TREATMENT OF MILD HYPERHOMOCYSTEINEMIA IN VASCULAR-DISEASE PATIENTS

Mild hyperhomocysteinemia is recognized as a risk factor for premature arteriosclerotic disease. A few vitamins and other substances have be en reported to reduce blood homocysteine levels, but normalization of elevated blood homocysteine concentrations with any of these substance s has not been reported. Therefore, we screened 421 patients suffering from premature peripheral or cerebral occlusive arterial disease by o ral methionine loading tests for the presence of mild hyperhomocystein emia. Thirty-three percent of patients with peripheral and 20% of pati ents with cerebral occlusive arterial disease were identified with mil d hyperhomocysteinemia (14% of the men, 34% of the premenopausal women , and 26% of the postmenopausal women). Mildly hyperhomocysteinemic pa tients were administered vitamin B-6 250 mg daily. After 6 weeks methi onine loading tests were again assessed to evaluate the effect of trea tment. Patients with nonnormalized homocysteine concentrations were fu rther treated with vitamin B-6 250 mg daily and/or folic acid 5 mg dai ly and/or betaine 6 g daily, solely or in any combination. Vitamin B, treatment normalized the afterload homocysteine concentration in 56% o f the treated patients (71% of the men, 45% of the premenopausal women , and 88% of the postmenopausal women). Further treatment resulted in a normalization of homocysteine levels in 95% of the remaining cases. Thus, mild hyperhomocysteinemia, which is frequently encountered in pa tients with premature arteriosclerotic disease, can be reduced to norm al in virtually all cases by safe and simple treatment with vitamin B- 6, folic acid, and betaine, each of which is involved in methionine me tabolism. (Arterioscler Thromb. 1994;14:465-470.)