Le Aiping, Zhang Lunli, Liu Wei, Li Xiaopeng, Ren Jianwei, Ning An
Departments of Blood Transfusion Department of Infectious Diseases, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Health Department of the PLA General Staff Headquarters of the Security Council, Beijing Jiangxi Institute of Parasitology, Nanchang, Jiangxi, P.R. China.
Medicine (Baltimore). 2017 Feb;96(7):e6116. doi: 10.1097/MD.0000000000006116.
A structural equation model was used for verification with chronic schistosomiasis to investigate the coagulation-anticoagulation system imbalance and to deduce the mechanism of D-dimer (D-D) level elevation in patients with advanced schistosome hepatic disease. We detected the plasma levels of tissue-type fiber plasminogen activator (tPA), urokinase type plasminogen activator (uPA), plasmin-antiplasmin complex (PAP), plasminogen (PLG), antithrombin (AT), plasminogen activator inhibitor 1 (PAI1), D-D, factor VIII: C (FVIII:C), antithrombin-III (AT-III), PLG, protein S (PS), and protein C (PC) in the healthy people as control (69), patients with chronic schistosomiasis (150) or advanced chronic schistosomiasis (90). FVIII, PAP, D-D, tPA, and uPA plasma levels were significantly higher in the chronic group than in the control group and were also significantly higher in the advanced group. However, AT-III, PC, PS, AT, PLG, and PAI1 plasma levels in the advanced and chronic groups were significantly lower than those in the control group. With progression of disease in patients with schistosomiasis japonica, a hypercoagulable state is induced by the coagulation-anticoagulation imbalance, eventually leading to patients with high levels of D-D. Furthermore, we established a structural equation model path of a "chronic schistosomiasis disease stage-(coagulation-anticoagulation-fibrinolysis)-D-D." By using analysis of moment structures (AMOS), it was shown that the chronic schistosomiasis stage was positively related to factor VIII and had negative correlation with AT-III; a good positive correlation with PAP, tPA, and uPA; and a good negative correlation with PLG and PAI1. In addition, our results show that the path coefficient of anticoagulation-fibrinolysis system to the chronic stage of schistosomiasis or D-D levels was significantly higher than that of the coagulation system. In conclusion, the coagulation and fibrinolysis imbalance in patients with chronic schistosomiasis, especially with advanced schistosomiasis, is due to the progression of disease stages.
采用结构方程模型对慢性血吸虫病进行验证,以研究凝血 - 抗凝系统失衡,并推导晚期血吸虫肝病患者D - 二聚体(D - D)水平升高的机制。我们检测了健康对照者(69例)、慢性血吸虫病患者(150例)和晚期慢性血吸虫病患者(90例)血浆中组织型纤溶酶原激活物(tPA)、尿激酶型纤溶酶原激活物(uPA)、纤溶酶 - 抗纤溶酶复合物(PAP)、纤溶酶原(PLG)、抗凝血酶(AT)、纤溶酶原激活物抑制剂1(PAI1)、D - D、因子VIII:C(FVIII:C)、抗凝血酶III(AT - III)、PLG、蛋白S(PS)和蛋白C(PC)的水平。慢性组的FVIII、PAP、D - D、tPA和uPA血浆水平显著高于对照组,且在晚期组中也显著更高。然而,晚期组和慢性组的AT - III、PC、PS、AT、PLG和PAI1血浆水平显著低于对照组。随着日本血吸虫病患者病情的进展,凝血 - 抗凝失衡导致高凝状态,最终导致患者D - D水平升高。此外,我们建立了“慢性血吸虫病疾病阶段 - (凝血 - 抗凝 - 纤溶) - D - D”的结构方程模型路径。通过矩结构分析(AMOS)表明,慢性血吸虫病阶段与因子VIII呈正相关,与AT - III呈负相关;与PAP、tPA和uPA呈良好正相关;与PLG和PAI1呈良好负相关。此外,我们的结果表明,抗凝 - 纤溶系统对血吸虫病慢性期或D - D水平的路径系数显著高于凝血系统。总之,慢性血吸虫病患者,尤其是晚期血吸虫病患者的凝血和纤溶失衡是由于疾病阶段的进展所致。