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The role of coagulation disorders in patients with retinal vein occlusion.
QJM : Monthly Journal of the Association of Physicians 2016 Februrary
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.
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.
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