Pathophysiology of Hypercalcemia
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David Goltzman [1]
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[1] Calcium Research Laboratory, Department of Medicine and Physiology, McGill University, Research Institute of the McGill University Health Centre, Glen Site, 1001 Decarie Boulevard, Room EM1.3220, Montreal, Quebec H4A 3J1, Canada
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- Localización: Endocrinology and metabolism clinics of North America, ISSN 0889-8529, Vol. 50, Nº. 4, 2021 (Ejemplar dedicado a: Hypercalcemia), págs. 591-607
- Idioma: inglés
- Texto completo no disponible (Saber más ...)
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Resumen
Extracellular calcium is normally tightly regulated by parathyroid hormone (PTH), 1,25-dihydroxyvitamin D, as well as by calcium ion (Ca++) itself. Dysregulated PTH production leading to hypercalcemia occurs most commonly in sporadic primary hyperparathryoidism (PHPT) but may also result from select genetic mutations in familial disorders. Parathyroid hormone-related protein shares molecular mechanisms of action with PTH and is the most common cause of hypercalcemia of malignancy. Other cytokines and mediators may also cause resorptive hypercalcemia once bone metastases have occurred. Less commonly, extrarenal production of calcitriol can occur in malignancies and in infectious and noninfectious inflammatory conditions and can cause hypercalcemia.
