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• W2978633952 abstract "Purpose: Portal vein thrombosis (PVT) and systemic venous thromboembolism are significantly increased in cirrhotic patients even without hepatocellular carcinoma. The risk of developing such complications is usually associated with advanced cirrhosis. When cirrhosis is mild and compensated, other possible causes of PVT should also be considered. We present a case of PVT in chronic hepatitis C infection with focal cirrhosis and portal hypertension with history of splenectomy. A 47-year-old Caucasian woman presented with chronic hepatitis C, genotype 1. She was treated with pegylated interferon and ribavirin for 48 weeks, but developed viral relapse. She had splenectomy when she was young for unclear reason. Her findings on pathologic examination of the liver biopsy were consistent with focal cirrhosis in mild to moderate chronic hepatitis; the Knodell's histologic activity index (HAI) score was 7-9/22. Her MELD score was 6. An annual esophagogastroduodenoscopy revealed non-bleeding grade II esophageal varices and cardial gastric varices. A computerized tomography scan revealed the sub-occlusive thrombus at the bifurcation of the main portal vein. The workup for hypercoagulable state showed low protein C, protein S, and antithrombin III levels. The inferior vena caval venogram showed thrombotic occlusion in left, right, and common portal vein with a portal systemic pressure gradient of 11 mmHg. Collateralization was present at portal hiatus. The ultrasound guided thrombus removal with interventional thrombolysis was attempted in order to avoid systemic anticoagulation therapy. However, the guidewire failed to pass through the obstructed portal vein. She eventually was evaluated for liver transplantation. This is a case that demonstrates the presence of PVT in a patient with mild compensated cirrhosis (based on both histological and clinical evaluation) without hepatocellular carcinoma. The incidence of PVT in well-compensated cirrhosis is reported between 0.6-16%. An increased frequency is reported in decompensated cirrhosis and in up to 35% of cirrhotic patients with hepatocellular carcinoma. The origin of PVT is multifactorial in most cirrhotic patients. Low serum protein C, protein S, and antithrombin III level secondary to decreased protein synthesis in cirrhosis can contribute to a prothrombotic state. Splenectomy is another possible cause of PVT in this case, since PVT after splenectomy occurs in 6-8%. However, the late onset of presentation makes it a less likely cause since most PVT occurs in days to weeks after splenectomy." @default.
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• W2978633952 date "2012-10-01" @default.
• W2978633952 modified "2023-09-26" @default.
• W2978633952 title "Portal Vein Thrombosis in Splenectomized Cirrhotic Patient: A Case Report" @default.
• W2978633952 doi "https://doi.org/10.14309/00000434-201210001-00985" @default.
• W2978633952 hasPublicationYear "2012" @default.
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