Thrombophilia as a cause for central and branch retinal artery occlusion in patients without an apparent embolic source.
PURPOSE: To assess the prevalence of vascular risk factors and thrombophilias in central and branch retinal artery occlusion in patients in whom an embolic source is not apparent. METHODS: The study group consisted of 21 consecutive patients with retinal artery occlusion ( RAO) in whom Doppler ultrasonography of the carotid arteries and transthoracic or transoesophageal echocardiography were normal. Laboratory methods included polymerase chain reaction for detection of factor V G1691A, factor II G20210A and methylentetrahydrofolate reductase C677T mutations, assays of plasma levels of protein C, free protein S, antithrombin, fibrinogen and homocysteine; and tests for the presence of lupus anticoagulant and anticardiolipin antibodies. Controls for the laboratory tests were 243 healthy subjects. RESULTS: Nine of the 21 (43%) patients had at least one thrombophilic marker: 4 were homozygous for MTHFR C677T, 1 was heterozygous for factor V G1691A, 1 had a high titre of IgM anticardiolipin, 2 were heterozygous for factor V G1691A and homozygous for MTHFR C677T, and 1 had lupus anticoagulant, a high titre of IgM anticardiolipin, homozygosity for MTHFR C677T and hyperhomocysteinaemia. An interaction between vascular risk factors and thrombophilias seemed important since out of 14 patients with hypertension, diabetes and/or hypercholesterolaemia 7 (50%) had a thrombophilia. Homozygous MTHFR C677T was a significant risk factor with odds ratio of 3.18 (95% CI 1.20-8.47). The prevalence of factor V G1691A was also higher in the RAO patients versus controls with an odds ratio of 2.36 (95% CI 0.63-8.88), but this value did not reach significance, probably due to the small sample size. CONCLUSION: A search for thrombophilia in RAO is advisable in patients without evident source of emboli even when vascular risk factors are identified.[1]References
- Thrombophilia as a cause for central and branch retinal artery occlusion in patients without an apparent embolic source. Salomon, O., Huna-Baron, R., Moisseiev, J., Rosenberg, N., Rubovitz, A., Steinberg, D.M., Davidson, J., Sela, B.A., Seligsohn, U. Eye (London, England) (2001) [Pubmed]
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