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Metabolic and Clinical Consequences of Hyperthyroidism on Bone Density

Overview
Publisher Wiley
Specialty Endocrinology
Date 2013 Aug 24
PMID 23970897
Citations 27
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Abstract

In 1891, Von Recklinghausen first established the association between the development of osteoporosis in the presence of overt hyperthyroidism. Subsequent reports have demonstrated that BMD loss is common in frank hyperthyroidism, and, to a lesser extent, in subclinical presentations. With the introduction of antithyroid medication in the 1940s to control biochemical hyperthyroidism, the accompanying bone disease became less clinically apparent as hyperthyroidism was more successfully treated medically. Consequently, the impact of the above normal thyroid hormones in the pathogenesis of osteoporosis may be presently underrecognized due to the widespread effective treatments. This review aims to present the current knowledge of the consequences of hyperthyroidism on bone metabolism. The vast number of recent papers touching on this topic highlights the recognized impact of this common medical condition on bone health. Our focus in this review was to search for answers to the following questions. What is the mechanisms of action of thyroid hormones on bone metabolism? What are the clinical consequences of hyperthyroidism on BMD and fracture risk? What differences are there between men and women with thyroid disease and how does menopause change the clinical outcomes? Lastly, we report how different treatments for hyperthyroidism benefit thyroid hormone-induced osteoporosis.

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References
1.
Lupoli G, Nuzzo V, Di Carlo C, Affinito P, VOLLERY M, Vitale G . Effects of alendronate on bone loss in pre- and postmenopausal hyperthyroid women treated with methimazole. Gynecol Endocrinol. 1996; 10(5):343-8. DOI: 10.3109/09513599609012821. View

2.
Bianco A, Salvatore D, Gereben B, Berry M, Larsen P . Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev. 2002; 23(1):38-89. DOI: 10.1210/edrv.23.1.0455. View

3.
Thomas F, Caldwell J, Greenberger N . Steatorrhea in thyrotoxicosis. Relation to hypermotility and excessive dietary fat. Ann Intern Med. 1973; 78(5):669-75. DOI: 10.7326/0003-4819-78-5-669. View

4.
Faber J, Jensen I, Petersen L, Nygaard B, Hegedus L, Siersbaek-Nielsen K . Normalization of serum thyrotrophin by means of radioiodine treatment in subclinical hyperthyroidism: effect on bone loss in postmenopausal women. Clin Endocrinol (Oxf). 1998; 48(3):285-90. DOI: 10.1046/j.1365-2265.1998.00427.x. View

5.
Morimura T, Tsunekawa K, Kasahara T, Seki K, Ogiwara T, Mori M . Expression of type 2 iodothyronine deiodinase in human osteoblast is stimulated by thyrotropin. Endocrinology. 2005; 146(4):2077-84. DOI: 10.1210/en.2004-1432. View