Is thrombocytopenia in liver failure dependent on an inadequate synthesis of thrombopoietic stimulating factor by the liver?

Thrombocytopenia in liver diseases has been considered secondary to portal hypertension or to a consumption mechanism associated with fibrinolytic disorders. Several conflicting clinical reports and evidence from experimental models justify the above mentioned mechanisms only in part. We propose that thrombocytopenia may be consequent to an inadequate synthesis of a factor stimulating thrombopoiesis produced by the liver.