Hypercoagulable states in branch retinal vein occlusion
Answers
Hyper-globular condition of patients with retinal venous projection.
Intangible
Background and purpose:
The retina of the thrombus formation in the retina vein causes the retina of the nerves to occur, which is not well understood. This study was done to detect the role of hypercoagulable states in patients with retinal vein.
Method:
Seven consecutive patients were examined with the emergence of intense retinal veins (average age 48+/- 11.5 years) for acute hypercoagulable states. Protein C (PC), Protein S (PS), Factor XII and Fibrinogen were tested, along with antithrombin levels, with the presence of antiphospophilipid antibody (APA) III (on third). The results of the APA and fibrinogen results obtained in these patients were compared to healthy control.
result:
We have detected the APA of 15 out of 57 patients in 15 out of 57 (P = 0.0002). Compared to the control (P <0.001), the level of fibrinogen in patients was very high. Naturally, protein anticognosider III (among 54 54 patients), decreased in PC (out of 8 42 patients), and PS (12 out of 56 patients) were diagnosed. Seven out of 32 patients had reduced the test XII level. Sub-group analysis of thrombophilic differences between patients with major trunk and patient patients, patients of branch vein veins have not shown any significant differences.
Conclusion:
hypercoagulable states are common in patients with delirium of retinal veins and can contribute to the etiology of the disease.
Answer:
Background: The role of a hypercoagulable state in the pathogenesis of retinal vein occlusion (RVO) has not been conclusively established.
Aim: To analyse the prevalence of thrombophilia in RVO.
Design: Prospective case–control study.
Methods: All the patients diagnosed with RVO were referred to an Internal Medicine clinic and compared with sex- and age-matched individuals from a population-based cohort. Demographic, clinical and laboratory variables (including a thrombophilia panel) were analysed.
Results: One hundred and seventy patients (93 men and 77 women; 68 ± 11 years) and 170 controls (80 men and 90 women; 67 ± 10 years) were included. RVO was peripheral in 113 cases. Genetic thrombophilia was detected in 13% of patients. Acquired thrombophilia was observed in 10% of cases and 4.7 % of controls (P < 0.01). Sixty-three percent of cases and 24.6% of controls had serum hyperhomocysteinemia (odds ratio [OR] 5.2, IC 95% 2.7–10.1; P < 0.0001). In RVO patients aged <50 years (n = 11), 36.4% had genetic thrombophilia (P = 0.04), as well as 50% of those without vascular risk factors (n = 18; P = 0.01). Forty-one (24%) patients with RVO received antiplatelet agents and 13 (7.6%) were on anticoagulants due to preexistent atrial fibrillation.
Conclusions: We suggest that, in patients with RVO, hyperhomocysteinemia and antiphospholipid syndrome should be ruled out. Moreover, a study of genetic thrombophilia should only be considered in those aged <50 years or without cardiovascular risk factors. Antiplatelet therapy with aspirin is probably the treatment of choice of RVO, to reduce the overall vascular risk. Anticoagulation should only be considered in patients with high-risk thrombophilia.