Physiological and Metabolic Changes During the Transition from Hyperthyroidism to Euthyroidism in Graves' Disease

Chng, Chiaw Ling; Lim, Adoree Yi Ying; Tan, Hong Chang; Kovalik, Jean‐Paul; Tham, Kwang Wei; Bee, Yong Mong; Lim, Wan Yen; Acharyya, Sanchalika; Lai, Oi Fah; Chong, Mary Foong‐Fong; Yen, Paul M.

doi:10.1089/thy.2015.0602

Cited by 47 publications

(58 citation statements)

References 41 publications

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“…Average weight gain from presentation to establishment of euthyroidism was 3.9 kg and thereafter patients continued to gain an average of 2 kg in weight by 3 months which was maintained at 6 and 9 months whilst euthyroid. In other small studies, which recruited young, healthy, thin individuals at baseline, weight gains of 1‐3 kg were reported at various time points up to 1 year post‐ATD treatment . Similar weight changes have been reported in studies that utilized block‐and‐replace therapy with an increase of 7 kg vs presentation weight and 2.4 kg vs premorbid weight; after cessation of therapy for 3 months, and whilst the patients remained euthyroid, weight did not change significantly and neither did REE, respiratory quotient, fat or glucose oxidation or FM.…”

Section: Weight Changes Due To Hyperthyroidismsupporting

confidence: 66%

“…Neurotransmitters and hormones may also be affected with treatment; leptin, ghrelin and resistin appear to decrease to normal levels, but adiponectin remains unaltered . Some studies have reported that leptin levels were unaltered with treatment of hyperthyroidism . Overall, the changes in body composition and appetite with hyperthyroidism therapy seem independent of neurotransmitters .…”

Section: Pathophysiologymentioning

confidence: 95%

“…At a cellular level the restoration of euthyroidism coincides with reduction in energy output, with 24‐hour energy expenditure dropping by about 18%, and this is attributed to a reduction in REE as well as spontaneous physical activity levels; changes in REE are correlated with changes in free T3 . Energy intake (as also appetite) is reduced by approximately 500 kcal/24 hours, which reciprocally correlates with post‐therapy body weight changes . One hypothesis is that some neurocognitive defect persists such that reduction in appetite and energy intake is comparatively less than the reduction in REE.…”

Section: Pathophysiologymentioning

confidence: 99%

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Weight gain following treatment of hyperthyroidism—A forgotten tale

Kyriacou

Makris

et al. 2019

Clinical Obesity

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Summary Hyperthyroidism causes weight loss in the majority, but its effect is variable and 10% of patients gain weight. Its treatment usually leads to weight gain and some studies have reported an excess weight regain. However, there is considerable inter‐individual variability and a differential effect on body weight by different treatments, with some studies reporting more weight increase with radioiodine, and perhaps surgery, compared with anti‐thyroid drugs. The excess weight regain may relate to treatment‐induced hypothyroidism. Furthermore, the transition from hyperthyroidism to euthyroidism may unmask, or exacerbate, the predisposition that some patients have towards obesity. Other risk factors commonly implicated for such weight increase include the severity of thyrotoxicosis at presentation and underlying Graves' disease. Conflicting data exist whether lean body mass or fat mass or both are increased post‐therapy and whether such increments occur concurrently or in a sequential manner; this merits clarification. In any case, clinicians need to counsel their patients regarding this issue at presentation. Limited data on the effect of dietary interventions on weight changes with treatment of hyperthyroidism are encouraging in that they cause significantly lesser weight gain compared to standard care. More research is indicated on the impact of the treatment of hyperthyroidism on various anthropometric indices and the predisposing factors for any excessive weight gain. Regarding the impact of dietary management or other weight loss interventions, there is a need for well‐designed and, ideally, controlled intervention studies.

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Section: Weight Changes Due To Hyperthyroidismsupporting

confidence: 66%

Section: Pathophysiologymentioning

confidence: 95%

Section: Pathophysiologymentioning

confidence: 99%

See 1 more Smart Citation

Weight gain following treatment of hyperthyroidism—A forgotten tale

Kyriacou

Makris

et al. 2019

Clinical Obesity

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“…However, in our study, no difference in hepatic (assessed by HOMA2-IR) or whole-body insulin sensitivity (assessed by Matsuda index) was noted during follow-up. Recently, in the study by Chng et al [13], no significant change in HOMA-IR was noted within 4 weeks of achieving a euthyroid state in patients with GD.…”

Section: Discussionmentioning

confidence: 99%

“…The rate of glycogenolysis has shown to be increased in animal models [9, 10]. However, changes in insulin sensitivity/resistance in patients with GD have not been consistently demonstrated in the literature [11-13]. …”

Section: Introductionmentioning

confidence: 99%

Insulin Sensitivity and Beta-Cell Function in Graves’ Disease and Their Changes with the Carbimazole-Induced Euthyroid State

et al. 2019

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Background and Objective: Thyroid hormones play an important role in intermediate metabolism, and abnormal glucose tolerance is often observed in patients with hyperthyroidism. Several pathogenic mechanisms have been proposed as contributors. However, there is no conclusive evidence in the existing literature regarding the predominant underlying pathophysiology. Our objective was to determine the changes in insulin resistance parameters and beta-cell function in patients with Graves’ disease following restoration of a euthyroid state. Methodology: This was an observational study with a before-after study design. Forty-five treatment-naïve adults with Graves’ diseases were included and 36 completed the study. An oral glucose tolerance test was performed at baseline and after 3 months of achieving a stable euthyroid state to assess glucose tolerance, insulin sensitivity, and beta-cell function. All patients were treated with antithyroid medication. The outcome measures studied were the Homeostasis Model Assessment-2 Insulin Resistance (HOMA2-IR), Matsuda index, and Insulin Secretion-Sensitivity Index (ISSI)-2. Results: Two-thirds of the patients had abnormal glucose tolerance at baseline. Among those with abnormal glucose tolerance at baseline, 34.7% had persistent abnormality during follow-up. During follow-up, no significant change was noted in the indices of insulin resistance. Patients with abnormal glucose tolerance had a significantly lower ISSI-2 index at baseline and it improved after achieving a euthyroid state. Conclusions: Abnormal glucose tolerance is a significant metabolic consequence in patients with Graves’ disease. Decreased beta-cell function was observed among those with abnormal glucose tolerance and it improved during follow-up. In a proportion of patients, abnormal glucose tolerance persisted after 3 months, emphasizing the need for continued follow-up.

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Immunometabolic signatures predict recovery from thyrotoxic myopathy in patients with Graves' disease

Setoyama

Lee

Moon

et al. 2021

J cachexia sarcopenia muscle

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Background Thyroid hormone excess induces protein energy wasting, which in turn promotes muscle weakness and bone loss in patients with Graves' disease. Although most studies have confirmed a relationship between thyrotoxicosis and muscle dysfunction, few have measured changes in plasma metabolites and immune cells during the development and recovery from thyrotoxic myopathy. The aim of this study was to identify specific plasma metabolites and T-cell subsets that predict thyrotoxic myopathy recovery in patients with Graves' disease. Methods One hundred patients (mean age, 40.0 ± 14.2 years; 67.0% female), with newly diagnosed or relapsed Graves' disease were enrolled at the start of methimazole treatment. Handgrip strength and Five Times Sit to Stand Test performance time were measured at Weeks 0, 12, and 24. In an additional 35 patients (mean age, 38.9 ± 13.5 years; 65.7% female), plasma metabolites and immunophenotypes of peripheral blood were evaluated at Weeks 0 and 12, and the results of a short physical performance battery assessment were recorded at the same time. ResultsIn both patient groups, methimazole-induced euthyroidism was associated with improved handgrip strength and lower limb muscle function at 12 weeks. Elevated plasma metabolites including acylcarnitines were restored to normal levels at Week 12 regardless of gender, body mass index, or age (P trend <0.01). Senescent CD8 + CD28 À CD57 + Tcell levels in peripheral blood were positively correlated with acylcarnitine levels (P < 0.05) and decreased during thyrotoxicosis recovery (P < 0.05). High levels of senescent CD8 + T cells at Week 0 were significantly associated with small increases in handgrip strength after 12 weeks of methimazole treatment (P < 0.05), but not statistically associated with Five Times Sit to Stand Test performance. Conclusions Restoring euthyroidism in Graves' disease patients was associated with improved skeletal muscle function and performance, while thyroid hormone-associated changes in plasma acylcarnitines levels correlated with muscle dysfunction recovery. T-cell senescence-related systemic inflammation correlated with plasma acylcarnitine levels and was also associated with small increases in handgrip strength.

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Physiological and Metabolic Changes During the Transition from Hyperthyroidism to Euthyroidism in Graves' Disease

Cited by 47 publications

References 41 publications

Weight gain following treatment of hyperthyroidism—A forgotten tale

Weight gain following treatment of hyperthyroidism—A forgotten tale

Insulin Sensitivity and Beta-Cell Function in Graves’ Disease and Their Changes with the Carbimazole-Induced Euthyroid State

Immunometabolic signatures predict recovery from thyrotoxic myopathy in patients with Graves' disease

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