Monomeric serum calcitonin and bone turnover during anticonvulsant treatment and in congenital hypothyroidism.

Decreased basal and calcium-stimulated calcitonin serum levels have been found in children with congenital hypothyroidism and in those receiving anticonvulsant drugs. The purpose of our investigation was to confirm these results using a new technique for calcitonin measurement and to study the effect on bone turnover. Calcitonin serum levels were measured with two different antibodies before and after a low-dose Ca infusion in patients receiving phenytoin, primidone, carbamazepine, or valproate and in patients with congenital hypothyroidism receiving L-thyroxine. In comparison with control values, basal and Ca-stimulated extractable calcitonin, representing the monomeric and biologically active form of the hormone, were moderately decreased in patients with epilepsy receiving phenytoin and primidone, and severely decreased in patients with hypothyroidism. Ca and bone metabolism were normal, except for an elevated renal threshold for phosphate (indicating phosphate conservation) in patients receiving phenytoin and primidone, and increased fasting urinary excretion of Ca and hydroxyproline (indicating increased bone resorption) in patients with hypothyroidism. The secretory capacity of the C cells for monomeric calcitonin is decreased in children receiving treatment with some, but not all, anticonvulsant drugs, and lacking in patients with hypothyroidism. Patients with calcitonin deficiency may be prone to osteopenia if the tendency to increased osteoclastic activity is aggravated by secondary hyperparathyroidism in patients with epilepsy receiving phenytoin and primidone or by inappropriate thyroid replacement therapy in patients with hypothyroidism.