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Biotin catabolism is accelerated in adults receiving long-term therapy with anticonvulsants

From the Department of Pediatrics (Dr. Mock), University of Arkansas for Medical Sciences, Arkansas Children's Hospital, Little Rock, AR; and Department of Neurology (Dr. Dyken), University of Iowa, College of Medicine, Iowa City, IA.

Address correspondence and reprint requests to Dr. Donald M. Mock, Department of Pediatrics, Arkansas Children's Hospital, 800 Marshall Street, Little Rock, AR 72202-3591.

Using serum biotin concentration as the indicator, a previous study reported biotin deficiency resulting from long-term anticonvulsant therapy. However, serum biotin may not be a good indicator of tissue biotin status. Using better indicators of biotin status in anticonvulsant-treated subjects, we found increased urinary excretion of biotin catabolites and 3-hydroxyisovaleric acid, an organic acid produced in greater quantities secondary to reduced activity of a biotin-dependent carboxylase. We conclude that anticonvulsant treatment led to increased biotin catabolism and probably to reduced biotin status.

Supported by a grant from the National Institutes of Health DK36823(D.M.).

Received January 24, 1997. Accepted in final form April 10, 1997.

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