Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone

Sclerostin, a protein expressed by osteocytes, is a negative regulator of bone formation. The aim of the study was to investigate the relationship between parathyroid hormone (PTH) and markers of bone metabolism and changes of sclerostin concentrations before and after treatment of hyperthyroidism....

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Main Authors: Elżbieta Skowrońska-Jóźwiak, Krzysztof C. Lewandowski, Zbigniew Adamczewski, Kinga Krawczyk-Rusiecka, Andrzej Lewiński
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2015/948384
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author Elżbieta Skowrońska-Jóźwiak
Krzysztof C. Lewandowski
Zbigniew Adamczewski
Kinga Krawczyk-Rusiecka
Andrzej Lewiński
author_facet Elżbieta Skowrońska-Jóźwiak
Krzysztof C. Lewandowski
Zbigniew Adamczewski
Kinga Krawczyk-Rusiecka
Andrzej Lewiński
author_sort Elżbieta Skowrońska-Jóźwiak
collection DOAJ
description Sclerostin, a protein expressed by osteocytes, is a negative regulator of bone formation. The aim of the study was to investigate the relationship between parathyroid hormone (PTH) and markers of bone metabolism and changes of sclerostin concentrations before and after treatment of hyperthyroidism. Patients and Methods. The study involved 33 patients (26 women), age (mean ± SD) 48 ± 15 years, with hyperthyroidism. Serum sclerostin, PTH, calcium, and bone markers [osteocalcin (OC) and collagen type I cross-linked C-telopeptide I (CTX)] were measured at diagnosis of hyperthyroidism and after treatment with thiamazole. Results. After treatment of hyperthyroidism a significant decrease in free T3 (FT3) and free T4 (FT4) concentrations was accompanied by marked decrease of serum sclerostin (from 43.7 ± 29.3 to 28.1 ± 18.4 pmol/L; p<0.001), OC (from 35.6 ± 22.0 to 27.0 ± 14.3 ng/mL; p<0.001), and CTX (from 0.49 ± 0.35 to 0.35 ± 0.23 ng/dL; p<0.005), accompanied by an increase of PTH (from 29.3 ± 14.9 to 39.8 ± 19.8; p<0.001). During hyperthyroidism there was a positive correlation between sclerostin and CTX (rs=0.41, p<0.05) and between OC and thyroid hormones (with FT3  rs=0.42, with FT4  rs=0.45, p<0.05). Conclusions. Successful treatment of hyperthyroidism results in a significant decrease in serum sclerostin and bone markers concentrations, accompanied by an increase of PTH.
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spelling doaj-art-483d97a1352548e1b1b8939b2c05c8702025-08-20T03:36:07ZengWileyInternational Journal of Endocrinology1687-83371687-83452015-01-01201510.1155/2015/948384948384Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid HormoneElżbieta Skowrońska-Jóźwiak0Krzysztof C. Lewandowski1Zbigniew Adamczewski2Kinga Krawczyk-Rusiecka3Andrzej Lewiński4Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, 281/289 Rzgowska Street, 90-338 Lodz, PolandDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, 281/289 Rzgowska Street, 90-338 Lodz, PolandDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, 281/289 Rzgowska Street, 90-338 Lodz, PolandDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, 281/289 Rzgowska Street, 90-338 Lodz, PolandDepartment of Endocrinology and Metabolic Diseases, Medical University of Lodz, 281/289 Rzgowska Street, 90-338 Lodz, PolandSclerostin, a protein expressed by osteocytes, is a negative regulator of bone formation. The aim of the study was to investigate the relationship between parathyroid hormone (PTH) and markers of bone metabolism and changes of sclerostin concentrations before and after treatment of hyperthyroidism. Patients and Methods. The study involved 33 patients (26 women), age (mean ± SD) 48 ± 15 years, with hyperthyroidism. Serum sclerostin, PTH, calcium, and bone markers [osteocalcin (OC) and collagen type I cross-linked C-telopeptide I (CTX)] were measured at diagnosis of hyperthyroidism and after treatment with thiamazole. Results. After treatment of hyperthyroidism a significant decrease in free T3 (FT3) and free T4 (FT4) concentrations was accompanied by marked decrease of serum sclerostin (from 43.7 ± 29.3 to 28.1 ± 18.4 pmol/L; p<0.001), OC (from 35.6 ± 22.0 to 27.0 ± 14.3 ng/mL; p<0.001), and CTX (from 0.49 ± 0.35 to 0.35 ± 0.23 ng/dL; p<0.005), accompanied by an increase of PTH (from 29.3 ± 14.9 to 39.8 ± 19.8; p<0.001). During hyperthyroidism there was a positive correlation between sclerostin and CTX (rs=0.41, p<0.05) and between OC and thyroid hormones (with FT3  rs=0.42, with FT4  rs=0.45, p<0.05). Conclusions. Successful treatment of hyperthyroidism results in a significant decrease in serum sclerostin and bone markers concentrations, accompanied by an increase of PTH.http://dx.doi.org/10.1155/2015/948384
spellingShingle Elżbieta Skowrońska-Jóźwiak
Krzysztof C. Lewandowski
Zbigniew Adamczewski
Kinga Krawczyk-Rusiecka
Andrzej Lewiński
Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone
International Journal of Endocrinology
title Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone
title_full Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone
title_fullStr Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone
title_full_unstemmed Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone
title_short Mechanisms of Normalisation of Bone Metabolism during Recovery from Hyperthyroidism: Potential Role for Sclerostin and Parathyroid Hormone
title_sort mechanisms of normalisation of bone metabolism during recovery from hyperthyroidism potential role for sclerostin and parathyroid hormone
url http://dx.doi.org/10.1155/2015/948384
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