Abstract

Thyrotoxicosis increases bone turnover. This accentuation of the normal remodelling sequence increases the number of osteoclasts and resorption sites, and alters the ratio of resorptive to formative bone surfaces. One result of this increase in bone resorption is hypercalcemia, which has been reported to occur in approximately 20% of patients with thyrotoxicosis. Ionized calcium levels appear to be increased in as many as 50% of patients with thyrotoxicosis (1). Since serum PTH and 1,25-dihydroxyvitamin D3 levels are decreased and intestinal calcium absorption blunted in patients with thyrotoxicosis, the increased calcium levels are thought to directly reflect the accelerated bone resorption. Hypercalciuria is also common in patients with thyrotoxicosis, occurring in individuals with and without hypercalcemia. The suppression of PTH secretion in patients with thyrotoxicosis, and the resultant decrease in renal tubular calcium reabsorption mediated by PTH, are thought to be the mechanisms responsible for h...

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