Portal Vein Thrombosis: Pathogenetic Mechanisms, Clinical Variants, and Prognosis

Portal vein thrombosis (PVT) is a rare but potentially life-threatening condition encountered in internal medicine, which often presents asymptomatically during the so-called “therapeutic window,” complicating timely diagnosis. PVT can be classified as acute or chronic, occlusive or non-occlusive, progressive or spontaneously regressing. Risk factors include both inherited and acquired, local and systemic causes. The most common among them are oral contraceptive use, antiphospholipid syndrome, pregnancy and the postpartum period, antithrombin III deficiency, hyper- and dysfibrinogenemia, hyperhomocysteinemia, prothrombin gene and factor V Leiden mutations, and deficiencies of protein C and protein S. The risk increases in the presence of malignancies, chronic inflammatory diseases, nephrotic syndrome, liver cirrhosis, obesity, post-liver transplantation status, parasitic infections of the abdominal organs, and during diuretic therapy. Diagnosis involves a thorough medical history, clinical assessment, imaging of the hepatobiliary vasculature, and laboratory evaluation including biochemical markers and thromboelastography. Acute PVT is often associated with abdominal pain and/or signs of systemic inflammatory response: leukocytosis, lymphopenia, hypoalbuminemia, and elevated levels of C-reactive protein, D-dimer, fibrinogen, procalcitonin, and LDH. Detection of a dense thrombus on imaging suggests its chronicity (approximately one month). Recurrent PVT may present with a cavernoma, obstruction of portal vein branches, abdominal pain, and ascites. Repeated episodes of abdominal pain in PVT are alarming signs of progressive intestinal ischemia and an unfavorable prognosis. Early initiation of anticoagulant therapy is essential to prevent thrombus extension and recurrence. Preferred medications include unfractionated or low-molecular-weight heparin, as well as vitamin K antagonists (warfarin) to achieve an INR (International Normalized Ratio) of 2.0–3.0. Warfarin is preferable in the absence of liver cirrhosis. In cases of heparin-induced thrombocytopenia or when INR monitoring is impractical, direct oral anticoagulants may be used as alternatives: rivaroxaban (10–20 mg once daily), apixaban (2.5–5 mg twice daily), or edoxaban (15–30 mg, less often 60 mg daily). Liver and kidney function should be monitored during therapy to reduce the risk of hemorrhagic complications. Local thrombolysis is indicated for acute thrombosis, while balloon angioplasty and/or stenting without thrombectomy may be a safe and effective alternative. Recanalization of the portal vein may take 6 to 12 months. The article presents a clinical case of portal vein thrombosis in a 31-year-old female patient in the late postpartum period associated with antiphospholipid syndrome.