title: Hypercoagulability in cirrhosis: causes and consequences.
abstract: Decreased levels of most coagulation factors and thrombocytopenia are the main haemostatic abnormalities of cirrhosis. As a consequence, this condition was, until recently, considered as the prototype acquired coagulopathy responsible for bleeding. However, recent evidence suggests that it should, rather, be regarded as a condition associated with normal or even increased thrombin generation. The bleeding events that occur in these patients should, therefore, be explained by the superimposed conditions that frequently occur in this setting. Due to elevated levels of factor VIII (procoagulant driver) in combination with decreased protein C (anticoagulant driver), which are typically found in patients with cirrhosis, a procoagulant imbalance, defined as a partial resistance to the in vitro anticoagulant action of thrombomodulin, can be demonstrated. Whether this in vitro hypercoagulability is truly representative of what occurs in vivo remains to be established. However, the hypothesis that it may have clinical consequences is attractive and deserves attention. The possible consequences that we discuss herein include whether (i) cirrhosis is a condition associated with increased risk of venous thromboembolism or portal vein thrombosis; (ii) the hypercoagulability associated with cirrhosis has any other role outside coagulation (i.e. progression of liver fibrosis); and (iii) anticoagulation should be used in cirrhosis. Although apparently provocative, considering anticoagulation as a therapeutic option in patients with cirrhosis is now supported by a rationale of increasing strength. There may be subgroups of patients who benefit from anticoagulation to treat or prevent thrombosis and to slow hepatic fibrosis. Clinical studies are warranted to explore these therapeutic options.
authors: Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Department of Internal Medicine, IRCCS Cà Granda Ospedale Maggiore Policlinico Foundation and Università degli Studi di Milan, Milan, Italy. armando.tripodi@unimi.it
authors: A
authors: A
authors: Tripodi
authors: Q M
authors: QM
authors: Anstee
authors: K K
authors: KK
authors: Sogaard
authors: M
authors: M
authors: Primignani
authors: D C
authors: DC
authors: Valla
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use; D005169:Factor VIII / Q000378:metabolism; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood* / Q000150:complications* / Q000188:drug therapy; D011169:Portal Vein; D011486:Protein C / Q000378:metabolism; D011655:Pulmonary Embolism / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood* / Q000188:drug therapy / Q000209:etiology*; D054556:Venous Thromboembolism / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D020246:Venous Thrombosis / Q000097:blood / Q000209:etiology / Q000517:prevention & control
chemical_list: D000925:Anticoagulants; D011486:Protein C; D005169:Factor VIII