ABSTRACT
Objective To evaluate the endogenous anticoagulation potential of bone fracture patients and its relationship with deep venous thrombosis formation (DVT).Methods A total of 95 DVT patients after bone fracture and 100 healthy subjects as control from Beijing Jishuitan Hospital were included in this study.On the third day after orthopedic surgery,the citrated anticoagulant plasma samples were collected and fibrin degradation products (FDP) and D-dimer (DD) were measured.Protac-induced coagulation inhibition percentage (PICI) was measured with ThromboPath (ThP) chromogenic assay as the marker of endogenous anticoagulation potential.The serum samples from patients were collected to measure the concentration of high-density lipoprotein cholesterol (HDL-C).Results Both FDP and DD values of DVT patient group were significantly higher than those of healthy control group (all P ＜ 0.01).The PICI (％) of DVT patients group was significantly lower than that of healthy control group (82.8 ± 7.2 vs 87.8 ± 3.6,P ＜ 0.01).The PICI of patients ≥65 years old was 4.8 percent lower than that of the patients ＜65 years old (P ＜0.05) in DVT group.When the cut-off value for PICI was set as 84.2％,a significant difference was showed between DVT and control group by Chi-Square test (P ＜0.0 1).PICI was negatively correlated with FDP and DD (r =-0.318,-0.336,both P ＜ 0.01),but positively correlated with HDLC (r =0.284,P ＜ 0.01).Logistic regression analysis suggested that PICI was a risk factor of DVT with odds ratio 1.243 (P ＜ 0.01).Conclusion The endogenous anticoagulation potential may be severely impaired in DVT patient after bone fracture.
ABSTRACT
BACKGROUND & AIMS: Cirrhosis is associated with a plasmatic procoagulant imbalance, detected in vitro by thrombin generation tests performed in the presence vs. absence of such activators of protein C as thrombomodulin or Protac. This imbalance is thought to be due to decreased protein C and increased factor VIII, but this has never been directly demonstrated. To test this hypothesis we analyzed plasma from 50 patients with cirrhosis before and after in vitro addition of purified protein C meant to restore normal levels. METHODS: Results for two thrombin generation assays were expressed as ratios of endogenous thrombin potential (ETP) with-to-without thrombomodulin or as Protac-induced coagulation inhibition (PICI%). By definition, high ETP ratios or low PICI% reflect a resistance to the anticoagulant action of thrombomodulin or Protac, respectively, and can be taken as indexes of in vitro procoagulant imbalance. RESULTS: The median (range) protein C level before addition was 40% (4-101%) and increased to 156% (110-305) after addition (p<0.001). The procoagulant imbalance, which was high before protein C addition [ETP ratio=0.83 (0.44-1.00)], was reduced after addition [ETP ratio=0.60 (0.14-0.84)], p<0.001. ETP-ratios were inversely correlated with protein C activity (rho=-0.46, p<0.001). Similar results were obtained with the Protac assay. CONCLUSIONS: The results provide evidence that low protein C contributes to the procoagulant imbalance in plasma from patients with cirrhosis. The findings may have clinical implications for the treatment or prophylaxis of thrombosis in these patients.