A fourteen-year-old boy developed severe symptomatic hypercalcaemia following prolonged supine bed rest for major trauma. Treatment consisted initially of intravenous saline and frusemide together with oral phosphate, followed by intramuscular salmon calcitonin. Only after mobilisation and weight bearing was a sustained fall of plasma calcium to normal achieved. Plasma immunoreactive parathormone levels using both N-terminal and mixed terminal specific antisera were always undetectable and urinary cyclic AMP levels were within the normal range throughout. However, before mobilisation, the tubular reabsorption of phosphate was reduced and that of calcium was increased thus indirectly suggesting increased parathormone activity. The hypercalcaemia was due to a combination of increased calcium release from bone and increased tubular reabsorption. We suggest that a factor other than parathormone is responsible for altered tubular handling of calcium and phosphate which develop following prolonged immobilisation in these patients.