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- Title
The adaptation and relationship of FGF-23 to changes in mineral metabolism in Graves’ disease.
- Authors
Se Eun Park; Mi Ae Cho; Se Hwa Kim; Yumie Rhee; Eun Seok Kang; Chul Woo Ahn; Bong Soo Cha; Eun Jig Lee; Kyung Rae Kim; Hyun Chul Lee; Sung-Kil Lim
- Abstract
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.
- Subjects
MINERAL metabolism; FIBROBLAST growth factors; GRAVES' disease; AUTOIMMUNE diseases; MINERALS in nutrition; EXTRACELLULAR matrix proteins; PHYSIOLOGICAL control systems
- Publication
Clinical Endocrinology, 2007, Vol 66, Issue 6, p854
- ISSN
0300-0664
- Publication type
Article
- DOI
10.1111/j.1365-2265.2007.02824.x