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Homocysteine (Hcy) is a sulfur amino acid formed from methionine during transmethylation. Once formed, it is either remethylated to methionine or irreversibly catabolized to cystathionine. The remethylation is catalyzed by methionine synthase (EC 2.1.1.13), which requires cobalamin as cofactor and 5-methyltetrahydrofolate as substrate (1) . This explains why the fasting total homocysteine (tHcy) concentration is related to overall folate or cobalamin status and that increased tHcy has been used to diagnose deficiencies of these vitamins (2)(3)(4) .Methotrexate (MTX) is an antifolate drug that inhibits dihydrofolate reductase, thereby depleting the cells of reduced folates, including 5-methyltetrahydrofolate (5) . In cell culture studies, MTX inhibits Hcy remethylation, leading to increased Hcy export to the medium (6)(7)(8) .Plasma tHcy is a sensitive indicator of the antifolate effect of MTX, as demonstrated by an increased plasma tHcy concentration. The increase is maximal after ∼2 days in psoriasis patients given only 25 mg of MTX (9) . In cancer patients receiving intermediate or high doses of MTX, there is a rapid increase in plasma tHcy within hours. However, the increased tHcy induced by MTX is normalized after rescue therapy with folinic acid (7)(10) .We have previously shown that tHcy clearance in folate-deficient subjects with hyperhomocysteinemia is close to that observed in healthy individuals (11) . However, it has been suggested that folate status predominately affects concentrations of fasting, i.e., low tHcy concentrations. Therefore, the present study was undertaken to examine tHcy elimination in subjects with plasma tHcy within reference values and to investigate whether the antifolate effect of MTX had any influence on plasma clearance. This was carried out by monitoring elimination of [14C]Hcy injected …

Kinetics of Plasma Total Homocysteine in Patients Receiving High-Dose Methotrexate Therapy