AIM： To assess the hypercoagulability in PBC and its relationship with homocysteine （HCY） and various components of the haemostatic system. METHODS： We investigated 51 PBC patients （43F/8M; mean age： 63±13....AIM： To assess the hypercoagulability in PBC and its relationship with homocysteine （HCY） and various components of the haemostatic system. METHODS： We investigated 51 PBC patients （43F/8M; mean age： 63±13.9 yr） and 102 healthy subjects （86 women/16 men, 63±13 yr）, and evaluated the haemostatic process in whole blood by the Sonoclot analysis and the platelet function by PFA-100 device. We then measured HCY （fasting and after methionine loading）, tissue factor （TF）, thrombin-antithrombin complexes （TAT）, D-dimer （D-D）, thrombomodulin （TH）, folic acid, vitamin B6 and B12 plasma levels. C677T 5,10-methylenetetrahydrofolate reductase （HTHFR） polymorphism was analyzed. RESULTS： Sonoclot RATE values of patients were significantly （P〈 0.001） higher than those of controls. Sonoclot time to peak values and PFA-100 closure times were comparable in patients and controls. TAT, TF and HCY levels, both in the fasting and post-methionine loading, were significantly （P〈0.001） higher in patients than in controls. Vitamin deficiencies were detected in 45/51 patients （88.2%）. The prevalence of the homozygous TT677 MTHFR genotype was significantly higher in patients （31.4%） than in controls （17.5%） （P〈 0.05）. Sonodot RATE values correlated significantly with HCY levels and TF.CONCLUSION： In PBC, hyper-HCY is related to hypovitaminosis and genetic predisposing factors. Increased TF and HCY levels and signs of endothelial activation areassociated with hypercoagulability and may have an important role in blood clotting activation.展开更多
AIM： To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease （IBD） and to characterize bhe anti-inflammatory action of antithrombin Ⅲ （ATⅢ） on...AIM： To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease （IBD） and to characterize bhe anti-inflammatory action of antithrombin Ⅲ （ATⅢ） on leukocyte kinetics and liver damage. METHODS： Hepatic and intestinal microcirculation was investigated by intravital videomicroscopy. Standardized models of experimental chronic liver cirrhosis and bowel inflammation were employed. Animals were divided into four groups （n = 6/group）： controls, animals with cirrhosis, animals with cirrhosis and IBD, animals with cirrhosis and IBD treated with ATIII. RESULTS： Cirrhosis facilitated leukocyte rolling and sticking in hepatic sinusoids （1.91±0.28 sticker/μm vs 0.5±0.5 sticker/μm in controls, P〈0.05）. The effect enhanced in animals with cirrhosis and IBD （5.4±1.65 sticker/μm）, but reversed after ATIII application （3.97±1.04 sticker/μm, P〈0.05）. Mucosal blood flow showed no differences in cirrhotic animals and controls （5.3±0.31 nL/min vs5.4±0.25 nL/min） and was attenuated in animals wibh cirrhosis and IBD significantly （3.49±0.6 nL/min）. This effect was normalized in the treatment group （5.13±0.4 nL/min, P〈0.05）. Enzyme values rose during development of cirrhosis and bowel inflammation, and reduced after ATIII application （P〈0.05）. CONCLUSION： Liver cirrhosis in the presence of IBD leads to a significant reduction in mucosal blood flow and an increase in hepatic leukocyte adherence with consecutive liver injury, which can be prevented by administration of ATⅢ.展开更多
Objective: To determine whether polymorphisms in the genes for coagulation factor II,V, VII could predispose an individual to increase risk for coronary artery disease (CAD) and/or myocardial infarction (MI) in Chines...Objective: To determine whether polymorphisms in the genes for coagulation factor II,V, VII could predispose an individual to increase risk for coronary artery disease (CAD) and/or myocardial infarction (MI) in Chinese. Methods: We screened coagulation factor II(G20210A),V(G1691A),VII (R353Q and HVR4) genotype in 374 patients undergoing coronary angiography by polymerase chain reaction and restriction fragment length polymorphism (PCR RFLP) assay. Results: The R353Q and HVR4 genotype of the factor VII distribution was in accordance with Hardy Weinberg equilibrium. The frequencies of FVII genotype or allele did not show statistically significant differences between CAD group and controls or between male and female. The frequencies of the Q allele and (RQ+QQ) genotype were significantly higher among the CAD patients without myocardial infarction (MI) history than among those with MI history ( P <0.05). However, HVR4 polymorphism was not significantly different within groups. We only find one normal control of factorII(G20210A) mutation. No coagulation factor V(G1691A) mutation was found in the CAD patients and controls. Conclusion: The factor II(G20210A),V(G1691A) mutation is absent and may not be a major genetic factor for CAD and/or MI; the Q allele of the R353Q polymorphism of the factor VII gene may be a protective genetic factor against myocardial infarction in Chinese.展开更多
文摘AIM： To assess the hypercoagulability in PBC and its relationship with homocysteine （HCY） and various components of the haemostatic system. METHODS： We investigated 51 PBC patients （43F/8M; mean age： 63±13.9 yr） and 102 healthy subjects （86 women/16 men, 63±13 yr）, and evaluated the haemostatic process in whole blood by the Sonoclot analysis and the platelet function by PFA-100 device. We then measured HCY （fasting and after methionine loading）, tissue factor （TF）, thrombin-antithrombin complexes （TAT）, D-dimer （D-D）, thrombomodulin （TH）, folic acid, vitamin B6 and B12 plasma levels. C677T 5,10-methylenetetrahydrofolate reductase （HTHFR） polymorphism was analyzed. RESULTS： Sonoclot RATE values of patients were significantly （P〈 0.001） higher than those of controls. Sonoclot time to peak values and PFA-100 closure times were comparable in patients and controls. TAT, TF and HCY levels, both in the fasting and post-methionine loading, were significantly （P〈0.001） higher in patients than in controls. Vitamin deficiencies were detected in 45/51 patients （88.2%）. The prevalence of the homozygous TT677 MTHFR genotype was significantly higher in patients （31.4%） than in controls （17.5%） （P〈 0.05）. Sonodot RATE values correlated significantly with HCY levels and TF.CONCLUSION： In PBC, hyper-HCY is related to hypovitaminosis and genetic predisposing factors. Increased TF and HCY levels and signs of endothelial activation areassociated with hypercoagulability and may have an important role in blood clotting activation.
文摘AIM： To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease （IBD） and to characterize bhe anti-inflammatory action of antithrombin Ⅲ （ATⅢ） on leukocyte kinetics and liver damage. METHODS： Hepatic and intestinal microcirculation was investigated by intravital videomicroscopy. Standardized models of experimental chronic liver cirrhosis and bowel inflammation were employed. Animals were divided into four groups （n = 6/group）： controls, animals with cirrhosis, animals with cirrhosis and IBD, animals with cirrhosis and IBD treated with ATIII. RESULTS： Cirrhosis facilitated leukocyte rolling and sticking in hepatic sinusoids （1.91±0.28 sticker/μm vs 0.5±0.5 sticker/μm in controls, P〈0.05）. The effect enhanced in animals with cirrhosis and IBD （5.4±1.65 sticker/μm）, but reversed after ATIII application （3.97±1.04 sticker/μm, P〈0.05）. Mucosal blood flow showed no differences in cirrhotic animals and controls （5.3±0.31 nL/min vs5.4±0.25 nL/min） and was attenuated in animals wibh cirrhosis and IBD significantly （3.49±0.6 nL/min）. This effect was normalized in the treatment group （5.13±0.4 nL/min, P〈0.05）. Enzyme values rose during development of cirrhosis and bowel inflammation, and reduced after ATIII application （P〈0.05）. CONCLUSION： Liver cirrhosis in the presence of IBD leads to a significant reduction in mucosal blood flow and an increase in hepatic leukocyte adherence with consecutive liver injury, which can be prevented by administration of ATⅢ.
文摘Objective: To determine whether polymorphisms in the genes for coagulation factor II,V, VII could predispose an individual to increase risk for coronary artery disease (CAD) and/or myocardial infarction (MI) in Chinese. Methods: We screened coagulation factor II(G20210A),V(G1691A),VII (R353Q and HVR4) genotype in 374 patients undergoing coronary angiography by polymerase chain reaction and restriction fragment length polymorphism (PCR RFLP) assay. Results: The R353Q and HVR4 genotype of the factor VII distribution was in accordance with Hardy Weinberg equilibrium. The frequencies of FVII genotype or allele did not show statistically significant differences between CAD group and controls or between male and female. The frequencies of the Q allele and (RQ+QQ) genotype were significantly higher among the CAD patients without myocardial infarction (MI) history than among those with MI history ( P <0.05). However, HVR4 polymorphism was not significantly different within groups. We only find one normal control of factorII(G20210A) mutation. No coagulation factor V(G1691A) mutation was found in the CAD patients and controls. Conclusion: The factor II(G20210A),V(G1691A) mutation is absent and may not be a major genetic factor for CAD and/or MI; the Q allele of the R353Q polymorphism of the factor VII gene may be a protective genetic factor against myocardial infarction in Chinese.
