AIM To evaluate the different roles of thrombophiliain patients with and without viral etiology. The thrombophilicgenetic factors （THRGFs）, PAI-1 4G-4G, MTHFR677TT, V Leiden 506Q and prothrombin 20210A,were studied ...AIM To evaluate the different roles of thrombophiliain patients with and without viral etiology. The thrombophilicgenetic factors （THRGFs）, PAI-1 4G-4G, MTHFR677TT, V Leiden 506Q and prothrombin 20210A,were studied as risk factors in 1079 patients with livercirrhosis （LC）, enrolled from January 2000 to January2014.METHODS： All Caucasian LC patients consecutivelyobserved in a seven year period were included; thepresence of portal vein thrombosis （PVT） and BuddChiari syndrome （BCS） was registered. The differencesbetween the proportions of each THRGF with regardto the presence or absence of viral etiology and thefrequencies of the THRGF genotypes with those predictedin a population by the Hardy-Weinberg equilibriumwere registered.RESULTS： Four hundred and seventeen/one thousandand seventy-six patients （38.6%） showed thrombophilia：217 PAI-1 4G-4G, 176 MTHFR C677TT, 71 V Leidenfactor and 41 prothrombin G20210 A, 84 with morethan 1 THRGF; 350 presented with no viral liver cirrhosis（NVLC） and 729 with, called viral liver cirrhosis （VLC）,of whom 56 patients were hepatitis C virus ＋ hepatitisB virus. PAI-1 4G-4G, MTHFR C677TT, the presence ofat least one TRHGF and the presence of 〉 1 THRGF,were statistically more frequent in patients with NVLC vspatients with VLC： All χ 2 〉 3.85 and P 〈 0.05. Patientswith PVT and/or BCS with at least one TRHGF were189/352 （53.7%）. The Hardy-Weinberg of PAI-1 andMTHFR 677 genotypes deviated from that expectedfrom a population in equilibrium in patients with NVLC（respectively χ 2 = 39.3; P 〈 0.000 and χ 2 = 27.94; P 〈0.05）, whereas the equilibrium was respected in VLC.CONCLUSION： MTHFR 677TT was nearly twofold andPAI-1 4G-4G more than threefold more frequently foundin NVLC vs patients with VLC; the Hardy-Weinbergequilibrium of these two polymorphisms confirms thisdata in NVLC. We suggest that PAI-1 4G-4G and MTHFR677TT could be considered as factors of fibrosis andthrombosis mechanisms, increasing the inflammationresponse, and causing the hepatic fibrosis and augmentedintrahepatic vascular resistance typical of LC. PAI-14G-4G and MTHFR 677TT screening of LC patientscould be useful, mainly in those with NVLC, to identifypatients in which new drug therapies based on theattenuation of the hepatic stellate cells activation orother mechanisms could be more easily evaluated.展开更多
文摘AIM To evaluate the different roles of thrombophiliain patients with and without viral etiology. The thrombophilicgenetic factors （THRGFs）, PAI-1 4G-4G, MTHFR677TT, V Leiden 506Q and prothrombin 20210A,were studied as risk factors in 1079 patients with livercirrhosis （LC）, enrolled from January 2000 to January2014.METHODS： All Caucasian LC patients consecutivelyobserved in a seven year period were included; thepresence of portal vein thrombosis （PVT） and BuddChiari syndrome （BCS） was registered. The differencesbetween the proportions of each THRGF with regardto the presence or absence of viral etiology and thefrequencies of the THRGF genotypes with those predictedin a population by the Hardy-Weinberg equilibriumwere registered.RESULTS： Four hundred and seventeen/one thousandand seventy-six patients （38.6%） showed thrombophilia：217 PAI-1 4G-4G, 176 MTHFR C677TT, 71 V Leidenfactor and 41 prothrombin G20210 A, 84 with morethan 1 THRGF; 350 presented with no viral liver cirrhosis（NVLC） and 729 with, called viral liver cirrhosis （VLC）,of whom 56 patients were hepatitis C virus ＋ hepatitisB virus. PAI-1 4G-4G, MTHFR C677TT, the presence ofat least one TRHGF and the presence of 〉 1 THRGF,were statistically more frequent in patients with NVLC vspatients with VLC： All χ 2 〉 3.85 and P 〈 0.05. Patientswith PVT and/or BCS with at least one TRHGF were189/352 （53.7%）. The Hardy-Weinberg of PAI-1 andMTHFR 677 genotypes deviated from that expectedfrom a population in equilibrium in patients with NVLC（respectively χ 2 = 39.3; P 〈 0.000 and χ 2 = 27.94; P 〈0.05）, whereas the equilibrium was respected in VLC.CONCLUSION： MTHFR 677TT was nearly twofold andPAI-1 4G-4G more than threefold more frequently foundin NVLC vs patients with VLC; the Hardy-Weinbergequilibrium of these two polymorphisms confirms thisdata in NVLC. We suggest that PAI-1 4G-4G and MTHFR677TT could be considered as factors of fibrosis andthrombosis mechanisms, increasing the inflammationresponse, and causing the hepatic fibrosis and augmentedintrahepatic vascular resistance typical of LC. PAI-14G-4G and MTHFR 677TT screening of LC patientscould be useful, mainly in those with NVLC, to identifypatients in which new drug therapies based on theattenuation of the hepatic stellate cells activation orother mechanisms could be more easily evaluated.
