Increased bone remodeling is attributed to both suppressed TSH and increased thyroid hormone
Presentation Number: SAT-265
Date of Presentation: June 15th, 2013
Hyun Ji Chun*1, Kwang-Woo Lee2 and Ki-Hyun Baek3
1St Mary's Hospital, The Catholic University of Korea, Seoul, 2Catholic Univ Med Coll, Seoul, Korea, Republic of (South), 3Division of Endocrinology and Metabolism, Department of Internal Medicine, Yeouido St. Mary’s Hospital, Seoul, Korea, Seoul, Korea, Republic of (South)
Background: Thyroid function is closely associated with bone metabolism whilst the related mechanism has not been clearly established. Our study was aimed to investigate whether TSH has independent relationship with bone turnover markers in addition to thyroid hormone.
Method: A total of 214 patients were included after excluding postmenopausal women and thyroid function affecting drugs users. The baseline thyroid function and bone turnover markers were examined. Patients with Graves’ disease were followed up after treatment and compared with baseline state and controls for thyroid function and bone biomarkers in addition to RANK, OPG, M-CSF.
Results: Hyperthyroid patients had increased bone turnover markers. In the multivariate regression analysis, suppressed TSH was significantly associated with elevated osteocalcin (β = -0.54, P = 0.034) in addition to FT4 (β = 1.39, P <.001) and also associated with higher levels of ICTP (β = -0.28, P = 0.036) besides FT4 (β = 1.21, P <.001). In the treatment of patients with Graves’ disease, FT4 was decreased promptly followed by lowered 1CTP whereas TSH was increased in the late period followed by lowered osteocalcin. However, there were no difference in RANKL, OPG, and M-CSF between patients before and after treatment and controls.
Conclusion: Both TSH and thyroid hormone was significantly associated with bone metabolism. As shown in the temporal change after treatment of Graves’ disease, bone remodeling could be largely attributed to elevated FT4 by activating osteoclast and TSH seemed to have additional role by suppressing osteoblast. Future studies are needed to elucidate related molecular mechanism to enlarge our knowledge in bone metabolism and to find new treatment candidate for osteoporosis.
Nothing to Disclose: HJC, KWL, KHB