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JANE S. LEWIS, DPH; MARION T. BAER, MSNS; MARGARET A. LAUFER, MA
University Affiliated Training Program Childrens Hospital of Los Angeles

Home Economics Department California State University at Los Angeles Los Angeles, CA 90032

Tualatin, Ore

Am J Dis Child. 1975;129(3):394.

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

Sir.—Hill et al in their article on infants exposed in utero to anticonvulsant drugs, which appeared in the May issue of the JOURNAL (127:645, 1974), mentioned folic acid deficiency states and altered calcium metabolism occurring among subjects who have been taking diphenylhydantoin. Other deficiency states may also occur.

We conducted a pilot study of riboflavin status of eight children under 10 years of age who were being followed up at the Seizure Clinic, Childrens Hospital of Los Angeles, while being given anticonvulsant drugs (diphenylhydantoin [Dilantin] sodium plus another drug). We found, using the method of Slater and Morell,¹ that they had significantly lower 24-hour urinary riboflavin excretion (0.28 mg ±0.17; range, 0.056 to 0.45 mg), than 28 normal children in the same age range (0.55 mg ± 0.28; range, 0.13 to 1.37 mg) (J. S. Lewis, unpublished data). A urinary excretion of less than 20% of riboflavin intake . . . [Full Text PDF of this Article]

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