{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:06:01Z","timestamp":1791417961083,"version":"4.3.3"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2005,11,1]],"date-time":"2005-11-01T00:00:00Z","timestamp":1130803200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Serum FGF-23 regulation was studied in patients with hypoparathyroidism or pseudohypoparathyroidism treated with calcitriol. Serum FGF-23 levels changed in parallel in response to changes in serum 1,25-D, suggesting that FGF-23 may be regulated by 1,25-D. In addition, the phosphaturic effect of FGF-23 may be diminished in the absence of PTH action on the kidney.<\/jats:p>\n               <jats:p>Introduction: Fibroblast growth factor (FGF)-23 is a recently described hormone that has been shown to be involved in the regulation of phosphate and vitamin D metabolism. The physiologic role of FGF-23 in mineral metabolism and how serum FGF-23 levels are regulated have yet to be elucidated. Three patients with mineral metabolism defects that allowed for the investigation of the regulation of FGF-23 were studied.<\/jats:p>\n               <jats:p>Materials and Methods: Patient 1 had postsurgical hypoparathyroidism and Munchausen's syndrome and consumed a pharmacologic dose of calcitriol. Patient 2 had postsurgical hypoparathyroidism and fibrous dysplasia of bone. She was treated with increasing doses of calcitriol followed by synthetic PTH(1\u201334). Patient 3 had pseudohypoparathyroidism type 1B and tertiary hyperparathyroidism. She underwent parathyroidectomy, which was followed by the development of hungry bone syndrome and hypocalcemia, requiring treatment with calcitriol. Serum FGF-23 and serum and urine levels of mineral metabolites were measured in all three patients.<\/jats:p>\n               <jats:p>Results: Patient 1 had an acute and marked increase in serum FGF-23 (70 to 670 RU\/ml; normal range, 18\u2013108 RU\/ml) within 24 h in response to high-dose calcitriol administration. Patient 2 showed stepwise increases in serum FGF-23 from 117 to 824 RU\/ml in response to increasing serum levels of 1\u03b1,25-dihydroxyvitamin D (1,25-D). Finally, before parathyroidectomy, while hypercalcemic, euphosphatemic, with low levels of 1,25-D (10 pg\/ml; normal range, 22\u201367 pg\/ml), and with very high serum PTH (863.7 pg\/ml; normal range, 6.0\u201340.0 pg\/ml), patient 3 had high serum FGF-23 levels (217 RU\/ml). After surgery, while hypocalcemic, euphosphatemic, and with high serum levels of serum 1,25-D (140 pg\/ml), FGF-23 levels were higher than preoperative levels (305 RU\/ml). It seemed that the phosphaturic effect of FGF-23 was diminished in the absence of PTH or a PTH effect.<\/jats:p>\n               <jats:p>Conclusions: Serum FGF-23 may be regulated by serum 1,25-D, and its phosphaturic effect may be less in the absence of PTH.<\/jats:p>","DOI":"10.1359\/jbmr.050718","type":"journal-article","created":{"date-parts":[[2006,4,27]],"date-time":"2006-04-27T07:27:46Z","timestamp":1146122866000},"page":"1944-1950","source":"Crossref","is-referenced-by-count":89,"title":["Fibroblast Growth Factor-23 Is Regulated by 1\u03b1,25-Dihydroxyvitamin D"],"prefix":"10.1093","volume":"20","author":[{"given":"Michael T","family":"Collins","sequence":"first","affiliation":[{"name":"Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John 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