Activation of the coagulation cascade in untreated primary open-angle glaucoma

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).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.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 (P0.05) systemic vascular disease than the control group. The patients with POAG had higher (P0.05) 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.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.