpuscular elements of the blood,
predominantly thrombocytes in the enlarged spleen. The concept of
hypersplenism was never proven beyond any doubt but was widely
accepted for the lack of alternative explanations.With the discovery of the lineage‐specific cytokine thrombopoietin
(TPO) the missing link between hepatocellular function
and thrombopoiesis was found. TPO is predominantly produced
by the liver and constitutively expressed by hepatocytes.TPOproduction
in humans is dependent on functional liver cell mass and
is reduced when liver cell mass is severely damaged. This leads to
reduced thrombopoiesis in the bone marrow and consequently to
thrombocytopenia in the peripheral blood of patients with
advanced‐stage liver disease.With recombinant TPOs in development, patients with liver disease
and TPO seem to be the ideal target population for this drug.
Once the efficacy of thrombopoietin in patients with liver disease
is proven, a potent yet safe drug may be available to treat cirrhotic
patients undergoing invasive or surgical procedures, during bleeding
episodes or when undergoing therapy with myelosuppressive
drugs such as interferon‐alpha.
