Increased plasma levels of homocystine are a significant risk fac-tor not only for venous thrombosis (eg, deep venous thrombosis [DVT], pulmonary embolism) but also for arterial thrombosis (eg, stroke, myocardial infarction). This disorder can be hereditary, or it can result from a nutritional deficiency of folic acid and, to a lesser extent, of vitamin B12 and B6, because these vitamins are cofactors in homocystine metabolism. For unknown reasons, people who are elderly, have renal failure, or smoke tobacco may also have elevated levels of homocystine in the absence of nutri-tional deficiencies of these vitamins. Although a simple fasting measurement of plasma homocystine can serve as a useful screen-ing test, people with heterozygous defects in this gene and those who are vitamin B6 deficient may have normal or minimally ele-vated levels. A much more sensitive method involves obtaining a second measurement 4 hours after the patient consumes methio-nine; the prevalence of hyperhomocystinemia is twice as great when this method is used. In hyperhomocystinemia, the en-dothelial lining of the vessel walls is denuded; this can precipitate unnecessary thrombus formation. Recent studies have deter-mined that this disorder is much more common than previously thought. In a long-term epidemiologic study on nurses’ health (Rimm et al., 1998), women who used dietary supplements with folic acid and vitamin B6 were found to have a lower incidence of thrombotic conditions such as DVT. Patients who are found to have hyperhomocystinemia should receive folic acid, B6, and/or B12 supplements and should be instructed in the rationale for their use to enhance compliance.
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