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Comment & Response
May 2015

Should the Term Coagulopathy in Cirrhosis Be Abandoned?

Author Affiliations
  • 1Department of Internal Medicine, Sapienza University, Rome, Italy
JAMA Intern Med. 2015;175(5):862-863. doi:10.1001/jamainternmed.2015.90

To the Editor The case reported by Roberts and Bambha1 regarding a 61-year-old woman with cirrhosis is of particular interest because it reflects the difficulty to face an old concept, which still continues to influence the clinical practice. This cirrhotic patient was planned for a surgical intervention and treated with a fresh-frozen plasma because of a prolonged prothrombin time and a putative risk of bleeding. Such an approach was based on the common belief that cirrhosis is complicated by the so-called coagulopathy, which theoretically should increase the risk of bleeding. The term coagulopathy has been coined because of impaired clotting activation detected by laboratory tests in association with deterioration of liver function; the frequent coexistence of hyperfibrinolysis, low platelet count, and platelet dysfunction reinforced the concept that coagulopathy is associated with cirrhosis.2 This concept has been recently challenged for several reasons. The prolongation of global tests of clotting activation does not actually reflect hemostatic changes in vivo and may be a laboratory artifact.3 Also, cirrhotic patients actually disclose a tendency to a hypercoagulation state, which is related to endotoxemia and may be detected in both peripheral and portal circulation, and to an increased platelet activation.4,5 It is difficult to believe that under these circumstances patients with cirrhosis are at high risk of bleeding; thus, apart from gastrointestinal tract bleeding, which is independent from changes of clotting system, spontaneous bleeding in cirrhosis is rare.2 Conversely, in vivo data reporting the existence of platelet and clotting activation may explain the increased risk for thrombosis overall in portal circulation. This opens a new and challenging scenario as portal vein thrombosis, which may occur in approximately 20% of cirrhotic patients,2 should be treated with antithrombotic drugs. However, planning trials with anticoagulants in cirrhosis will be very difficult because the persistent concept of “coagulopathy in cirrhosis” is likely to be a barrier against the use of anticoagulants. For this reason, a consensus should be reached that cirrhosis is characterized by a tendency to thrombosis more than to bleeding and that the term coagulopathy is inadequate to depict the clinical picture of this setting.

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