{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T14:31:14Z","timestamp":1791988274806,"version":"4.4.0"},"reference-count":460,"publisher":"The Endocrine Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Hypercalcemia occurs in up to 4% of the population in association with malignancy, primary hyperparathyroidism, ingestion of excessive calcium and\/or vitamin D, ectopic production of 1,25-dihydroxyvitamin D [1,25(OH)2D], and impaired degradation of 1,25(OH)2D. The ingestion of excessive amounts of vitamin D3 (or vitamin D2) results in hypercalcemia and hypercalciuria due to the formation of supraphysiological amounts of 25-hydroxyvitamin D [25(OH)D] that bind to the vitamin D receptor, albeit with lower affinity than the active form of the vitamin, 1,25(OH)2D, and the formation of 5,6-trans 25(OH)D, which binds to the vitamin D receptor more tightly than 25(OH)D. In patients with granulomatous disease such as sarcoidosis or tuberculosis and tumors such as lymphomas, hypercalcemia occurs as a result of the activity of ectopic 25(OH)D-1-hydroxylase (CYP27B1) expressed in macrophages or tumor cells and the formation of excessive amounts of 1,25(OH)2D. Recent work has identified a novel cause of non-PTH-mediated hypercalcemia that occurs when the degradation of 1,25(OH)2D is impaired as a result of mutations of the 1,25(OH)2D-24-hydroxylase cytochrome P450 (CYP24A1). Patients with biallelic and, in some instances, monoallelic mutations of the CYP24A1 gene have elevated serum calcium concentrations associated with elevated serum 1,25(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and on occasion, reduced bone density. Of interest, first-time calcium renal stone formers have elevated 1,25(OH)2D and evidence of impaired 24-hydroxylase-mediated 1,25(OH)2D degradation. We will describe the biochemical processes associated with the synthesis and degradation of various vitamin D metabolites, the clinical features of the vitamin D-mediated hypercalcemia, their biochemical diagnosis, and treatment.<\/jats:p>","DOI":"10.1210\/er.2016-1070","type":"journal-article","created":{"date-parts":[[2016,9,2]],"date-time":"2016-09-02T13:00:13Z","timestamp":1472821213000},"page":"521-547","source":"Crossref","is-referenced-by-count":397,"title":["Vitamin D-Mediated Hypercalcemia: Mechanisms, Diagnosis, and Treatment"],"prefix":"10.1210","volume":"37","author":[{"given":"Peter J.","family":"Tebben","sequence":"first","affiliation":[{"name":"Divisions of Endocrinology (P.J.T., R.K.) Mayo Clinic College of Medicine, Rochester, Minnesota 55905"},{"name":"Departments of Pediatric and Adolescent Medicine (P.J.T.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905"},{"name":"Internal Medicine (P.J.T., R.K.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravinder J.","family":"Singh","sequence":"first","affiliation":[{"name":"Laboratory Medicine and Pathology (R.J.S.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajiv","family":"Kumar","sequence":"first","affiliation":[{"name":"Divisions of Endocrinology (P.J.T., R.K.) Mayo Clinic College of Medicine, Rochester, Minnesota 55905"},{"name":"Nephrology and Hypertension (R.K.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905"},{"name":"Internal Medicine (P.J.T., R.K.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905"},{"name":"Biochemistry in Molecular Biology (R.K.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2016,9,2]]},"reference":[{"key":"2020071613130814600_B1","doi-asserted-by":"crossref","first-page":"131","DOI":"10.1111\/j.0954-6820.1976.tb08208.x","article-title":"Prevalence of hypercalcaemia in a health screening in Stockholm","volume":"200","author":"Christensson","year":"1976","journal-title":"Acta Med Scand"},{"key":"2020071613130814600_B2","doi-asserted-by":"crossref","first-page":"745","DOI":"10.1136\/pgmj.63.743.745","article-title":"The incidence and causes of hypercalcaemia","volume":"63","author":"Dent","year":"1987","journal-title":"Postgrad Med J"},{"key":"2020071613130814600_B3","first-page":"405","article-title":"Hypercalcaemia\u2013a hospital survey","volume":"49","author":"Fisken","year":"1980","journal-title":"Q J Med"},{"key":"2020071613130814600_B4","first-page":"436","article-title":"Prevalence of hypercalcaemia in normal and in hospital populations","volume":"45","author":"Fr\u00f8lich","year":"1998","journal-title":"Dan Med Bull"},{"key":"2020071613130814600_B5","doi-asserted-by":"crossref","first-page":"119","DOI":"10.1097\/00000441-200603000-00002","article-title":"Hypercalcemia in the emergency department","volume":"331","author":"Lee","year":"2006","journal-title":"Am J Med Sci"},{"key":"2020071613130814600_B6","doi-asserted-by":"crossref","first-page":"657","DOI":"10.1016\/j.ajem.2012.11.010","article-title":"Hypercalcemia in the ED: prevalence, etiology, and outcome","volume":"31","author":"Lindner","year":"2013","journal-title":"Am J Emerg Med"},{"key":"2020071613130814600_B7","doi-asserted-by":"crossref","first-page":"535","DOI":"10.4158\/EP.12.5.535","article-title":"Causes of hypercalcemia in a population of military veterans in the United States","volume":"12","author":"Newman","year":"2006","journal-title":"Endocr Pract"},{"key":"2020071613130814600_B8","doi-asserted-by":"crossref","first-page":"732","DOI":"10.1177\/000313481408000819","article-title":"Hypercalcemia in the emergency department: a missed opportunity","volume":"80","author":"Royer","year":"2014","journal-title":"Am Surg"},{"key":"2020071613130814600_B9","doi-asserted-by":"crossref","first-page":"S51","DOI":"10.1002\/jbmr.5650061413","article-title":"Differential diagnosis of hypercalcemia","volume":"6","author":"Lafferty","year":"1991","journal-title":"J Bone Miner Res"},{"key":"2020071613130814600_B10","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/j.bone.2014.12.003","article-title":"Secular trends in the incidence of primary hyperparathyroidism over five decades (1965\u20132010)","volume":"73","author":"Griebeler","year":"2015","journal-title":"Bone"},{"key":"2020071613130814600_B11","doi-asserted-by":"crossref","first-page":"171","DOI":"10.1359\/JBMR.050910","article-title":"Incidence of primary hyperparathyroidism in Rochester, Minnesota, 1993\u20132001: an update on the changing epidemiology of the disease","volume":"21","author":"Wermers","year":"2006","journal-title":"J Bone Miner Res"},{"key":"2020071613130814600_B12","doi-asserted-by":"crossref","first-page":"433","DOI":"10.7326\/0003-4819-126-6-199703150-00003","article-title":"The rise and fall of primary hyperparathyroidism: a population-based study in Rochester, Minnesota, 1965\u20131992","volume":"126","author":"Wermers","year":"1997","journal-title":"Ann Intern Med"},{"key":"2020071613130814600_B13","doi-asserted-by":"crossref","first-page":"204","DOI":"10.1016\/S0140-6736(80)90092-6","article-title":"Primary hyperparathyroidism","volume":"2","author":"Heath","year":"1980","journal-title":"Lancet"},{"key":"2020071613130814600_B14","doi-asserted-by":"crossref","first-page":"189","DOI":"10.1056\/NEJM198001243020402","article-title":"Primary hyperparathyroidism. 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