Thrombocytopenia is considered one of the hallmarks of patients with cirrhosis. Several mechanisms have been implicated in the pathophysiology of thrombocytopenia in cirrhosis. Hypersplenism caused by splenomegay, classically regarded as an indirect marker of portal hypertension has been considered the main factor implicated [200]. Nevertheless, portal hypertension is best estimated by the hepatic venous pressure gradient (HVPG) [32, 189], although contradictory results have been reported regarding the association between HVPG and platelet count [195-197]. The identification of thrombopoietin (TPO), a growth factor that enhances the maturation of megakaryocytes and the release of platelets from the bone marrow, has shed new light on the physiolgy of platelets [217]. In normal conditions in adults, TPO is mainly produced in the liver [93, 96] and the circulating leves of platelets are controlled by a negative feedback mechanism [99], so there is an inverse relationship between the amount of circulating platelets, and the amount of TPO that can reach the bone marrow to stimulate thrombopoiesis. In liver cirrhosis perhaps a decreased syntehesis of TPO could be implicated in the development of thrombocytopenia. Controversial findings regarding the role of each mechanism in thrombocytopenia of liver cirrhosis have been reported [142, 146, 160-161, 184] and no study has simultaneously evaluated the influence of the different mechanisms including portal hypertension and TPO production nor whether their influence could change in different stages of the disease..
