Abstract
The inadequacy of long-term treatment for control of hypercalcemia is exemplified by the difficulties encountered in patients with recurrent parathyroid carcinoma. Among the approaches currently used, phosphate1,2and mithramycin,3although effective, may be associated with toxic effects, while calcitonin, which theoretically should be ideal for this problem because of its specific ability to inhibit parathyroid hormone-stimulated bone resorption and its lack of toxic effects, has been disappointing clinically because the initial effects are often not sustained.4"Escape" from the inhibitory effects of calcitonin has been observed in organ culture5as well as in vivo6and may be due to changes in cellular responses to calcitonin rather than to the development of secondary increase in parathyroid hormone output,7or to development of antibodies to calcitonin.8Recent studies in organ culture showed that the escape of parathyroid hormone-stimulated resorption from calcitonin inhibition can be prevented by simultaneous treatment with glucocorticoids.9This report