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61 AMAUROSIS FUGAX CAUSED BY THROMBOPHILIA-HYPOFIBRINOLYSIS IN CASES WITHOUT CAROTID ATHEROSCLEROSIS: THERAPY WITH COUMADIN-LOVENOX OR FOLIC ACID-B6-B12 PREVENTS SUBSEQUENT TRANSIENT MONOCULAR PARTIAL BLINDNESS
  1. C. J. Glueck,
  2. L. Sieve,
  3. D. Aregawi,
  4. P. Wang
  1. Jewish Hospital, Cincinnati

Abstract

In 8 men and 9 women, age 60 ± 14, all white) without carotid atherosclerosis, whose amaurosis fugax was caused by thrombophilia-hypofibrinolysis, we hypothesized that case-specific intervention for coagulation disorders (Coumadin-Lovenox or folic acid [5 mg]-B6 [100 mg]-B12 [2000 μg]) would prevent subsequent episodes of transient monocular partial or total blindness. PCR measures of thrombophilia (V Leiden, prothrombin, MTHFR, platelet glycoprotein PL A1/A2 mutations) and hypofibrinolysis (plasminogen activator inhibitor-1 4G4G mutation) were compared in 17 cases vs 276 healthy controls, 145 male, 131 female, 240 white, 32 black, 4 other. MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity was more common in cases (7/16 [44%]) than controls (35/276 [13%]), Fisher's p = .003. Serologic measures of thrombophilia (proteins C, antithrombin III, free S, homocysteine, anticardiolipin antibody IgG and IgM, lupus anticoagulant, Factor VIII, Factor XI) and hypofibrinolysis (plasminogen activator inhibitor-1 [PAI-Fx], Lp[a]) were compared in the 17 cases vs 78 healthy adults. High (> 150%) Factor VIII was more common in cases (4/16 [25%]) than controls (5/72 [7%]), Fisher's p = .053. All 17 cases had ≥ 1 thrombophilic-hypofibrinolytic disorder, with the most common being MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity (7 cases), 4G4G homozygosity (5 cases), high Factor VIII (4 cases), lupus anticoagulant (4 cases), the platelet PL A1/A2 mutation (4 cases), low free protein S (2 cases), high PAI-Fx (2 cases), V Leiden heterozygosity (1 case), prothrombin gene mutation (1 case), and protein C deficiency (1 case). In 4 cases on Coumadin for 3, 5, 11, and 84 months, in 1 case for 8 months of pregnancy on Lovenox, and in 4 cases on folic acid-B6-B12 for 2, 3, 10, and 13 months, amaurosis fugax disappeared, usually within 1 month of starting therapy. Amaurosis fugax stopped in 2 cases when exogenous estrogens-SERMS were discontinued, stopped in 1 case on aspirin alone, and stopped spontaneously in 1 case. When amaurosis fugax occurs in the absence of carotid artery atherosclerosis, thrombophilia and/or hypofibrinolysis are nearly universal, reversible pathoetiologies.

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