OBJECTIVE AND METHODS: We compared frequencies of three common prothrombotic mutations (factor V Leiden, the G20210A mutation of the prothrombin gene, and homozygosity for C677T methylenetetrahydrofolate reductase) in 219 cirrhotic patients, 43 with and 176 without portal vein thrombosis (PVT). The following variables were related to PVT: prothrombin levels, platelet count, Child-Pugh classification, previous abdominal surgery, number of decompensation events, size of varices, red markers on varices, and sclerotherapy. All patients were followed up for a mean period of 18 months (range 10-30). RESULTS: Prothrombotic mutations were detected in 64 of the 219 cirrhotic patients (29.2%), at equal frequency in patients with or without PVT. At univariate analysis, PVT was associated with Child-Pugh classes B and C, signs of liver decompensation, large varices with red markings, sclerotherapy, and abdominal surgery. At multivariate analysis, PVT was associated with sclerotherapy [odds ratio (OR) 4.9, 95% confidence interval (CI) 2.2-11] and previous surgery (OR 2.8, 95% CI 1.2-6.3). The combination of the two acquired factors increased the risk of PVT, whereas the combination of local with genetic defects did not. Only a single patient with genetic thrombophilia and without PVT at inclusion developed the complication during follow-up, concomitantly with the development of hepatocellular carcinoma. CONCLUSION: In cirrhotic patients prothrombotic mutations by themselves are not causative of PVT. Sclerotherapy and previous abdominal surgery favour the development of two-thirds of cases of PVT; in the remaining cases the pathogenesis remains elusive.
OBJECTIVE AND METHODS: We compared frequencies of three common prothrombotic mutations (factor V Leiden, the G20210A mutation of the prothrombin gene, and homozygosity for C677T methylenetetrahydrofolate reductase) in 219 cirrhotic patients, 43 with and 176 without portal vein thrombosis (PVT). The following variables were related to PVT: prothrombin levels, platelet count, Child-Pugh classification, previous abdominal surgery, number of decompensation events, size of varices, red markers on varices, and sclerotherapy. All patients were followed up for a mean period of 18 months (range 10-30). RESULTS: Prothrombotic mutations were detected in 64 of the 219 cirrhotic patients (29.2%), at equal frequency in patients with or without PVT. At univariate analysis, PVT was associated with Child-Pugh classes B and C, signs of liver decompensation, large varices with red markings, sclerotherapy, and abdominal surgery. At multivariate analysis, PVT was associated with sclerotherapy [odds ratio (OR) 4.9, 95% confidence interval (CI) 2.2-11] and previous surgery (OR 2.8, 95% CI 1.2-6.3). The combination of the two acquired factors increased the risk of PVT, whereas the combination of local with genetic defects did not. Only a single patient with genetic thrombophilia and without PVT at inclusion developed the complication during follow-up, concomitantly with the development of hepatocellular carcinoma. CONCLUSION: In cirrhotic patients prothrombotic mutations by themselves are not causative of PVT. Sclerotherapy and previous abdominal surgery favour the development of two-thirds of cases of PVT; in the remaining cases the pathogenesis remains elusive.
Authors: Tawfik Khoury; Muhammad Massarwa; Wadi Hazou; Saleh Daher; David Hakimian; Ariel A Benson; Toni Ashqar; Mahmud Mahamid; Shaul Yaari Journal: J Gastrointest Cancer Date: 2019-12