Calcitonin Therapy for Bone Disease and Hypercalcemia

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Abstract
Since a "hypocalcemic substance" (ie, calcitonin) was first demonstrated in extracts of rat thyroid tissue by Hirsch et al1 in 1963, its role in maintaining mineral homeostasis has undergone extensive analyses. Mechanisms that regulate the secretion and the biological activity of calcitonin in healthy humans, patients with medullary carcinoma, and in lower animal species have been defined, and the sequence for the 32—amino acid calcitonin peptide isolated from human, bovine, ovine, salmon, and porcine thyroid glands established.2,3 Despite these many observations, which stem primarily from a combination of in vitro experiments on thyroid or ultimobranchial tissue, in situ perfusions of the thyroid gland of pigs, goats, cows, and dogs, and in vivo studies in rats following a multitude of dietary pertubations,2,4 the functional role of calcitonin in either conditioning or regulation mineral and skeletal metabolism in healthy humans is still conjectural at best. Women have lower basal