Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review

Approach to Hypercalcemia

In: Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.
.
Affiliations
Free Books & Documents
Review

Approach to Hypercalcemia

David Goltzman.
Free Books & Documents

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, WWW.ENDOTEXT.ORG.

PubMed Disclaimer

References

    1. Walser M. Ion association: VI. Interactions between calcium, magnesium, inorganic phosphate, citrate, and protein in normal human plasma. J. Clin. Invest. 1961;40:723–730. - PMC - PubMed
    1. 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.
    1. 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.
    1. 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.
    1. 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.

LinkOut - more resources