Portal vein thrombosis with protein C-S deficiency in a noncirrhotic patient

There are several conditions that can lead to portal vein thrombosis(PVT), including including infection, malignancies, and coagulation disorders. Anew condition of interest is protein C and S deficiencies, associated with hypercoagulation and recurrent venous thromboembolism. We report the case of a non-cirrhotic 63-year-old male diagnosed with acute superior mesenteric vein thrombosis and PVT and combined deficiencies in proteins C and S, recanalized by short-term low molecular heparin plus oral warfarin therapy.     

Portal vein thrombosis in a patient with HIV treated with a protease inhibitor-containing regimen

We report a case of an HIV seropositive female patient treated with a protease inhibitor-containing regimen who developed recurrent severe life-threathening episodes of haematemesis over time, caused by ruptured oesophageal varices as a consequence of a portal vein thrombosis. Coagulation tests revealed a protein S deficiency, an elevated homocysteinemia and a constitutional elevated plasma factor VIII coagulant activity. These coagulopathies and the HIV infection are independent risk factors for developing venous thromboembolic events. The protease inhibitor treatment may have played a role in increasing the thromboembolic risk. The recurrent bleedings only stopped after invasive surgery. The invasive splenorenal shunt operation was in this case a life-saving procedure.     

肝硬化门静脉血栓药物性再通1例并文献复习

本文报道了1例经过抗凝治疗后门静脉血栓再通的乙型肝炎肝硬化病例。回顾近年肝硬化合并门静脉血栓的文献,总结抗凝治疗的重要性。     

Portal and mesenteric vein thrombosis after portal vein embolization in a patient with protein S deficiency

Portal vein embolization can be performed safely, and so far no major complications have been reported. We report an extremely rare complication of portal vein embolization, a case of portal and mesenteric thrombosis in a 65-year-old patient with protein S deficiency. Right portal vein embolization was carried out prior to extended right hepatectomy for advanced gallbladder carcinoma involving the hepatic hilus. Computed tomography 14 days after embolization revealed massive thrombosis of the portal and the superior mesenteric veins. A protein S deficiency was found by means of an extensive workup for hypercoagulable state. Portal vein embolization may have triggered a cascade of events that was expressed as portal and mesenteric vein thrombosis resulting from deficiency of protein S. It may be better to determine the concentrations of such coagulation regulators prior to portal vein embolization.     

Portal vein thrombosis

Opinion statement Portal vein thrombosis (PVT) can be a difficult clinical problem to assess and manage. A high index of suspicion is needed for a PVT diagnosis given the subtle presentation and potentially serious long-term complications. It should be considered a clue to the presence of one or several underlying disorders, including prothrombotic disorders, whether or not a local precipitating factor is identified. The accruing evidence shows that acute PVT can and probably should be treated with anticoagulation or thrombolytic agents in an effort to prevent extension of thrombus, mesenteric vessel occlusion, and portal hypertension. However, chronic PVT should be treated conservatively with measures to control major consequences related to portal hypertension. Anticoagulation therapy duration should be tailored to the identified predisposing factors.     

Portal vein thrombosis in a patient with hepatitis C virus-related cirrhosis complicated with antiphospholipid syndrome

We report a rare case of portal vein thrombosis (PVT) associated with antiphospholipid syndrome (APS) and hepatitis C virus-related cirrhosis. A 59-year-old woman with hepatitis C virus (HCV) infection was admitted because of coma. The blood test showed a typically cirrhosis pattern including an elevated serum ammonia level. Abdominal computed tomography showed liver cirrhosis and thrombus in the right branch of the portal vein. To elucidate the cause of PVT, antiphospholipid antibodies were examined. Both IgG anti-cardiolipin antibody (ELISA) and IgG anti-cardiolipin-β2 -glycoprotein I complex antibody (ELISA) were positive. When PVT is detected in a patient with cirrhosis, it might be necessary to examine antiphospholipid antibodies to clarify the cause of PVT.     

Left branch portal vein thrombosis associated with hyperhomocysteinemia

A 34 year-old man, who was a smoker, was hospitalised because of severe epigastric and right upper quadrant pain. An isolated left branch portal vein thrombosis was diagnosed using ultrasonography and arteriography. Two thrombogenic pathologies were found: i) a latent myeloproliferative syndrome with spontaneous presence of erythroid colony forming unit (CFU-E) in bone marrow culture, normal blood cell count, platelet count and medullogram; ii) a hyperhomocysteinemia associated with low serum folate levels and a methyl tetrahydrofolate reductase mutation. The association of these two factors probably resulted in portal vein thrombosis. This is the first adult case of a portal vein thrombosis associated with hyperhomocysteinemia. Increased homocysteine serum levels could be a previously unrecognized factor for portal vein thrombosis. Homocysteinemia should be systematically investigated in patients with idiopathic portal vein thrombosis since folate supplements could prevent deleterious vascular effects of hyperhomocysteinemia.     

Portal vein thrombosis: a concise review

Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. Although several predisposing conditions are known to exist in the background of PVT, there still remains a proportion of patients in whom the etiology is not known and the pathogenesis is unclear. In this review we summarize the literature on PVT and present the current knowledge about the precipitating factors of PVT. Further, we discuss the advances in the radiological diagnosis that have improved diagnostic accuracy and are noninvasive. Finally, we discuss the treatment options for patients who have varying extents of thrombosis in the portal vein and specifically focus on PVT that is encountered before and after liver transplantation.     

Portal vein thrombosis associated with ischemic colitis

We report the case of a 52-year-old male who was admitted for sudden abdominal pain and hematochezia. Colonoscopy showed erosion and edema in the mucosa of the descending colon, leading to a diagnosis of ischemic colitis. Blood tests revealed hepatic dysfunctions. Using abdominal ultrasonography (US), thrombus was observed in the left branch of the portal vein and a part of the right branch. Although the Doppler method detected blood flow in the right branch, no blood flow signal was observed in the left branch. Since coagulation examinations were almost normal, and there was no past history of liver cirrhosis or malignancy, it was diagnosed to be portal vein thrombosis (PVT) associated with ischemic colitis. Anticoagulation therapy was initiated for PVT. According to the results of the US and abdominal computed tomography performed 3 months after starting the treatment, thrombus in the right branch had diminished but remained in the umbilical region of the left branch. Due to atrophy of the lateral segment of the liver, we terminated the treatment. Ischemic colitis is not a rare disease; however, when accompanying hepatic dysfunction, it is necessary to take the complications associated with PVT into consideration.