Serum fibroblast growth factor 23 and mineral metabolism in patients with euthyroid Graves’ diseases: a case-control study
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This study investigated the alterations of mineral metabolism in patients with Graves’ disease (GD) who achieved euthyroidism. They had higher fibroblast growth factor 23 (FGF23) and phosphorus as compared with healthy subjects. Serum FGF23 was negatively correlated with serum phosphorus. These indicated abnormal mineral metabolism even after 1.6 years of euthyroid status.
FGF23 is involved in the mineral homeostasis, especially the regulation of serum phosphorus. Graves’ disease (GD) is associated with accelerated bone turnover, hyperphosphatemia, and elevated serum FGF23. Evidence suggested that serum FGF23 decreased after a 3-month treatment of GD. However, it remains unclear whether serum FGF23, serum phosphorus, and other markers of mineral metabolism will be normalized after euthyroid status achieved.
A total of 62 patients with euthyroid GD and 62 healthy control subjects were enrolled, and the median duration of euthyroid status was 1.6 years. Endocrine profiles including thyroid function test, autoantibodies, serum FGF23, and bone turnover markers were obtained and compared between the two groups.
Euthyroid GD patients had significantly higher serum FGF23 and phosphorus, and lower 25-hydroxyvitamin D (25(OH)D) and intact parathyroid hormone (iPTH) levels as compared with the control group. Serum FGF23 was significantly and negatively correlated with phosphorus level after adjusted for age, gender, calcium, iPTH, and 25(OH)D in the euthyroid GD group.
Serum phosphorus and FGF23 levels remain higher in GD patients even after euthyroid status has been achieved for a median of 1.6 years. Serum FGF23 was negatively correlated with serum phosphorus in euthyroid GD patients. Underlying mechanisms warrant further investigations.
Registration number: NCT01660308 and NCT02620085
KeywordsFibroblast growth factor 23 Graves’ disease Osteoporosis Phosphorus
The authors thank the staff of the Eighth Core Lab in the Department of Medical Research of the National Taiwan University Hospital for technical support during the study. The authors also thank Professor Tien-Shang Huang for the support funding.
This work was financially supported by Liver Disease Prevention and Treatment Research Foundation, Taiwan, National Taiwan University Hospital (grant number: 107-S3859), National Taiwan University and Wong-Yuan Endocrine Fund in Taiwan.
Compliance with ethical standards
Informed consents were signed by all participants prior to the study, and ethical approval was obtained from the Ethics Committee of NTUH (protocol number 201105045RC, 201107013RC, and 201411013RINB).
Conflicts of interest
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