Risk for Fracture in Women with Low Serum Levels of Thyroid-Stimulating Hormone

Bauer, Douglas C.; Ettinger, Bruce; Nevitt, Michael C.; Stone, Katie L.

doi:10.7326/0003-4819-134-7-200104030-00009

Cited by 433 publications

(271 citation statements)

References 55 publications

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“…Hyperthyroidism is characterized by increased bone turnover and reduced BMD, followed by increased risk of fractures, which persists even after 5 years of treatment (9,10,24). Consistent with the published literature (9, 10), we also found increased bone turnover markers P1NP, osteocalcin, and b-CTX in hyperthyroid patients.…”

Section: Discussionsupporting

confidence: 91%

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Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Yavropoulou¹,

Tomos²,

Tsekmekidou³

et al. 2011

European Journal of Endocrinology

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Objective: Postprandial suppression of bone resorption is considered one of the main contributors in the circadian rhythm of bone turnover markers. The aim of this study was to investigate this physiological response of bone tissue in diseases that affect bone metabolism. Patients and methods: In this study, 118 patients (45 hypothyroid, 40 hyperthyroid, and 33 b-thalassemic patients) and 78 healthy individuals matched for age and body mass index were included. An oral glucose test (75 g glucose) was performed after overnight fasting. Serum levels of procollagen type-I N-terminal propeptide (P1NP), b-C-terminal telopeptide of type I collagen (b-CTX), and osteocalcin were assayed at 0, 60, and 120 min. Results: Baseline values of bone turnover markers were significantly elevated in hyperthyroid and b-thalassemic patients but not in hypothyroid patients compared with the control group. After oral glucose, the levels of b-CTX but not P1NP or osteocalcin were significantly suppressed in all groups (mean change from baseline is 46.9% for b-CTX, 7.9% for P1NP, and 8% for osteocalcin). The percentage change from baseline for b-CTX was significantly augmented in hypothyroidism (52 vs 42%, PZ0.009). Conclusion: The preservation or even augmentation of postprandial suppression of bone resorption in diseases that affect bone metabolism through distinct pathogenetic mechanisms suggests the importance of this physiological response to nutrients for the general homeostasis and functional integrity of the skeleton.

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Section: Discussionsupporting

confidence: 91%

“…Several studies have reported a marked relationship between thyroid status and bone mineral density (BMD) or fracture risk in healthy individuals as well as in patients with thyroid dysfunction (6)(7)(8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Yavropoulou¹,

Tomos²,

Tsekmekidou³

et al. 2011

European Journal of Endocrinology

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“…This risk augments with advancing age and returns to normal upon treatment of the hyperthyroid state (9,19,20). Untreated subclinical hyperthyroidism in postmenopausal women has also been associated with decreased aBMD and a higher fracture risk compared with women who received treatment, although findings have not been unequivocal (21)(22)(23)(24). Little data exists on the influence of subclinical hyperthyroidism on the skeleton in men (5).…”

Section: Discussionmentioning

confidence: 99%

Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

Roef

Lapauw

Goemaere

et al. 2011

European Journal of Endocrinology

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Context: The hormonal factors involved in the regulation of peak bone mass (PBM) in men have not been fully investigated. Apart from gonadal steroids and somatotropic hormones, thyroid hormones are known to affect bone maturation and homeostasis and are additional candidate determinants of adult bone mass. Objective: We aimed to investigate between-subject physiological variation in free and total thyroid hormone concentrations, TSH, and thyroid binding globulin (TBG) in relation to parameters of bone mass, geometry, and mineral density in healthy men at the age of PBM. Design and setting: We recruited 677 healthy male siblings aged 25-45 years in a cross-sectional, population-based study. Areal and volumetric bone parameters were determined using dual-energy x-ray absorptiometry (DXA) and peripheral quantitative computed tomography (pQCT). Total and free thyroid hormones, TBG, and TSH were determined using immunoassays. Results: Free and total thyroid hormone concentrations were inversely associated with bone mineral density (BMD) and bone mineral content (BMC) at the hip and total body (free triiodothyronine (FT 3 ), total T 3 (TT 3 ), and total T 4 (TT 4 )) and at the spine (FT 3 ). TBG was negatively associated with BMC and areal BMD at all sites. At the radius, cortical bone area was inversely associated with TT 3 , TT 4 , and TBG, and trabecular bone density was inversely associated with free thyroxine, TT 4 , and TBG. We observed inverse associations between cortical bone area at the mid-tibia and FT 3 , TT 3 , TT 4 , and TBG. No associations between TSH and DXA or pQCT measurements were found. Conclusion: In healthy men at the age of PBM, between-subject variation in thyroid hormone concentrations affects bone density, with higher levels of FT 3 , TT 3 , TT 4 , and TBG being associated with less favorable bone density and content.

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“…An increase in the risk of developing dementia (especially of vascular origin) and Alzheimer's disease was observed. 14,15 Because thyroid hormones influence the skeletal and cardiovascular systems, associations have been described between SH and osteoporosis, 16,17,18 atrial fibrillation, 3,19,20,21 hypertrophy of the left ventricle (LV), tachycardia, impaired diastolic function and increased rate of cardiovascular mortality. 12,13,22,23 Laboratory diagnosis is made through the finding of a low plasma concentration of TSH and normal levels of free T3 and T4, usually obtained during routine screening.…”

Section: B Introductionmentioning

confidence: 99%

Clinical and therapeutic controversies on subclinical hyperthyroidism

Salles¹,

Salles²

2014

Medical Express

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Subclinical hyperthyroidism is defined as low or undetectable serum thyrotropin concentration in the presence of levels of free thriiodothyronine and thyroxine within the reference range. Despite the conflicting results from many observational studies, this thyroid disorder has been associated with an increased risk of developing atrial fibrillation, left ventricular hypertrophy, increased heart rate and diastolic function impairment. In addition, a relation between subclinical hyperthyroidism, skeletal disorders and cognitive changes has been reported. Treatment of subclinical hyperthyroidism remains controversial, given the lack of prospective randomized studies showing clinical benefits with restoration of the euthyroid state. Nevertheless, this review recommends the treatment of subclinical hyperthyroidism to individuals aged over 65, postmenopausal women, patients with cardiac risk factors, heart disease, osteoporosis or hyperthyroidism symptoms, whenever TSH is persistently suppressed (,0.1 mU/L). When TSH is between 0.1 -0.5 mU/L, treatment should be considered for individuals over age 65, patients with heart disease or hyperthyroidism symptoms.

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Risk for Fracture in Women with Low Serum Levels of Thyroid-Stimulating Hormone

Cited by 433 publications

References 55 publications

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Response of biochemical markers of bone turnover to oral glucose load in diseases that affect bone metabolism

Thyroid hormone status within the physiological range affects bone mass and density in healthy men at the age of peak bone mass

Clinical and therapeutic controversies on subclinical hyperthyroidism

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