Portal vein thrombosis (PVT) is a frequent complication in cirrhotic patients, but it may also exist as a basic vascular condition even without any liver damage. Local and systemic factors play a significant role in the pathogenesis of PVT; yet, in practice, more than one factor may be identified. PVT can be considered a result of liver fibrosis and hepatic insufficiency. The JAK2mutation has been accepted as a factor producing PVT. In general, the anticoagulants are recom- mended but this therapy should be used carefully in treating patients that associate coagulopathy or thrombocytopenia and esophageal varices. Acute PVT without bowel infarction has a good prognosis. In liver cirrhosis, the mortality due to hemor- rhage is higher than in chronic PVT. Therefore, for the patients with PVT, the survival rate is decreased by 55% in two years, due to hepatic insufficiency. Regarding the treatment, LMWH (low molecular weight heparine) is the most utilized in patients with cirrhosis, non-malignancies, infections, or those who are awaiting a liver transplant. DOACs (direct-acting oral anticoagulants) may be used in the rest of the medical conditions, being safe and equal to LMWH.Copyright © 2021 Spandidos Publications. All rights reserved.
CITATION STYLE
Costache, R., Dragomirică, A., Dumitraș, E., Mariana, J., Căruntu, A., Popescu, A., & Costache, D. (2021). Portal vein thrombosis: A concise review (Review). Experimental and Therapeutic Medicine, 22(1). https://doi.org/10.3892/etm.2021.10191
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