Endocrine Abstracts

Introduction: Fibroblast growth factor 23 (FGF23) and PTH have been identified as major players in the bone-parathyroid-kidney axis controlling phosphate homeostasis. In patients with primary hyperparathyroidism (PHPT) data on the relationship between PTH and FGF23 are scarce and not always concordant.

Objective: The aim of our study was to evaluate whether the relationship between PTH and FGF23 was altered in patients with primary hyperparathyroidism and whether, if present, this alteration was sustained after cure following successful parathyroidectomy.

Patients and methods: We identified 22 patients with primary hyperparathyroidism (PHPT) and 24 patients with long-term cure after successful PTx (EuPTH). All patients underwent biochemical evaluation of renal function, parathyroid status, vitamin D status, bone turnover markers and serum intact FGF23 levels.

Results: Mean serum FGF23 concentration was significantly higher in PHPT than in EuPTH patients (50.4±27.2 vs 33.1±12.5 pg/ml, P=0.011). FGF23 levels significantly correlated with PTH levels (r=0.362, P=0.013), even after correction for 1,25(OH)₂D levels (r=0.422, P=0.01). FGF23 levels showed a significant negative correlation with 1,25(OH)₂D, which was more pronounced in PHPT than in EuPTH patients (r=−0.780, P=0.000 vs r=−0.519, P=0.023).

Conclusion: Our findings suggest that in PHPT, increased PTH levels can directly stimulate FGF23 production and that this increase is reversible when euparathyroidism is achieved. Based on the greater negative relationship between FGF23 and 1,25(OH)₂D in PHPT patients, we propose that the PTH-induced increase in FGF23 levels may be an adaptive mechanism to prevent the potential deleterious effects of 1,25(OH)₂D levels on phosphate homeostasis.