Endocrine Abstracts

Sclerostin, a product of a SOST gene, is a protein expressed by osteocytes that inhibits osteoblastic bone formation. Several hormones including PTH and glucocorticosteroids and have been suggested as possible regulators of sclerostin production. The influence of thyroid hormones on sclerostin synthesis has not been investigated so far. The aim of the study was to evaluate sclerostin concentrations in patients before and after treatment of thyrotoxicosis.

Patients and methods: The study involved 15 patients (four men), mean age 51.8±15.3, mean BMI 24.7±3.5, with thyrotoxicosis due to Graves’ disease or toxic multinodular goitre. Serum sclerostin was measured by immunoassays at diagnosis of thyrotoxicosis and after 6–10 weeks of treatment with thiamazole. The data were analysed by means of simple descriptive statistics of location and dispersion and Mann–Whitney U test for pairs of results ‘before’ and ‘after’ therapy. Association between variables was evaluated with use of Spearman correlation coefficient.

Results: Here was a significant decrease in free T₃ and free T₄ concentrations (from 8.74±4.79 to 3.54±2.40 pg/ml, and from 4.48±2.21 to 1.02±1.07 ng/ml, P<0.001), for free T₃ and free T₄ respectively. This was accompanied by a marked decrease of serum sclerostin levels from 55.46±20.90 to 35.73±15.70 pmol/l, P<0.0015). Interestingly, however, sclerostin levels did not correlate with serum free T₃ or free T₄ concentrations.

Conclusions: Restoration of a euthyroid state in patients with thyrotoxicosis results in a significant decrease in serum sclerostin concentrations. The above mentioned phenomenon may reflect lowering of bone metabolism, but possible direct influence of thyroid hormones on SOST gene needs to be investigated.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.