Activation of the coagulation cascade in untreated primary open-angle glaucoma
Activation of the coagulation cascade in untreated primary open-angle glaucoma
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DOI：
10.1016/s0161-6420(97)30245-0
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发表时间：
1997-04-01
期刊：
影响因子：
13.7
通讯作者：
Detkova, P
中科院分区：
文献类型：
--
作者：
OBrien, C;Butt, Z;Detkova, P
目的：作者研究了未经治疗的青光眼患者的凝血级联和纤溶途径（分别为P = 0.00001和P = 0.0003）和正常眼压性青光眼患者（[NPG] P = 0.00001和P = 0.03），方法：招募了42名未经治疗的NPG患者，25名未经治疗的原发性开角型青光眼（POAG）患者和32名年龄匹配的正常对照。排除了接受抗凝治疗、β受体阻滞剂或钙通道阻滞剂的患者。使用酶联免疫吸附试验techniques.Results：POAG患者的凝血酶原片段1 + 2和D-二聚体水平升高相比，NPG和对照组（P = 0.00001和P = 0.0003，分别）的凝血和纤溶途径的标志物进行了评估。两组青光眼患者的全身血管病变均多于对照组（P < 0.05）。POAG患者的收缩压和脉压均高于正常对照组和NPG组（P < 0.05）。两个青光眼组有更大的纤维蛋白原水平（这是边界的统计学意义）比control group.Conclusion：凝血酶原片段1 + 2和D-二聚体水平升高表示激活的凝血级联和纤溶途径，分别导致高凝状态在未经治疗的POAG。这些发现可能有助于报道青光眼视网膜静脉血栓形成的患病率增加，也有助于青光眼视神经损伤的发病机制。
Purpose: The authors studied the coagulation cascade and fibrinolysis pathway in patients with untreated glaucoma (P = 0.00001 and P = 0.0003, respectively) and patients with normal pressure glaucoma ([NPG] P = 0.00001 and P = 0.03, respectively),Methods: Forty-two untreated patients with NPG, 25 untreated patients with primary open-angle glaucoma (POAG), and 32 age-matched normal controls were recruited. Patients taking anticoagulant therapy beta blockers or calcium channel blockers were excluded. Venous blood was assessed for markers of the coagulation and fibrinolysis pathways using enzyme-linked immunosorbent assay techniques.Results: Patients with POAG had elevated levels of prothrombin fragments 1 + 2 and D-dimer compared with both the NPG and controls (P = 0.00001 and P = 0.0003, respectively). Both glaucoma groups had more (P < 0.05) systemic vascular disease than the control group. The patients with POAG had higher (P < 0.05) systemic blood pressure (systolic and pulse pressure) than the control and NPG groups. Both glaucoma groups had greater levels of fibrinogen (which was of borderline statistical significance) than the control group.Conclusion: Elevated levels of prothrombin fragments 1 + 2 and D-dimer indicate activation of the coagulation cascade and fibrinolysis pathway, respectively, leading to a hypercoagulable state in untreated POAG. These findings may contribute to the reported increased prevalence of retinal venous thrombosis in glaucoma and also to the pathogenesis of optic nerve damage in glaucoma.