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Parathyroid function and serum calcitonin in children receiving anticonvulsant drugs
Insights
Anticonvulsant drugs like phenytoin may lower calcitonin (CT) levels in epileptic children, potentially contributing to bone disease by increasing parathyroid hormone (PTH) effects.
Area of Science:
- Endocrinology
- Pediatric Neurology
- Pharmacology
Background:
- Epilepsy treatment often involves long-term anticonvulsant drug use.
- Calcium metabolism and bone health are crucial in pediatric patients.
Purpose of the Study:
- To investigate serum calcitonin (CT) levels and calcium metabolism in epileptic children on anticonvulsants.
- To explore the relationship between anticonvulsant drugs and bone disease markers.
Main Methods:
- Measured serum calcitonin (CT) and immunoreactive parathyroid hormone (iPTH) levels.
- Assessed urinary cyclic AMP (cAMP) and hydroxyproline excretion.
- Compared 40 epileptic children on anticonvulsants with 38 age-matched controls.
Main Results:
- Epileptic children had significantly lower CT levels compared to controls.
- Elevated iPTH levels were observed in 11 patients, correlating with urinary cAMP and hydroxyproline.
- Low CT levels were drug-related, not due to hypocalcemia.
Conclusions:
- Anticonvulsant drugs may directly lower CT levels.
- Drug-induced low CT and secondary hyperparathyroidism could contribute to anticonvulsant bone disease in children.
Abstract:
Serum calcitonin (CT) levels and other aspects of calcium metabolism were investigated in 40 epileptic children receiving long-term treatment with phenytoin and/or other anticonvulsant drugs, and in 38 age-matched controls. In the patients CT levels were significantly lower. Immunoreactive parathyroid hormone (iPTH) was significantly elevated exceeding the upper limit of controls in 11 patients. We also observed a highly significant correlation between iPTH and urinary cyclic AMP (cAMP) excretion but a lack of such a correlation with the renal handling of phosphate; this indicates to us a dissociation between cAMP production and phosphaturia. A significant correlation between iPTH levels and urinary hydroxyproline excretion points to a normal action of PTH on bone in the patients. The low CT levels are not due to hypocalcemia and may be directly attributed to the effects of anticonvulsant drugs. As the primary effect of CT is a direct inhibition of PTH induced calcium loss from bone, the drug-related low CT levels in association with secondary hyperparathyroidism possibly is an additional factor in anticonvulsant bone disease.