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FRANK C. CARTER, M.D.; PAUL HELLER, M.D.; GERTRUD SCHAFFNER, A.B.; ROY J. KORN, M.D.

Arch Intern Med. 1961;108(1):41-46.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Increased excretion of formiminoglutamic acid (FIGLU) in the urine has been demonstrated in experimental animals and in patients with folic acid deficiency.^1-6 FIGLU is an intermediate metabolite in the degradation of histidine (Figure). In the presence of tetrahydrofolic acid, the formimino group is transferred from FIGLU to the tetrahydrofolic acid which is thus converted to 5-formiminotetrahydrofolic acid.^7-9 This conversion apparently is facilitated by the enzyme FIGLU transferase, which has been found in hog liver.¹⁰ 5-Formiminotetrahydrofolic acid is then converted by a series of reactions to 10-formyltetrahydrofolic acid, a labile, highly active compound in formyl transfer reactions.^9,10 If tetrahydrofolic acid is not present, which is the case in folic-acid-deficient subjects, this transfer of the formimino group cannot take place, and FIGLU is then excreted in the urine. Normally, only a very small amount is demonstrable in the urine. Even in folic-acid-deficient persons the FIGLU excretion may be . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO

From the Medical Service and Research Laboratory, Veterans Administration West Side Hospital and Department of Medicine, University of Illinois College of Medicine.

Footnotes
Submitted for publication July 5, 1960.

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