ACTA ENDOCRINOLOGICA (BUC)

Context. Thyrotoxicosis is an important cause of secondary osteoporosis, but the extent of bone loss and its\r\nreversibility with therapy have not been clearly determined yet.\r\nObjective. We assessed the impact of thyrotoxicosis on bone mineral density (BMD) and the recovery of bone loss with\r\ntherapy. We also tested, in this context, the hypothesis that low TSH levels, even within reference range, increase fracture risk.\r\nDesign, Subjects and Methods. In this retrospective study we compared 78 women with thyrotoxicosis and osteopenia /\r\nosteoporosis (TX ? study group), with 82 age matched, euthyroid women with primary osteopenia /osteoporosis (C-control group). All patients had a baseline and at least one follow-up assessment of lumbar spine BMD by dual-emission X-ray absorptiometry (DXA) and thyroid function (thyrotropin ? TSH and free thyroxine ? fT4, measured by electrochemiluminescence immunoassay).\r\nResults. Mean BMD and T scores were similar at baseline (0.764 g/cm2, -2.50 SD in the TX group 0.747 g/cm2, -2.59 SD\r\nin C group); 17 thyrotoxic patients and 17 patients with primary osteoporosis had previous fractures. Both groups showed a significant BMD increase with therapy, over a similar period of time (TX ? mean 10.38 months; C ? 10.74 months). BMD gain was significantly higher in the study\r\ngroup (p = 0.04). In hyperthyroid patients, the best predictor for bone density increase was the TSH raise, while in controls the main determinant was treatment duration.\r\nConclusions. In comparison to primary osteoporosis, bone loss recovery rate with appropriate therapy is higher in\r\nthyrotoxicosis, confirming its contribution to the pathogenesis of osteoporosis.