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Mechanism of Triamterene-Induced Megaloblastosis

JOSÉ CORCINO, M.D.; SAMUEL WAXMAN, M.D.; and VICTOR HERBERT, M.D.
[+] Article and Author Information

Supported in part by grants AM 13358 and AM 11048, U. S. Public Health Service, Washington, D. C.; the Mount Sinai Research Foundation, New York, N. Y.; and the Veterans Administration.

Dr. Corcino was supported by Senior Postdoctoral Fellowship AM 39795, U. S. Public Health Service. Dr. Herbert was supported by New York City Health Research Council Career Scientist Award I-435 and a Veterans Administration Medical Investigatorship.

▸Requests for reprints should be addressed to José Corcino, M.D., University (District) Hospital, Puerto Rico, Medical Center, San Juan, P.R. 00935


New York, New York


Ann Intern Med. 1970;73(3):419-424. doi:10.7326/0003-4819-73-3-419
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A patient with cirrhosis of the liver who developed megaloblastosis despite normal serum and red cell folate levels after receiving conventional doses of triamterene for 2 weeks is described. Studies using short-term human bone marrow cultures indicate that triamterene interferes with the de novo deoxyribonucleic-acid-thymine synthesis from deoxyuridine and that this interference is completely corrected by reduced (folinic acid) but only partially by oxidized (pteroylglutamic acid) folate. These findings support the concept that triamterene inhibits dihydrofolate reductase activity in human bone marrow, as it does in other mammalian systems, and suggest this drug should be used with caution in patients who may have borderline folate stores (such as pregnant women and alcoholics).

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