The adaptation and relationship of FGF-23 to changes in mineral metabolism in Graves’ disease
Yumie Rhee
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorEun Seok Kang
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorChul Woo Ahn
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorBong Soo Cha
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorEun Jig Lee
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorKyung Rae Kim
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorHyun Chul Lee
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorSung-Kil Lim
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorYumie Rhee
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorEun Seok Kang
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorChul Woo Ahn
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorBong Soo Cha
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorEun Jig Lee
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorKyung Rae Kim
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorHyun Chul Lee
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorSung-Kil Lim
Department of Internal Medicine and
Endocrine Research Institute, College of Medicine, Yonsei University, Seoul, Korea
Search for more papers by this authorSummary
Objective The aim of this study was to observe the changes in bone and mineral metabolism and to confirm the regulation of fibroblast growth factor-23 (FGF-23) in untreated Graves’ disease.
Patients and measurements The study comprised 39 patients, with or without Graves’ disease. The Graves’ disease group was made up of 21 newly diagnosed patients, enrolled before starting treatment. Their disease was determined by biochemical and radiological means. The control group was composed of 18 people who were proven to be euthyroid without any diseases affecting bone and mineral metabolism. FGF-23, calcium, phosphate, PTH, 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and bone turnover markers were compared between these groups.
Results Serum calcium and phosphate, plasma FGF-23 and free T4 were significantly higher in the Graves’ disease group than in the healthy control group (P < 0·05). The bone turnover markers serum osteocalcin and C-terminal cross-linked telopeptide of type 1 collagen (s-CTx) were also significantly elevated in the Graves’ disease group, and had a positive correlation with free T4 levels. However, there was no significant decrease in PTH and 1,25(OH)2D in the Graves’ disease group. Plasma levels of FGF-23 exhibited a positive correlation with serum phosphate levels and with free T4 levels (P < 0·05).
Conclusions These findings suggest that FGF-23 is physiologically related to serum phosphate homeostasis, as indicated indirectly by the changes in bone and mineral metabolism, in untreated Graves’ disease.
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