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Abstract
The response of kidney and bone to parathyroid extract (PTE) was investigated in 8 epileptic children on long-term treatment with primidone in combination with phenytoin or other anticonvulsant drugs. The results indicate a dissociation between normal and cyclic AMP excretion and disturbed renal handling of phosphate which resembles type II pseudohypoparathyroidism suggesting an anticonvulsant drug related inhibition of cyclic AMP-induced phosphaturia. It is speculated that antiepileptic drugs may provoke renal conservation of phosphate which may explain the relative low incidence of manifest rickets or osteomalacia in site of low 25-hydroxy-vitamin D levels in epileptic patients. A normal bone response of PTE indicates that antiepileptic treatment with phenobarbital and phenytoin does not affect PTH-stimulated bone resorption in the investigated patients.
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