Purpose of reviewThe importance of parathyroid hormone in maintaining bone health has long been appreciated. Recent advances in the understanding of the cellular and molecular actions of this hormone have enhanced our treatment of parathyroid disorders and osteoporosis. Recent findingsParathyroid hormone has been shown to act at the cellular level through the activation of the RANK ligand system, which is a new target for drug development for osteoporosis. Our understanding of the natural history of primary hyperparathyroidism and the potential for medical management has recently come under greater scrutiny. An increased recognition of vitamin D inadequacy is changing our understanding of secondary hyperparathyroidism. Newer calcimimetic drugs are enhancing our therapy of both primary and secondary hyperparathyroidism. Synthetic parathyroid hormone has been shown to be both safe and effective in the treatment of osteoporosis. Summary Synthetic parathyroid hormone, the first anabolic agent for osteoporosis, has changed the therapeutic approach in severe osteoporosis. Although newer drugs have been used for primary hyperparathyroidism, surgery remains the definitive therapy. Increased understanding of the molecular biology of parathyroid hormone has allowed the development of new classes of therapeutic agents for osteoporosis.
Hypocalcemia is a known risk following bariatric surgery and can contribute to the development of osteoporosis. Osteoporosis is commonly treated with denosumab, though denosumab can exacerbate underlying abnormalities in calcium homeostasis. We present the case of a 59-year-old female with severe hypocalcemia who had been treated with denosumab for osteoporosis three months before and had Billroth II gastric bypass surgery 15 years before, for bariatric purposes. Intravenous calcium supplementation was used to correct the initial electrolyte abnormality, and the patient was able to maintain appropriate calcium levels on high doses of oral calcium before discharge. Denosumab-induced hypocalcemia has been previously reported in patients with predisposing conditions including chronic kidney disease, primary sclerosing cholangitis, Crohn’s disease, and a history of sleeve gastrectomy for marginal gastric ulcers. A few cases of hypocalcemia have been reported in patients with a history of bariatric surgery secondary to vitamin D deficiency, but this report is unique in demonstrating denosumab-induced hypocalcemia after bariatric surgery with normal vitamin D levels, suggesting a primary malabsorption of calcium. The risk of severe hypocalcemia should be considered before initiating denosumab to treat osteoporosis in patients with a history of bariatric surgery. If denosumab is initiated, serum calcium levels should be closely monitored, and patients should be educated about the importance of adherence to calcium supplementation.
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