Portal vein thrombosis in patients with liver cirrhosis: Risk factors and clinical presentation

Abstract Background:Portal vein thrombosis (PVT) is a common complication of liver cirrhosis. PVT impact on disease progression is not clarified as yet. Anticoagulation therapy is considered effective in this setting, but is associated with potentially bleeding episodes. Aim : to assess the risk factors and clinical impact of non-neoplastic PVT complicating cirrhosis, as well as the treatment profile and its efficacy in clinical practice.Methods:A retrospective monocentric study over a period of 19 years including all patients diagnosed with cirrhosis and non-neoplastic PVT was conducted.Results:A total of 49 patients were enrolled in the present study.The mean age was 60.86±11.61 years old. Chronic viral hepatitis was the most frequent cause of cirrhosis (63.2%). Most of our cases had advanced liver disease (89.9% Child class B/C) with a mean MELD score of 19.27. The risk factors for thrombophilia, inherited or acquired, were: a deficiency in coagulation inhibitors, either isolated or combined (protein S, protein C and antithrombin III) in 19 patients, a heterozygous Factor V Leiden mutation in 2 patients, a heterozygous MTHFR mutation in one patient, an antiphospholipid antibodies syndrome in 2 patients, an essential thrombocythemia in one patient. Anticoagulant therapy was indicated in half of the cases. Multivariate analyses demonstrated that thrombus extension was the only independent predictive factor of portal vein recanalization (p=0.009). During follow-up, progression was observed in 8% of treated patients with anticoagulants versus 12.5% of untreated patients (p=0.12). Our study has shown that anticoagulant treatment is not associated with elevated risk of bleeding or developing other complications. The mean survival was higher in patients treated successfully (38.31 months Vs 23.41 months, p=0.204). Conclusions:Our outcomes confirm that anticoagulation therapy in cirrhotic patients with non-neoplastic PVT is not associated with increased risk of liver disease decompensation, including bleeding.