Anticoagulation in patients with advanced liver disease: an open issue
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IM - REVIEW
Anticoagulation in patients with advanced liver disease: an open issue Francesco Violi1,2 · Lorenzo Loffredo1 · Daniele Pastori1 Received: 20 June 2020 / Accepted: 30 September 2020 © Società Italiana di Medicina Interna (SIMI) 2020
Abstract Liver disease has been long considered as a risk factor for bleeding for the presence of prolongation of global tests of clotting activation and low platelet count. For this reason, the use of anticoagulants in patients with liver disease and an indication to anticoagulation, such as atrial fibrillation of venous thrombosis, has been poorly considered. Furthermore, recent studies underscored the fact that patients with chronic liver disease may experience thrombosis in portal as well as systemic circulation and treatment with anticoagulants should be considered. The introduction of direct oral anticoagulants has increased therapeutic options for thromboprophylaxis; however, evidence on their safety and efficacy in specific populations, such as patients with liver disease, is still scarce and needs further investigation. Thus, atrial fibrillation patients with coexistent liver disease have been excluded from clinical trials with direct oral anticoagulants. Here, we provide an overview on mechanisms of thrombosis in patients with advanced chronic liver disease and a summary of evidence on the use of oral anticoagulants in patients with liver disease and portal vein thrombosis or atrial fibrillation. Keywords Anticoagulation · Liver disease · Atrial fibrillation · Thrombosis
Introduction Liver disease may be of different etiology including viral, alcoholic, and nonalcoholic fatty liver disease (NAFLD). Liver cells play a key role in the biosynthesis of pro- and anticoagulants factors [1]. Almost all clotting factors are synthetized by liver cells, excepting for the factor VIII, produced by endothelial and stellate cells [2]. Similarly, liver cells synthetize almost all anticoagulants proteins with few exceptions, such as thrombomodulin, which is synthetized by endothelial cells [2]. It is, therefore, arguable that in case of severe liver damage, clotting system undergoes abnormal changes, which may predispose to hemostatic disorders. For decades, advanced liver damage has been considered as a risk factor for bleeding on the basis of a putative so called “coagulopathy”, depicted by a prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT) and * Francesco Violi [email protected] 1
Department of Clinical, Internal, Anesthesiologic and Cardiovascular Sciences, I Clinica Medica, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy
Mediterranea Cardiocentro, via Orazio 2, 80122 Naples, Italy
2
low platelet count. These three blood abnormalities may be detected alone or in association and are usually associated with a concomitant decrease of natural anticoagulants, such as antithrombin or proteins C and S [2]. For these reasons, the use of anticoagulants in patients with liver disease has been long consid
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