Emile L.E. de Bruijne, MD; Gonneke H.J.C. Keulen-de Vos, MD; Rob J.Th. Ouwendijk, MD, PhD
de Bruijne EL, Keulen-de Vos GH, Ouwendijk RJ. Ocular Venous Occlusion and Hyperhomocysteinemia. Ann Intern Med. 1999;130:78. doi: 10.7326/0003-4819-130-1-199901050-00026
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Published: Ann Intern Med. 1999;130(1):78.
TO THE EDITOR:
Classic homocysteinuria is an inborn error of metabolism with autosomal recessive inheritance. If homocysteinuria is untreated, about 50% of patients will have thromboembolic events, and mortality is about 20% before 30 years of age (1). Studies indicate that an elevated plasma homocysteine level is an important, independent risk factor for cardiovascular disease (2, 3).
Between July 1996 and January 1998, we studied 10 men and 12 women (mean age ± SD, 65.3 ± 11.5 years) in whom an ophthalmologist had diagnosed venous occlusion in the eye. Blood was drawn for measurement of serum total cholesterol, glucose, creatinine, folic acid, pyridoxine, and cyanocobalamin levels. The presence of coagulation abnormalities (factor V Leiden, protein S, protein C, lupus anticoagulant, and anticardiolipin antibodies) was studied. All patients underwent a methionine-loading test. The normal range for plasma total homocysteine level was less than 15 µmol/L for fasting and less than 45 µmol/L 6 hours after methionine loading.
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