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Correspondence
136 (
2
); 309-309
pmid:
22960904

Changes in markers of bone turnover during treatment of hyperthyroidism

Yıldırım Beyazıt University Medical School, Ataturk Teaching & Research Hospital, Department of Endocrinology, Bilkent, Ankara, Turkey

For correspondence: Ceyhun Atuf Kansu Cad Ehl-i BeytMah 1268. Sok 10/6, TR-06520, Balgat, Çankaya, Ankara, Turkey dredademir@gmail.com

Licence

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Disclaimer:
This article was originally published by Medknow Publications & Media Pvt Ltd and was migrated to Scientific Scholar after the change of Publisher.

Sir,

I read with great interest the article by Jyotsna et al1. They undertook a study to measure the bone mineral density (BMD) in patients with Graves disease in Indian population which is predominantly vitamin D deficient and to assess the changes in BMD after the patients became and remained euthyroid following treatment. BMD was found to be significantly lower at hip, spine and fore arm compared to healthy, euthyroid controls. When treated for hyperthyroidism, the absolute BMD improved at all sites. But the BMD corrected for body mass index showed a decrease which stabilized after one year. The authors concluded that damage in BMD caused by thyroid hormone excess was not corrected even after two years of patients being euthyroid1.

Biochemical markers that reflect remodelling or turnover of bone can be measured in urine or blood including resorption markers and formation markers. Resorption markers include tartrate resistant acid phosphatase and bone matrix degradation products like hydroxyproline, pyridinium cross-links, and telopeptides2. Bone formation markers include alkaline phosphatase enzyme, and three products of bone matrix synthesis which are osteocalcin, amino- and carboxy-terminal procollagen l extension peptide3.

Thyroid hormones affect bone cells both in vitro and in vivo by stimulating osteoblast and osteoclast cells with more bone resorption and increased skeletal remodelling. It was reported that bone resorption markers, such as urinary pyridinoline and deoxypyridinoline, were increased 7-8 times in hyperthyroidism than age and sex matched controls4. On the other hand, levels of bone formation markers increased to a less degree suggesting the imbalance between bone formation and resorption with subsequent bone loss in hyperthyroidism45. It was shown that the increased levels of markers of bone turnover declined during antithyroid treatment4.

It is felt that measurement of several bone formation and resorption markers in addition to serum calcium and alkaline phosphatase could have been an original contribution to the design of the present study under the light of the pertinent data in the literature.

References

  1. , , , , , . Bone mineral density in patients of Graves disease pre- & post-treatment in a predominantly vitamin D deficient population. Indian J Med Res. 2012;135:36-41.
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  2. , , . Measurement of biochemical markers of bone resorption. In: , , , eds. Dynamics in bone and cartilage metabolism. San Diego: Academic Press; . p. :541-64.
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  3. , , . Measurement of biochemical markers of bone resorption. In: , , , eds. Dynamics of bone and cartilage metabolism. San Diego: Academic Press; . p. :529-40.
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  4. , , . Changes of bone mineral density, quantitative ultrasound parameters and markers of bone turnover during treatment of hyperthyroidism. Neth J Med. 2008;66:428-32.
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  5. , , , , . Bone remodelling markers and serum cytokines in patients with hyperthyroidism. Clin Endocrinol (Oxf). 2002;57:125-9.
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