What are the mechanisms for coagulopathy and thrombophilia in patients with cirrhosis?

From Cirrhosis and its complications.  In:  Harrison’s Internal Medicine, 18th ed.

Under Major Complications, toward the bottom of the page.

Explains that patients with cirrhosis experience a decrease in production of clotting factors and diminished clearance of anticoagulants.  Portal hypertension may result in hypersplenism which is associated with thrombocytopenia.  Also, diminished vitamin K absorption (as in patients with chronic cholestatic syndrome or decreased hepatic mass) can interfere with production of some of the vitamin k-dependent clotting factors.

Regarding hypercoagulability, most studies seem to address portal vein thrombosis rather than a risk for any thrombosis.

Tripodi A, et al.  Hypercoagulability in cirrhosis: causes and consequences.  Journal of Thrombosis and Haemostasis, 2011; 9: 1713–1723.

This review identifies three case-control studies that look at the risk of VTE in hospitalized patients:  1) 625 cases with VTE & severe liver disease v. 625 controls – reduced risk of VTE in patients with severe liver disease; 2)  6500 cases VTE v. 10,000 controls – non-significant risk of VTE (RR 1.65) in patients with chronic liver disease.  The third study aimed to assess risk of VTE in patients with cirrhosis; 963 patients with cirrhosis v. 12,405 hospitalized patients without cirrhosis.  Incidence of DVT/PE in cases was 1.8% v. 0.9% in controls.  In multivariate analysis, the presence of cirrhosis was not associated with an increased risk in DVT/PE (OR, 0.87).  The article does discuss mechanisms for hypercoagulability that has been observed in plasma taken from cirrhotic patients.


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