Effect of calcitonin deficiency on bone density and bone turnover in totally thyroidectomized patients.

To investigate the influence of calcitonin deficiency on bone turnover and density we studied 25 premenopausal female and 12 male patients (age 23 to 49 years) who had undergone total thyroidectomy for differentiated thyroid cancer 1 to 15 years previously. Basal and calcium stimulated extractable calcitonin, representing the monomeric, biologically active form of the hormone, was lacking or markedly decreased in all patients. There was a relative increase of urine hydroxyproline excretion (an index of osteoclastic bone degradation) in relation to serum osteocalcin (an index of osteoblastic bone formation) indicating an imbalance of bone turnover with a tendency to increased degradation in all patients. Total and trabecular bone density, measured with quantitative computed tomography at the distal forearm were significantly decreased in the male and normal in the female patients, without a relation to the duration of the calcitonin deficiency. The study indicates that patients with calcitonin deficiency, suppressive thyroid hormone treatment, or both may have a higher risk of increased bone degradation and osteopenia. Whether the effect is more due to calcitonin deficiency or thyroid hormone therapy, cannot be concluded from this study design. The fact that only the male patients had a decreased bone density may be due to a lower parathyroid activity in our female patients and the greater thyroidectomy-induced decrement of monomeric calcitonin in our male patients compared with male controls.