The effects of l-thyroxine supressive treatment on bone mineral density, osteoporosis associated cytokines, receptor activator of nuclear factor ?b ligand, osteoprotogerin, and parameters of bone formation and resorbtion in patients with differantiated thyroid carcinoma

Due to the TSH dependent growth of the tumor tissue in differentialthyroid cancer, these patients are treated with L-thyroxine so that the THSlevel is lower than 0.1 ?U/ml. Long-term L-thyroxine treatment insupraphysiological doses may cause side effects such as weight loss, atrialfibrillation, psychological disorders. Furthermore, it may also adversely affectbone turnover and BMD, causing bone loss, osteoporosis and relatedfractures.In this study, we have attempted to research effects of the subclinicalhyperthyroidism arising from L-thyroxine suppression treatment of DTCpatients on BMD, bone turnover markers, some cytokines related to boneresorbtıon and the OPG-RANKL system.49 differential thyroid cancer patients (17 premenopausal and 22postmenopausal women and 10 men) with a mean of 46.32±10.54 years(range 22 to 64 years) were included in our research. The bone constructionand resorbtıon markers, cytokines, RANKL-OPG and BMD (gr/cm2) wereevaluated for all patients before TSH suppressive treatment with L-thyroxineand during the first year of the treatment. Significant reduction was observedin the BMD of the lumbar vertebrae L1-4 and the neck of the femur in the 1.year of the TSH suppressıve treatment. In subgroup analyses, while menexhibited significant reduction in BMD in L3, and premenopausal women inL2, L3 and L1-4, there was no significant change in the BMD ofpostmenopausal women in the first year of suppression.An increase in the bone turnover markers (especially DPD and ALP) wasobserved after the TSH suppression with L-thyroxine. While no significant74change was observed in the proinflammatory cytokines, RANKL and OPG,known as a protective marker for bone resorbtion, was reduced.In conclusion, it has been shown that the exogen subclinicalhyperthyroidism due to TSH suppression treatment with L-thyroxine causes;1) Increased bone turnover,2) Lowered levels of OPG, which suppresses osteoclastogenesis andprevents bone resorbtion,3) Lower BMD and bone loss.In future prospective, randomized, long term studies with a larger numberof patients will be necessary in order to better assess the relative risk ofosteoporosis in patients undergoing TSH suppressive treatment. Accordingto the results of such studies a protective treatment to prevent bone loss inDTC patients receiving TSH suppressive treatments with L-thyroxine may beimplemented.Key words: subclinical hyperthyroidism, differentiated thyroid cancer,osteoporosis, OPG, RANKL