Homocystine, atherosclerosis and thrombosis: implications for oral contraceptive users

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Abstract
Individuals with homocystinuria have been found to suffer from several types of inherited enzymatic deficiencies. Experiments indicated that vascular changes were subsequent to the metabolic effects of homocysteine derivatives in the tissues. Experimental studies in animals showed that homocysteine thiolactone, methionine, homocysteic acid, and homocystine cause fibrous arteriosclerotic plaques, arterial thrombosis or venous thrombosis with pulmonary embolism. The type which develops depends on the particular homocystine derivative, the dose, and the route of administration. The use of oral contraceptives causes similar alterations in nutrient metabolism. This fact suggests the possibility of increased risk of atherosclerosis, thrombosis, and embolism among long-term oral contraceptive users. Pyridoxine supplementation may reduce the risk. Further research is needed to assess the degree of risk involved.