PT  - JOURNAL ARTICLE
AU  - J. Silver
AU  - T. J. Davies
AU  - Emelia Kupersmitt
AU  - M. Orme
AU  - Aviva Petrie
AU  - F. Vajda
TI  - Prevalence and treatment of vitamin D deficiency in children on anticonvulsant drugs
AID  - 10.1136/adc.49.5.344
DP  - 1974 May 01
TA  - Archives of Disease in Childhood
PG  - 344--350
VI  - 49
IP  - 5
4099  - http://adc.bmj.com/content/49/5/344.short
4100  - http://adc.bmj.com/content/49/5/344.full
SO  - Arch Dis Child1974 May 01; 49
AB  - Bone metabolism was studied in a group of adolescent epileptic children given anticonvulsant drugs and compared with a matched group of nonepileptic children living in the same institutional environment. Biochemical evidence of vitamin D deficiency was more common in treated children than in controls, and 3 out of 60 children taking anticonvulsants had radiological evidence of rickets. The signs of vitamin D deficiency could not be corrected by giving 5 μg (200 IU) cholecalciferol daily for 12 weeks, but disappeared after treatment with 75 μg (3000 IU) cholecalciferol weekly for a further 12 weeks. Thus, in a residential home in southeast England the increased nutritional requirement for vitamin D caused by the administration of anticonvulsants to adolescent epileptic children was of the order of 10 μg cholecalciferol per day. It is likely that all epileptic subjects on anticonvulsants have increased needs for vitamin D and we advise regular supplementation of their diets. It is also shown that serum concentrations of γ-glutamyl transpeptidase, 5′nucleotidase, and leucine aminopeptidase are raised in children taking anticonvulsants. It seems likely that this is caused by drug induction of membrane-bound enzymes in the liver.