During the course of hospitalization for comprehensive rehabilitation, an 11-year-old boy with a C4-C5 spinal cord injury developed hypercalcemia which persisted for 131 days. The total serum calcium was closely monitored during six treatment periods during which calcitonin was administered. The response to calcitonin was variable and limited by the occurrence of the escape phenomenon. Glucocorticoids were also partly effective but other antihypercalcemic therapies including low calcium diet, diuretics, IV saline, wheelchair sitting, and oral phosphates were not. A review of the pathophysiology of immobilization hypercalcemia indicates that increased bone resorption is primarily responsible for the disorder. Both calcitonin and glucocorticoids are potent inhibitors of bone resorption, and glucocorticoids can prevent escape from calcitonin's calcium-lowering effect. We suggest that combination therapy with calcitonin and glucocorticoids be utilized in severe hypercalcemia in order to take advantage of the rapid effect of calcitonin and the more sustained effect of glucocorticoids.