Cureus · 2025
Serum Calcium as a Determinant of Fibroblast Growth Factor 23 Levels in Patients With Primary Hyperparathyroidism and Graves' Disease.
СтатьяНазвание и аннотация: Перевод в очереди
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Yamashita Hiroyuki, Mori Yusuke, Imanishi Yasuo, Shindo Hisakazu, Tatsushima Daisuke, Tachibana Seigo, Fukuda Takashi, Takahashi Hiroshi, Nagayama Yuji, Satoh Shinya
Аннотация
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.
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.