{"title":"Serum Calcium as a Determinant of Fibroblast Growth Factor 23 Levels in Patients With Primary Hyperparathyroidism and Graves' Disease.","authors":"Hiroyuki Yamashita, Yusuke Mori, Yasuo Imanishi, Hisakazu Shindo, Daisuke Tatsushima, Seigo Tachibana, Takashi Fukuda, Hiroshi Takahashi, Yuji Nagayama, Shinya Satoh","doi":"10.7759/cureus.93972","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Fibroblast growth factor 23 (FGF23) is a phosphate-regulating hormone with an emerging role in calcium homeostasis. However, its role in hypercalcemic conditions remains unclear. This study aimed to investigate the relationship between serum calcium and FGF23 levels in two hypercalcemic disorders: primary hyperparathyroidism (PHPT) and Graves' disease.</p><p><strong>Methods: </strong>A cross-sectional analysis was performed in 98 patients with PHPT and 45 patients with Graves' disease. Clinical and biochemical parameters, including parathyroid hormone (PTH), phosphate, and 1,25-dihydroxyvitamin D3 (1,25(OH)<sub>2</sub>D), were analyzed.</p><p><strong>Results: </strong>In PHPT, serum calcium was the only independent determinant of FGF23 levels (P < 0.0001), whereas in Graves' disease, both serum calcium (P < 0.001) and 1,25(OH)<sub>2</sub>D (P < 0.005) were independently associated with FGF23. A significant positive correlation between calcium and FGF23 was observed in both conditions. Interestingly, FGF23 levels were elevated despite different phosphate profiles: hypophosphatemia in PHPT and hyperphosphatemia in Graves' disease.</p><p><strong>Conclusions: </strong>These findings suggest that hypercalcemia may directly contribute to FGF23 elevation, independent of phosphate levels. However, the compensatory effect of FGF23 in modulating calcium homeostasis appears to be limited. This study provides new insights into the calcium sensitivity of FGF23 in endocrine disorders characterized by altered mineral metabolism.</p>","PeriodicalId":93960,"journal":{"name":"Cureus","volume":"17 10","pages":"e93972"},"PeriodicalIF":1.3000,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12500342/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cureus","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.7759/cureus.93972","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/10/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Fibroblast growth factor 23 (FGF23) is a phosphate-regulating hormone with an emerging role in calcium homeostasis. However, its role in hypercalcemic conditions remains unclear. This study aimed to investigate the relationship between serum calcium and FGF23 levels in two hypercalcemic disorders: primary hyperparathyroidism (PHPT) and Graves' disease.
Methods: A cross-sectional analysis was performed in 98 patients with PHPT and 45 patients with Graves' disease. Clinical and biochemical parameters, including parathyroid hormone (PTH), phosphate, and 1,25-dihydroxyvitamin D3 (1,25(OH)2D), were analyzed.
Results: In PHPT, serum calcium was the only independent determinant of FGF23 levels (P < 0.0001), whereas in Graves' disease, both serum calcium (P < 0.001) and 1,25(OH)2D (P < 0.005) were independently associated with FGF23. A significant positive correlation between calcium and FGF23 was observed in both conditions. Interestingly, FGF23 levels were elevated despite different phosphate profiles: hypophosphatemia in PHPT and hyperphosphatemia in Graves' disease.
Conclusions: These findings suggest that hypercalcemia may directly contribute to FGF23 elevation, independent of phosphate levels. However, the compensatory effect of FGF23 in modulating calcium homeostasis appears to be limited. This study provides new insights into the calcium sensitivity of FGF23 in endocrine disorders characterized by altered mineral metabolism.