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.
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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
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DOI: https://doi.org/10.1203/00006450-197610000-00157