Biotin catabolism is accelerated in adults receiving long-term therapy with anticonvulsants.
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.
Mock
D M
DM
Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children's Hospital, Little Rock, USA.
Dyken
M E
ME
D000293:Adolescent; D000328:Adult; D000927:Anticonvulsants / Q000378:metabolism* / Q000627:therapeutic use*; D001710:Biotin / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism* / Q000652:urine; D004827:Epilepsy / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D013997:Time Factors; D014631:Valerates / Q000097:blood / Q000652:urine
D000927:Anticonvulsants; D014631:Valerates; C002143:bisnorbiotin; C004961:beta-hydroxyisovaleric acid; D001710:Biotin