Approach to Hypercalcemia
- PMID: 25905352
- Bookshelf ID: NBK279129
Approach to Hypercalcemia
Excerpt
A reduction in serum calcium can stimulate parathyroid hormone (PTH) release which may then increase bone resorption, enhance renal calcium reabsorption, and stimulate renal conversion of 25-hydroxyvitamin D, to the active moiety 1,25-dihydroxyvitamin D [1,25(OH)2D] which then will enhance intestinal calcium absorption. These mechanisms restore the serum calcium to normal and inhibit further production of PTH and 1,25(OH)2D. Normal serum concentrations of total calcium generally range between 8.5 and 10.5 mg/dL (2.12 to 2.62 mM) and ionized calcium between 4.65-5.30 mg/dL (1.16-1.31 mM). Decreased PTH and decreased 1,25(OH)2D should accompany hypercalcemia unless PTH or 1,25(OH)2D is causal. Hypercalcemia may be caused by: Endocrine Disorders with Excess PTH including primary sporadic and familial hyperparathyroidism(syndromic and non-syndromic), and tertiary hyperparathyroidism; Endocrine Disorders Without Excess PTH including hyperthyroidism, pheochromocytoma, VIPoma, hypoadrenalism, and Jansen's Metaphyseal Chondrodysplasia; Malignancy-Associated Hypercalcemia, which can be caused by elevated PTH-related protein (PTHrP), or other factors (e.g. increased 1,25(OH)2D in lymphomas); Inflammatory Disorders including Granulomatous Diseases, where excess 1,25(OH)2D production may be causal, and viral syndromes (HIV); Pediatric Syndromes including Williams Syndrome and Idiopathic Infantile Hypercalcemia, where inappropriate levels of 1,25(OH)2D may occur due to a mutation in the 25-hydroxyvitamin D-24-hydroxylase gene (CYP24A1); medication, including thiazide diuretics, lithium, vitamin D, vitamin A, antiestrogens, theophylline; and prolonged immobilization, particularly in states of high bone turnover. Treatment should be aimed at the underlying disorder, however, if serum calcium exceeds 12 to 14mg/dL (3 to 3.5mM), acute hydration and agents that inhibit bone resorption are required. Under selected conditions, calcimimetics, calciuresis, glucocorticoids, or dialysis may be needed. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text,
Copyright © 2000-2025, MDText.com, Inc.
Sections
- ABSTRACT
- DEFINITION OF HYPERCALCEMIA
- PHYSIOLOGY OF CALCIUM HOMEOSTASIS
- REGULATION OF THE PRODUCTION AND ACTION OF HUMORAL MEDIATORS OF CALCIUM HOMEOSTASIS
- MEDIATORS OF BONE REMODELING
- HYPERCALCEMIC DISORDERS
- ENDOCRINE DISORDERS ASSOCIATED WITH HYPERCALCEMIA
- MALIGNANCY-ASSOCIATED HYPERCALCEMIA
- INFLAMMATORY DISORDERS CAUSING HYPERCALCEMIA
- PEDIATRIC SYNDROMES
- MEDICATION-INDUCED HYPERCALCEMIA
- ALTERATIONS IN MUSCLE AND BONE
- CLINICAL ASSESSMENT OF THE HYPERCALCEMIC PATIENT
- MANAGEMENT OF HYPERCALCEMIA
- REFERENCES
References
-
- Parfitt AM, Kleerekoper M. Clinical disorders of calcium, phosphorus and magnesium metabolism. in Maxwell MH, Kleeman CR. (eds): Clinical disorders of fluid and electrolyte metabolism, 3rd ed. New York, McGraw-Hill, 1980, pp 947-1153.
-
- Stewart AF, Broadus AE: Mineral metabolism. in Felig P, Baxter ID, Broadus AE, Frohman LA. (eds): Endocrinology and metabolism, 2nd ed. New York, McGraw-Hill, 1987, pp 1317-1453.
-
- Bringhurst FR, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism., in Wilson JD, Foster DW, Kronenberg HM, Larsen PR. (eds): Williams textbook of endocrinology, 9th ed. Philadelphia, Saunders, 1998, pp 1155-1200.
-
- Brown EM: Physiology of calcium homeostasis., in Bilezikian JP, Marcus R, Levine MA. (eds): The parathyroids: basic and clinical concepts, 2nd ed. San Diego, Academic Press, 2001, pp 167-181.
Publication types
LinkOut - more resources
Full Text Sources
Research Materials