Bone Turnover in Overt and Subclinical Hyperthyroidism Due to Autonomous Thyroid Adenoma

Menis, Ernesto De; Rin, Giorgio Da; Roiter, Ignazio; Legovini, P; Foscolo, G; Conte, N

doi:10.1159/000182315

Cited by 25 publications

(19 citation statements)

References 5 publications

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“…In contrast to these studies, De Menis et al reported that patients with overt hyperthyroidism displayed a significant enhancement of both bone resorption (increased serum calcium and urinary excretion of hydroxyproline) and bone formation (increased serum levels of osteocalcin and alkaline phosphatase) when compared both to controls and to patients with subclinical hypothyroidism, and that no significant alterations of bone metabolism parameters were found in patients with subclinical hyperthyroidism in comparison with healthy controls [16]. Similarly, Gurlek and Gedik reported that endogenous subclinical hyperthyroidism is not associated with increased bone turnover, and bone mineral density is not reduced in premenopausal women, at least in the short term [17].…”

Section: Discussionmentioning

confidence: 91%

Bone and Calcium Metabolism in Subclinical Autoimmune Hyperthyroidism and Hypothyroidism

et al. 2003

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Abstract. Bone turnover is reported to increase in favour of resorption in overt hyperthyroidism and the rate of resorption is associated with the levels of thyroid hormones. Hypothyroidism, on the other hand, was shown to cause no disturbance of calcium kinetics and found to associate lower trabecular resorption surfaces and increased bone cortical thickness. Similar studies are very rare in subclinical thyroid disorders and consequently we aimed to examine calcium and bone metabolism in subclinical thyroid disorders. Thirteen patients with subclinical hyperthyroidism secondary to untreated Graves' disease, 20 patients with subclinical hypothyroidism and 10 healthy subjects participated in this survey. Briefly calcium, phosphorus, and creatinine (Cre), urinary deoxypyridinoline (U-DPD) and serum osteocalcin (OC) were measured as biochemical markers for calcium metabolism. Concerning serum Ca and phosphorus levels, there were no differences between three of the groups, but urinary Ca excretion was higher in subclinical hyperthyroid patients compared to control and hypothyroid subjects. Hypothyroid patients had similar U-DPD levels with control subjects (p = 0.218). Serum OC and U-DPD were higher in subclinical hyperthyroid compared to control subjects ( p<0.001 and p<0.001 respectively). We demonstrated a higher bone turnover and greater calcium excretion in subclinical hyperthyroid patients. Additionally, we found that subclinical hypothyroidism is not associated with disturbed calcium metabolism. As persistent increase in bone turnover is responsible for accelerated bone loss, patients with Graves' disease may have increased risk for osteoporosis. THE combination of an undetectable serum thyrotropin concentration, as measured by an assay with a threshold of detection 0.1 mU per liter or less, and normal serum triiodothyronine and thyroxine concentrations (usually at the upper end of the normal range) is known as subclinical hyperthyroidism. It is not a rare finding; rates between 0.2% and 11.8% have been reported in different groups, according to age, sex, etc [1]. The etiology is usually the same as that of overt hyperthyroidism [1]. The health implications include general symptoms, effects on the cardiovascular system, and decreased bone density. Subclinical hypothyroidism is defined as a state where the patient is eumetabolic but has a modest increase in the serum TSH level (5 to 15 mU/L), a normal serum T 3 concentration, and low-normal or slightly decreased serum fT 4 levels. The overall prevalence has been reported to range from 4-10% in large general population screening surveys [2].There are a few studies performed to examine calcium and bone metabolism in subclinical thyroid disorders with conflicting results. Bone turnover is increased in favour of resorption and the rate of resorption is associated with the serum levels of thyroid hormones in hyperthyroidism [3]. Thyroid hormone exerts its effect on osteoblasts via nuclear receptors to stimulate osteoclastic bone resorption [4,5]; hyperthyroidism is...

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Section: Discussionmentioning

confidence: 91%

Bone and Calcium Metabolism in Subclinical Autoimmune Hyperthyroidism and Hypothyroidism

et al. 2003

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“…Some studies reported that subclinical hyperthyroid patients with nodular goiter showed accelerated bone loss at a rate of about 2% per year [12, 25], while others showed that no significant alteration of bone metabolism parameters was found in subclinical hyperthyroid patients when compared with healthy controls [14, 23]. …”

Section: Discussionmentioning

confidence: 99%

Effects on Bone Mineral Density by Treatment of Benign Nodular Goiter with Mildly Suppressive Doses of <i>L</i>-Thyroxine in a Cohort Women Study

Appetecchia

2005

Horm Res Paediatr

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Objectives: Thyroid diseases and their treatment may influence the osseous system. The influence that prolonged suppressive L-thyroxine (LT4) therapy may have on inducing subclinical hyperthyroidism on bone metabolism is still a matter of debate. The aim of the present study was to assess the effects of chronic LT4 treatment at mildly inhibiting serum thyroid-stimulating hormone (TSH) doses on bone mineral density (BMD) and biochemical bone remodeling markers in a cohort of women with benign nodular goiter, and to verify the efficacy of the treatment on nodule size. Subjects and Study Design: A total of 200 euthyroid Caucasian women with nodular goiter (age 52.1 ± 9; 80 pre- and 120 postmenopausal) were enrolled: 96 had been treated with LT4 for at least 3 years and a matched group of 104 had untreated goiter. LT4 therapy was given at a dose sufficient to reduce TSH under the lower limit of the normal range (0.27–4.20 µIU/ml) without suppressing it below the limit of assay sensitivity (0.005 µIU/ml) and maintaining normal serum values of free triiodothyronine (FT3) and free thyroxine (FT4). The adequacy of the dose was evaluated on the basis of serum TSH levels. The osteopenic effect of LT4 treatment was evaluated directly by total body and lumbar spine dual-energy X-ray absorptiometry (DEXA) and indirectly by biochemical parameters (alkaline phosphatase, osteocalcin, calcium, parathyroid hormone) at the baseline and throughout the follow-up. The efficacy of LT4 schedule on thyroid nodule size was assessed on the basis of the ultrasonographic evaluation. Results: Mineralometric data showed no significant difference between BMD values for treated and untreated patients in both pre- and postmenopausal status. In all patients, serum markers of bone turnover were in the normal range, with no differences in the treated and control groups. The TSH concentrations were significantly lower in treated than in untreated patients (p < 0.0001); FT3 and FT4 were in the normal range for all patients. Evaluation of nodule size during follow-up showed a reduction of ≧30% in 32 of 96 treated patients (33.3%) versus none in those untreated, whilst nodule size remained unmodified in 60 treated patients (62.5%) versus 35 (33.6%) in those untreated, and an increase in nodule size and/or development of new nodules was found in 4 treated patients (4.2%) versus 69 of the 104 untreated patients (66.3%). Conclusions: This study suggests that at slightly suppressing TSH doses, LT4 therapy has no adverse effects on BMD in both pre- and postmenopausal women, while having an efficacy on nodule size comparable with that reported using an LT4 schedule able to maintain TSH near or below the assay sensitivity limit.

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“…The major problem in assessing adverse skeletal effects of SHyper is the difficulty in establishing disease duration. There are conflicting results related to bone mineral density (BMD) [96,97,98,99,100,101,102,103,104]. However, the majority of studies show that Endo SHyper does not affect BMD in premenopausal women [96,97,98], whereas a decreased BMD has been reported in postmenopausal women [99,100,101,102,103,104].…”

Section: Risks Associated With Persistent and Untreated Endo Subclinimentioning

confidence: 99%

The 2015 European Thyroid Association Guidelines on Diagnosis and Treatment of Endogenous Subclinical Hyperthyroidism

Biondi¹,

Bartalena²,

Cooper³

et al. 2015

Eur Thyroid J

254

157

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Endogenous subclinical hyperthyroidism (SHyper) is caused by Graves' disease, autonomously functioning thyroid nodules and multinodular goitre. Its diagnosis is based on a persistently subnormal serum thyroid-stimulating hormone (TSH) level with free thyroid hormone levels within their respective reference intervals. In 2014 the European Thyroid Association Executive Committee, given the controversies regarding the treatment of Endo SHyper, formed a task force to develop clinical practice guidelines based on the principles of evidence-based medicine. The task force recognized that recent meta-analyses, including those based on large prospective cohort studies, indicate that SHyper is associated with increased risk of coronary heart disease mortality, incident atrial fibrillation, heart failure, fractures and excess mortality in patients with serum TSH levels <0.1 mIU/l (grade 2 SHyper). Therefore, despite the absence of randomized prospective trials, there is evidence that treatment is indicated in patients older than 65 years with grade 2 SHyper to potentially avoid these serious cardiovascular events, fractures and the risk of progression to overt hyperthyroidism. Treatment could be considered in patients older than 65 years with TSH levels 0.1-0.39 mIU/l (grade 1 SHyper) because of their increased risk of atrial fibrillation, and might also be reasonable in younger (<65 years) symptomatic patients with grade 2 SHyper because of the risk of progression, especially in the presence of symptoms and/or underlying risk factors or co-morbidity. Finally, the task force concluded that there are no data to support treating SHyper in younger asymptomatic patients with grade 1 SHyper. These patients should be followed without treatment due to the low risk of progression to overt hyperthyroidism and the weaker evidence for adverse health outcomes.

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Bone Turnover in Overt and Subclinical Hyperthyroidism Due to Autonomous Thyroid Adenoma

Cited by 25 publications

References 5 publications

Bone and Calcium Metabolism in Subclinical Autoimmune Hyperthyroidism and Hypothyroidism

Bone and Calcium Metabolism in Subclinical Autoimmune Hyperthyroidism and Hypothyroidism

Effects on Bone Mineral Density by Treatment of Benign Nodular Goiter with Mildly Suppressive Doses of <i>L</i>-Thyroxine in a Cohort Women Study

The 2015 European Thyroid Association Guidelines on Diagnosis and Treatment of Endogenous Subclinical Hyperthyroidism

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