Analysis of Subclinical Hyperthyroidism Influence on Parameters of Bone Metabolism

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I.V. Pankiv


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.

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Pankiv, I. “Analysis of Subclinical Hyperthyroidism Influence on Parameters of Bone Metabolism”. INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), no. 2.74, Apr. 2015, pp. 101-5, doi:10.22141/2224-0721.2.74.2016.70946.
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