Abstract
249 mentally severely retarded children were examined for se Ca,P, aminoacid N, alk. P-ase, tubular rejection of P, aminoacid N; urinary aminoacid chromatogram. They had not been treated with vit. D. 170/Group 1/did not take anticonvulsants, 79/Gr 2/ were on long-term anticonvulsant treatment. Gr 1 showed no abnormal findings, only 6/170 had hyperaminoaciduria. Gr 2 showed first markedly decreased se P, increased alk. P-ase, tubular rejection of P and aminoacid N. Hyperaminoaciduria occurred in 25/79. Gr 2 was then subdivided: 39 /Gr 2a/were left without vit. D, 40/Gr 2b/were treated with oral D3, 3000 IU/day. Both subgroups continued taking anticonvulsants. After 3 nios all determinations were repeated. Vit. D3 abolished nearly all abnormalities in Gr 2b,in Gr 2a all deviations got more pronounced, hyperaminoaciduria included.
Conclusions:
l. Hyperaminoaciduria in mental retardation is due mostly to anticonvulsant induced vit. D deficiency.
2. Measurement of tubular reabsorption of P and aminoacid N is useful in follow-up of patients on anticonvulsants.
Log in or create a free account to read this content
Gain free access to this article, as well as selected content from this journal and more on nature.com
or
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Cholnoky, P., Mangliár, K., Szabó, L. et al. 166: Hyperaminoaciduria and phosphate wasting in severe psychomotor retardation: An effect of anticonvulsants. Pediatr Res 10, 898 (1976). https://doi.org/10.1203/00006450-197610000-00157
Issue date:
DOI: https://doi.org/10.1203/00006450-197610000-00157
