How to treat non-tumoral portal vein thrombosis in cirrhosis? Towards the use of direct-acting oral anticoagulants

© AME Medical Journal. All rights reserved. AME Med J 2017;2:133 amj.amegroups.com Nagaoki et al. suggest that edoxaban a direct-acting oral anticoagulant (DOAC) may be more effective than warfarin in case of chronic portal vein thrombosis (PVT) complicating cirrhosis (1). Furthermore, the conclusions of the study are that edoxaban following an initial therapy with danaparoid sodium, is effective to reduce the volume of thrombosis, without significantly increasing the risk of bleeding. The presence of cirrhosis is associated with a relative risk of 7.3 of developing PVT in the general population. PVT is the most common thrombotic event occurring in cirrhotic patients, with a reported prevalence ranging from 2% to 23%. Complications of PVT may be an extension of thrombosis to the mesenteric vein, with intestinal infarction as a dreaded complication and may also jeopardize liver transplantation when extending to splenic and mesenteric vein. When treating with anticoagulation, [vitamin K antagonist (VKA) or low molecular weight heparin (LMWH)] recanalization rate ranged from 55% to 75% at a mean interval time of 6 months and overall bleeding complications were encountered in 5% of patients. Recommendations for anticoagulation in cirrhotic PVT are experts recommendations, all based on retrospective studies and none on blinded randomized controlled trials: EASL recommends anticoagulation after implementing an adequate prophylaxis for gastrointestinal bleeding at therapeutic dose for at least 6 months, or lifelong in patients candidates to liver transplantation, or with superior mesenteric vein thrombosis, or with a past history suggestive of intestinal ischemia (2). The first line treatment is usually a LMWH followed by VKAs. However, in patients with cirrhosis, anticoagulant dose adjustment is difficult to assess whatever the anticoagulant is administered and recommendations concerning monitoring of these drugs are scarce. First, the reliability of the anti-Xa assay to monitor LMWH is low due to the reduction of antithrombin, a typical feature in patients with advanced liver disease. Second, the prothrombin time is often prolonged because of spontaneous reduction of the clotting factors. The doses of VKAs usually necessary to reach the therapeutic target range may be lower (3-5). However there is currently no reliable data on the international normalized ratio (INR) target in cirrhotic patients in particular in patients with significant liver failure (e.g., factor V below 50%). EASL recommendations insist on the following point: INR target aims a therapeutic interval of 2.0–3.0, but the INR value might not be representative of the real anticoagulation and the results may vary between centers. Therefore, VKAs and LMWH have both a risk of under and over dose. DOACs unlike VKAs directly target clotting factors activated thrombin (dabigatran) or the factor Xa (rivaboxaban or apixaban, edoxaban) without the intermediary action of Editorial