ECE2022 Eposter Presentations Calcium and Bone (114 abstracts)
1Uppsala University Hospital, Uppsala, Sweden, Department of Endocrinology and Diabetes, Uppsala, Sweden; 2Akademiska Sjukhuset, Sweden; 3Institutionen för Medicinska Vetenskaper, Sweden.
Objective: Vitamin D and osteoporosis in Graves disease (GD) have previously been examined in cross-sectional studies with partly divergent results. Here, we prospectively studied vitamin D metabolism and bone health in patients with newly diagnosed GD.
Methods: Thirty consecutive patients with de novo overt thyrotoxicosis diagnosed with GD were included. None of the patients at diagnosis were treated with vitamin D supplementation or anti osteoporotic drugs. All patients were initially treated with antithyroid drugs. Blood samplings were performed at baseline and at 6 weeks, 3, 6, 12 and 24 months after treatment start. Serum levels of 25OHD3, 1,25OH2D3, calcium, parathyroid hormone (PTH), and C-terminal telopeptides of Type I collagen (CTX-I) were analyzed. Bone mineral density (BMD) was measured at baseline, and after one and two years after treatment initiation.
Results: At diagnosis patients with GD did not have vitamin D deficiency. There were no significant correlations between levels of 25OHD3 and thyrotoxicosis. Upon treatment of the thyrotoxicosis, serum calcium transiently fell, and PTH and 1,25OH2D3 increased. 25OHD3 fell within the normal range and stabilized at 6 months. CTX-I fell over 12 months, BMD increased significantly up to 2 years, P=0.002, <0.001 and 0.005 in spine, left total hip and left femoral neck respectively.
Conclusion: The present data underline that thyrotoxicosis negatively impacts bone health and demonstrate fine-tuned dynamics in bone and vitamin D metabolism. Upon treatment, bone health improved over a follow-up period of 24 months despite rising PTH. Increased conversion of 25OHD3 to 1,25OH2D3 occur during treatment of GD.