Anticoagulation in cirrhosis: Indications, drug selection, and disease-modifying potential.

Abstract

Anticoagulation in cirrhosis has evolved from a perceived contraindication to an integral component of modern liver disease management. Recognition of the fragile rebalanced hemostatic state has challenged the traditional concept of cirrhosis as an exclusively hemorrhagic disorder and provided the biological rationale for anticoagulation in selected patients. Beyond preventing thrombus extension and promoting portal vein recanalization, accumulating experimental and clinical evidence suggests that anticoagulants may exert disease-modifying effects by attenuating intrahepatic coagulation, hepatic fibrogenesis, sinusoidal dysfunction, and portal hypertension. The therapeutic landscape has also changed substantially. Direct oral anticoagulants have emerged as effective and generally safe alternatives to vitamin K antagonists and low-molecular-weight heparin in carefully selected patients, although important differences in pharmacokinetics, hepatic metabolism, renal elimination, and drug interactions require individualized anticoagulant selection. At the same time, management of portal vein thrombosis has shifted from a uniform treatment approach to a patient-centered strategy that considers thrombus characteristics, transplant candidacy, bleeding risk, and the increasing role of endovascular portal vein recanalization. This review summarizes current evidence regarding the indications for anticoagulation in cirrhosis, anticoagulant selection, management of portal vein thrombosis, and available clinical outcomes. It also examines the emerging concept of anticoagulation as a disease-modifying therapy and highlights key knowledge gaps that should guide future research. Together, these advances position anticoagulation as an increasingly important component of comprehensive cirrhosis care rather than a treatment reserved solely for thrombotic complications.