Subclinical Hyperthyroidism in Patients with Nodular Goiter Represents a Hypermetabolic State

Kvetny, Jan

doi:10.1055/s-2004-830541

Cited by 8 publications

(6 citation statements)

References 14 publications

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“…This is corroborated by the observation, that VO 2 correlate with T 3 , indicating that T 3 or a deiodination product of T 3 (T 2 ) stimulates oxygen consumption at the mitochondrial level within hours. We have previously demonstrated a correlation between TSH and VO 2 in euthyroid subjects [13] and in patients with subclinical hyperthyroidism [14] , but it was not possible to demonstrate a significant correlation between VO 2 and TSH in persons with subclinical hypothyroidism in the present study. An explanation may be that the feedback from the thyrotrope cells in the pituitary may be impaired in the present condition corresponding to a decreased pituitary D 2 activity as previously described [12] .…”

Section: Discussion ▼contrasting

confidence: 88%

Subclinical Hypothyroidism Affects Mitochondrial Function

Kvetny¹,

Wilms²,

Pedersen³

et al. 2010

Horm Metab Res

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The aim of the present study was to examine mitochondrial function in cells from persons with subclinical hypothyroidism and euthyroid controls. The participating persons were examined clinically and had basal oxygen consumption (VO(2)) determined. The concentrations of thyroid hormones and thyrotropine stimulating hormone were determined, and mitochondrial function in isolated mononuclear blood cells was examined by enzymatic methods [citrate synthase activity (CS)] and by flow cytometry (mitochondrial membrane potential by TMRM fluorescence and mitochondrial mass by MTG fluorescence). The ratio of T(4)/T(3) was lowered in subclinical hypothyroidism patients compared to controls (2.5+/-0.5 vs. 2.9+/-0.4, p=0.005). VO(2) was increased in persons with subclinical hypothyroidism compared to controls (adolescents: 134+/-27 ml O(2)/min*m(2) vs. 119+/-27 ml O(2)/min*m(2), p=0.006, adults: 139+/-14 ml O(2)/min*m(2) vs. 121+/-17 ml O(2)/min*m(2), p=0.001). The mitochondrial function, represented by citrate synthase activity, MTG, and TMRM fluorescence were all increased (CS in subclinical hypothyroidism vs. controls: 0.074+/-0.044 nmol/mg*min vs. 0.056+/-0.021 nmol/mg*min, p=0.005; MTG fluorescence in subclinical hypothyroidism vs. controls: 7,482+/-1,733 a.u. vs. 6,391+/-2,171 a.u., p=0.027; TMRM fluorescence in subclinical hypothyroidism vs. controls: 13,449+/-3,807 a.u. vs. 11,733+/-4,473 a.u, p=0.04). Our results indicate an increased mitochondrial stimulation, eventually caused by increased deiodination of T(4) to intracellular bioactive iodothyronines in adults and adolescents with subclinical hypothyroidism.

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Section: Discussion ▼contrasting

confidence: 88%

Subclinical Hypothyroidism Affects Mitochondrial Function

Kvetny¹,

Wilms²,

Pedersen³

et al. 2010

Horm Metab Res

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“…These data are in contrast to studies in endogenous subclinical hyperthyroidism, which have reported increased basal VO 2 , decreased lean body mass, and increased percent body fat (17)(18)(19). Subjects in one study were given methimazole, and basal VO 2 normalized when they became euthyroid (17).…”

Section: Discussioncontrasting

confidence: 50%

“…Subjects in one study were given methimazole, and basal VO 2 normalized when they became euthyroid (17). These studies suggest that endogenous Values shown are mean -standard error of the mean, unless otherwise indicated.…”

Section: Discussionmentioning

confidence: 98%

Effects of Levothyroxine Replacement or Suppressive Therapy on Energy Expenditure and Body Composition

Samuels

Kolobova

Smeraglio

et al. 2016

Thyroid

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Background: Thyrotropin (TSH)-suppressive doses of levothyroxine (LT4) have adverse effects on bone and cardiac function, but it is unclear whether metabolic function is also affected. The objective of this study was to determine whether women receiving TSH-suppressive LT4 doses have alterations in energy expenditure or body composition. Methods: This study was a cross-sectional comparison between three groups of women: 26 women receiving chronic TSH-suppressive LT4 doses, 80 women receiving chronic replacement LT4 doses, and 16 untreated euthyroid control women. Subjects underwent measurements of resting energy expenditure (REE), substrate oxidation, and thermic effect of food by indirect calorimetry; physical activity energy expenditure by accelerometer; caloric intake by 24-hour diet recall; and body composition by dual X-ray absorptiometry. Results: REE per kilogram lean body mass in the LT4 euthyroid women was 6% lower than that of the LT4-suppressed group, and 4% lower than that of the healthy control group ( p = 0.04). Free triiodothyronine (fT3) levels were directly correlated with REE, and were 10% lower in the LT4 euthyroid women compared with the other two groups ( p = 0.007). The groups of subjects did not differ in other measures of energy expenditure, caloric intake, or body composition. Conclusions: LT4 suppression therapy does not adversely affect energy expenditure or body composition in women. However, LT4 replacement therapy is associated with a lower REE, despite TSH levels within the reference range. This may be due to lower fT3 levels, suggesting relative tissue hypothyroidism may contribute to impaired energy expenditure in LT4 therapy.

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“…Women older than 65 years of age who have suppressed TSH have been reported to have a threefold increased risk for hip fractures and a fourfold increased risk for vertebral fracture [41]. Decreased BMD was observed in a small group of patients with subclinical hyperthyroidism with nodular goiter [50]. Similar data have been reported in preand postmenopausal women with subclinical hyperthyroidism caused by multinodular goiter.…”

Section: Endogenous Subclinical Hyperthyroidismsupporting

confidence: 58%

Thyroid Hormone Diseases and Osteoporosis

Delitala

Scuteri

Doria

2020

JCM

140

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Thyroid hormones are essential for normal skeletal development and normal bone metabolism in adults but can have detrimental effects on bone structures in states of thyroid dysfunction. Untreated severe hyperthyroidism influences the degree of bone mass and increases the probability of high bone turnover osteoporosis. Subclinical hyperthyroidism, defined as low thyrotropin (TSH) and free hormones within the reference range, is a subtler disease, often asymptomatic, and the diagnosis is incidentally made during screening exams. However, more recent data suggest that this clinical condition may affect bone metabolism resulting in decreased bone mineral density (BMD) and increased risk of fracture, particularly in postmenopausal women. The main causes of exogenous subclinical hyperthyroidism are inappropriate replacement dose of thyroxin and TSH suppressive L-thyroxine doses in the therapy of benign thyroid nodules and thyroid carcinoma. Available data similarly suggest that a long-term TSH suppressive dose of thyroxin may decrease BMD and may induce an increased risk of fracture. These effects are particularly observed in postmenopausal women but are less evident in premenopausal women. Overt hypothyroidism is known to lower bone turnover by reducing both osteoclastic bone resorption and osteoblastic activity. These changes in bone metabolism would result in an increase in bone mineralization. At the moment, there are no clear data that demonstrate any relationship between BMD in adults and hypothyroidism. Despite these clinical evidences, the cellular and molecular actions of thyroid hormones on bone structures are not complete clear.

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Subclinical Hyperthyroidism in Patients with Nodular Goiter Represents a Hypermetabolic State

Cited by 8 publications

References 14 publications

Subclinical Hypothyroidism Affects Mitochondrial Function

Subclinical Hypothyroidism Affects Mitochondrial Function

Effects of Levothyroxine Replacement or Suppressive Therapy on Energy Expenditure and Body Composition

Thyroid Hormone Diseases and Osteoporosis

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