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2017 | 64 | 4 | 597-602

Article title

Sclerostin and bone metabolism markers in hyperthyroidism before treatment and interrelations between them

Content

Title variants

Languages of publication

EN

Abstracts

EN
Sclerostin, which is a glycoprotein produced by osteocytes, reduces the formation of bones by inhibiting the Wnt signal pathway. Thyroid hormones are related with Wnt signal pathway and it has been reported that increased thyroid hormones in hyperthyroidism fasten epiphysis maturation in childhood, and increase the risk of bone fractures by stimulating the bone loss in adults. The aim of this study was to examine the sclerostin serum levels, the relation between sclerostin and thyroid hormones as well as the biochemical markers of the bone metabolism in patients with hyperthyroidism (including multinodular goiter and Graves' disease), whose treatments have not started yet. No difference was found in the serum sclerostin levels between the hyperthyroidism group (n=24) and the control group (n=24) (p=0.452). The serum osteocalcin levels and 24-hour urinary phosphorus excretion were found to be higher in the hyperthyroid group than in the control group (p<0.001, p=0.009). A positive correlation was determined between the sclerostin and bone alkaline phosphatase levels (p<0.001); a negative correlation between the osteocalcin and thyroid stimulating hormone (TSH) (p<0.05); a positive correlation between the osteocalcin and thyroid hormones (FT3,FT4) (p<0.001); and a positive correlation between the deoxypyridinoline and hydroxyproline (p<0.001). No correlation was determined between sclerostin and TSH,FT3,FT4 (p>0.05). Therefore, we consider that a long-term study that covers the pre-post treatment stages of hyperthyroidism, including both the destruction and construction of the skeleton would be more enlightening. Moreover, the assessment of the synthesis of sclerostin in the bone tissue and in the serum level might show differences.

Year

Volume

64

Issue

4

Pages

597-602

Physical description

Dates

published
2017
received
2016-04-20
revised
2017-07-05
accepted
2017-08-03
(unknown)
2017-10-25

Contributors

  • Department of Biochemistry, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
  • Department of Biochemistry, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
  • Department of Endocrine and Metabolism, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
author
  • Department of Endocrine and Metabolism, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
author
  • Department of Biochemistry, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
author
  • Department of Biochemistry, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
  • Department of Biochemistry, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
  • Department of Biostatistics, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey
  • Department of Physical Medicine and Rehabilitation, Faculty of Medicine, Bülent Ecevit University, 67630 Zonguldak, Turkey

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Document Type

Publication order reference

Identifiers

YADDA identifier

bwmeta1.element.bwnjournal-article-abpv64p597kz
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