Main Article Content
State of subclinical hypothyroidism can be considered as the optimal model for assessing the significance of thyroid stimulating hormone (TSH) for bone tissue in clinical practice. Objective: to make a comparative analysis of the impact of subclinical hyperthyroidism of various origins on the performance of bone mineral density (BMD) and bone metabolism parameters. Materials and methods. The study in an outpatient setting included 112 women with a diagnosis of subclinical hyperthyroidism and duration of menopause for at least 5 years. Among the examinees, endogenous subclinical hyperthyroidism has been detected in 78 women (group I), exogenous subclinical hyperthyroidism on the background of suppressive levothyroxine therapy (group II) — in 34. The control group (group III) included 20 women without thyroid dysfunction. Results. The study first conducted a comparative analysis of bone metabolism, BMD indicators, as well as parameters of phosphorus and calcium, blood lipids in women with subclinical hyperthyroidism of various origins. A positive correlation between markers of bone metabolism and free triiodothyronine (fT3) as hormones necessary for the development of the skeleton and to maintain its homeostasis indicates a physiological effect of parathyroid hormone and fT3 on bone tissue. It is shown that the bone metabolism and BMD depend not only on the content of TSH, but also on the causes of subclinical hyperthyroidism.Conclusions. In postmenopausal women with endogenous subclinical hyperthyroidism, there is a significant decline in BMD indices, more pronounced in the bones with the cortical structure. A negative correlation between markers of bone metabolism and TSH has been observed among all patients included in the study.
This work is licensed under a Creative Commons Attribution 4.0 International License.
Our edition uses the copyright terms of Creative Commons for open access journals.
Authors, who are published in this journal, agree with the following terms:
- The authors retain rights for authorship of their article and grant to the edition the right of first publication of the article on a Creative Commons Attribution 4.0 International License, which allows others to freely distribute the published article, with the obligatory reference to the authors of original works and original publication in this journal.
- Directing the article for the publication to the editorial board (publisher), the author agrees with transmitting of rights for the protection and using the article, including parts of the article, which are protected by the copyrights, such as the author’s photo, pictures, charts, tables, etc., including the reproduction in the media and the Internet; for distributing; for the translation of the manuscript in all languages; for export and import of the publications copies of the writers’ article to spread, bringing to the general information.
- The rights mentioned above authors transfer to the edition (publisher) for the unlimited period of validity and on the territory of all countries of the world.
- The authors guarantee that they have exclusive rights for using of the article, which they have sent to the edition (publisher). The edition (the publisher) is not responsible for the violation of given guarantees by the authors to the third parties.
- The authors have the right to conclude separate supplement agreements that relate to non-exclusive distribution of their article in the form in which it had been published in the journal (for example, to upload the work to the online storage of the journal or publish it as part of a monograph), provided that the reference to the first publication of the work in this journal is included.
- The policy of the journal permits and encourages the publication of the article in the Internet (in institutional repository or on a personal website) by the authors, because it contributes to productive scientific discussion and a positive effect on efficiency and dynamics of the citation of the article.
Balabolkin M.I. Fundamentalnaya i klinicheskaya tiroidologiya / M.I. Balabolkin, E.M. Klebanova, V.M. Kreminskaya. – M.: OAO Izdatelstvo «Meditsina», 2007. – 816 s.
Povoroznyuk V.V. Zahvoryuvannya kIstkovo-m’yazovoYi sistemi v lyudey rIznogo vIku (vibranI lektsIYi, oglyadi, stattI): u 3-h tomah / Povoroznyuk V.V. – K., 2009. – T. 3. – 664 s.
Kim TH, J.Y. Joung JY, Kang M. A modest protective effect of thyrotropin against bone loss is associated with plasma triiodothyronine levels. PLoS One. 2015; 10 (12):e0145292. doi: 10.1371/journal.pone.0145292. eCollection 2015.
Jódar E, Muñoz-Torres M, Escobar-Jiménez F. Antiresorptive therapy in hyperthyroid patients: longitudinal changes in bone and mineral metabolism. J Clin Endocrinol Metab. 1997; 82 (6): 1989-94.
Bianco AC, Salvatore D. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev. 2002; 23 (1): 38-89.
Boutin A, Eliseeva E, Gershengorn MC, Neumann S. β-Arrestin-1 mediates thyrotropin-enhanced osteoblast differentiation. FASEB J. 2014; 28 (8): 3446-55. doi: 10.1096/fj.14-251124.
González-Rodríguez LA, Felici-Giovanini ME, Haddock L. Thyroid dysfunction in an adult female population: A population-based study of Latin American Vertebral Osteoporosis Study (LAVOS). P.R. Health Sci. J. 2013; 32: 57-62.
Hudec SM, Camacho PM. Secondary causes of osteoporosis. Endocr Pract. 2013; 19(1): 120-128. doi: 10.4158/EP12059.
Svare A, Nilsen TI, Bjøro T. Hyperthyroid levels of TSH correlate with low bone mineral density: the HUNT 2 study. Europ. J. Endocrinol. 2009; 161: 779-86.
Kim BJ, Lee SH, Bae SJ. The association between serum thyrotropin levels and bone mineral density in healthy euthyroid men. Clin. Endocrinol. 2010; 73(3): 396-403.
Grimnes G, Emaus N, Joakimsen RM. The relationship between serum TSH and bone mineral density in men and postmenopausal women: the Tromsø study. Thyroid. 2008;18: 1147-55.
Abe E, Marians RC, Yu W. TSH is a negative regulator of skeletal remodeling. J. Cell. 2003; 115: 151-62.