PAI-1 4G-4G and MTHFR 677TT in non-hepatitis C virus/hepatitis B virus-related liver cirrhosis  

作　　者：Linda Pasta Francesca Pasta 

机构地区：[1]Department of Medicine,Clinica Candela

出　　处：《World Journal of Hepatology》2015年第29期2920-2926,共7页世界肝病学杂志（英文版）（电子版）

摘　　要：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 cauAIM: To evaluate the different roles of thrombophilia in patients with and without viral etiology. The thrombophilic genetic factors(THRGFs), PAI-1 4G-4G, MTHFR 677 TT, V Leiden 506 Q and prothrombin 20210 A, were studied as risk factors in 1079 patients with liver cirrhosis(LC), enrolled from January 2000 to January 2014. METHODS: All Caucasian LC patients consecutively observed in a seven year period were included; the presence of portal vein thrombosis(PVT) and Budd Chiari syndrome(BCS) was registered. The differences between the proportions of each THRGF with regard to the presence or absence of viral etiology and the frequencies of the THRGF genotypes with those predicted in a population by the Hardy-Weinberg equilibrium were registered.RESULTS: Four hundred and seventeen/one thousand and seventy-six patients(38.6%) showed thrombophilia: 217 PAI-1 4G-4G, 176 MTHFR C677 TT, 71 V Leiden factor and 41 prothrombin G20210 A, 84 with more than 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 + hepatitis B virus. PAI-1 4G-4G, MTHFR C677 TT, the presence of at least one TRHGF and the presence of > 1 THRGF, were statistically more frequent in patients with NVLC vs patients with VLC: All χ~2 > 3.85 and P < 0.05. Patients with PVT and/or BCS with at least one TRHGF were 189/352(53.7%). The Hardy-Weinberg of PAI-1 and MTHFR 677 genotypes deviated from that expected from 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 677 TT was nearly twofold and PAI-1 4G-4G more than threefold more frequently found in NVLC vs patients with VLC; the Hardy-Weinberg equilibrium of these two polymorphisms confirms this data in NVLC. We suggest that PAI-1 4G-4G and MTHFR677 TT could be considered as factors of fibrosis and thrombosis mechanisms, increasing the inflammation response, and causing the hepatic fibro

关 键 词：PAI-1 4G-4G MTHFR 677TT V Leiden506Q PROTHROMBIN 20210A Liver cirrhosis Portal veinthrombosis BUDD CHIARI syndrome FIBROGENESIS 

分 类 号：R512.62[医药卫生—内科学] R575.2[医药卫生—临床医学]