Abstract
Hyperfibrinolysis may be detected in patients with cirrhosis, particularly in case
of severe liver failure. Hyperfibrinolysis is usually associated with prolonged global
tests of clotting activation, which are then dependent on impaired synthesis of clotting
factors by liver cells. The term “coagulopathy” has therefore been coined to indicate
the existence of hyperfibrinolysis and blood hypocoagulation in cirrhosis, and, for
a long time, these changes have been believed to facilitate bleeding. However, apart
from gastrointestinal bleeding, which is related prevalently to hemodynamic factors
in the portal circulation, spontaneous bleeding is less frequent than would be expected
by the abnormality of laboratory tests. This apparent paradox may be explained by
studies questioning the term “coagulopathy,” instead documenting a hypercoagulation
state in portal as well as in peripheral circulation of cirrhotic patients. The support
of these findings by more recent data allows a redefinition of the overall clotting
picture, in particular hyperfibrinolysis, in cirrhosis. Thus, this review analyzes
prevalence and clinical impact of hyperfibrinolysis in cirrhosis, focusing in particular
on whether it is primary or secondary to clotting activation. Furthermore, we focused
such changes in the context of more recent data showing an association between cirrhosis
and thrombosis.
Keywords
liver cirrhosis - hyperfibrinolysis - portal vein thrombosis - anticoagulants
