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Abstract Context Because subclinical hyperthyroidism increases the risk of osteoporosis and fractures, concerns are growing about the long-term skeletal safety of TSH suppression therapy after total thyroidectomy in patients with differentiated thyroid cancer (DTC). Objective We aimed to determine the effect of TSH suppression therapy on bone mineral density (BMD) in DTC patients. Methods We searched PubMed, Embase, the Cochrane library, and other sources. Eligible observational studies included DTC patients who underwent TSH suppression therapy and BMD measurement. Two independent reviewers extracted data on the studies’ characteristics and outcomes and determined their risk of bias. Data were extracted from each study for postmenopausal/premenopausal women’s and men’s lumbar spine (LS), femoral neck (FN), and total hip (TH) BMD and summed using a random-effects meta-analysis model. The weighted mean differences with 95% CIs are expressed for the differences in outcome measurements between groups. Results Seventeen studies (739 patients and 1085 controls) were included for quantitative analysis. In postmenopausal women, TSH suppression therapy showed a significant decrease in LS BMD (-0.03; -0.05, -0.02), and a similar trend was seen in TH. In premenopausal women, TSH suppression therapy significantly increased LS BMD (0.04; 0.02, 0.06) and FN BMD (0.02; 0.01, 0.04). In men, there was no significant association between TSH suppression therapy and BMD at any site compared with the controls. Conclusion Evidence from observational studies suggests that postmenopausal women treated with TSH suppression therapy are at risk for lower BMD. Attention should be paid to long-term skeletal safety in DTC survivors.

BackgroundParathyroid glands (PGs) exhibit autofluorescence (AF) when excited by near-infrared laser. This multicenter study aims to analyze how this imaging could facilitate the detection of PGs during thyroidectomy and parathyroidectomy procedures.MethodsThis was a retrospective Institutional Review Board-approved analysis of prospectively collected data at three centers. Near-infrared fluorescence imaging (NIFI) was used to detect AF from PGs during thyroidectomy and parathyroidectomy procedures. Logistic regression analysis was performed to assess the utility of NIFI to identify PGs and concordance at these centers.ResultsOverall, 210 patients underwent total thyroidectomy (n = 95), thyroid lobectomy (n = 41), and parathyroidectomy (n = 74) (n = 70 per center). Using NIFI, AF was detected from 98% of visually identified PGs. Upon initial exploration, 46% of PGs were not visible to the naked eye due to coverage by soft tissue, but AF from these glands could be detected by NIFI without any further dissection. Overall, a median of one PG per patient was detected by NIFI in this fashion before being identified visually (p = nonsignificant between centers). On logistic regression, smaller PGs were more likely to be missed visually, but localized by AF on NIFI (odds ratio with increasing size, 0.91; p = 0.02).ConclusionsIn our experience, NIFI facilitated PG identification by detecting their AF, before conventional recognition by the surgeon, in 37–67% of the time. Despite the variability in this rate across centers, there was a concordance in detecting AF from 97 to 99% of the PGs using NIFI. We suggest the incorporation of AF on NIFI alongside conventional visual cues to aid identification of PGs during neck operations.

In this study, eight perfluorinated alkyl substances (PFASs) and five thyroid hormones (TSH, FT4, FT3, TGAb, and TMAb) were determined in 202 human serum samples of the general population of Guangdong, Guangxi and Hainan provinces in southern China. Σ 8 PFASs concentrations ranged from 0.85 to 24.3 ng/mL with a mean value of 4.66 ng/mL. The PFASs composition profiles of human serum samples nearly make no difference at different locations. A significant increase was observed for ∑ 8 PFASs, PFOS, and PFHxS concentrations with age (p < 0.01). Gender-related differences were found; PFOS, PFHxS, PFBS, and PFOA levels were higher in males (p < 0.05), and the mean concentration of ∑ 8 PFASs was 1.5 times greater in males (6.02 ng/mL) than in females (4.15 ng/mL). PFOS and ∑ 8 PFASs were significantly negatively correlated with FT3 and FT4 and positively correlated with TSH while PFPeA and PFHxA were significantly positively correlated with TGAb and TMAb in all the samples. The opposite associations between FT3, TSH and PFOS, PFOA and PFHxS levels in hypothyroidism and hyperthyroidism group indicate that the PFOS, PFOA and PFHxS enhance the negative feedback mechanisms of the thyroid gland.

Ten eleven translocation 1 (TET1) is a 5-methylcytosine dioxygenase, and its altered DNA demethylation has been implicated in human diseases. However, its role in regulating thyroid function remains totally unknown. Here we first generated thyroid-specific Tet1 knockout combined with thyroid-specific Braf V600E transgenic mouse model ( Thy-Braf V600E ; Tet1 −/− ) and their control mice ( Thy-Braf V600E ; Tet1 +/+ ). The latter developed severe hypothyroidism and lost reproductive ability owing to structural damages of thyroid gland, while thyroid-specific Tet1 knockout effectively restored thyroid structure and function of Thy-Braf V600E ; Tet1 +/+ mice and their reproductive ability. In addition, we also established thyroid-specific Tet1 knockout mouse model ( Thy-Tet1 −/− ) and demonstrated that these mice could develop hyperthyroidism with systemic hypermetabolic symptoms such as weight loss, increased heart rate and elevated systolic blood pressure, further supporting the inhibitory effect of TET1 on thyroid function. Transcriptomic sequencing revealed that key genes related to metabolism and synthesis of thyroid hormones such as PAX8 , SLC5A5 and TPO were significantly upregulated in Thy-Tet1 −/− mice. Mechanistically, TET1 recruits HDAC1 to reduce the levels of H3K27Ac and H3K9Ac in the PAX8 promoter, thereby inhibiting the expression of itself and its downstream targets NIS and TPO. Further studies showed that elevated miR-29c-3p in serum exosomes enhanced thyroid function by targeting TET1, which may be one of the causes of hyperthyroidism. Thus, this study uncovers a new mechanism by which TET1 suppresses thyroid function, providing a new perspective to explore the pathogenesis of hyperthyroidism. TET1 regulates thyroid function and hyperthyroidism mechanisms Hyperthyroidism is a condition in which the thyroid gland produces too many hormones, leading to symptoms such as weight loss and irritability. Here scientists are exploring the role of a protein called TET1 in thyroid function. TET1 is known for its role in modifying DNA, which can affect how genes are turned on or off. In this study, researchers investigated whether TET1 influences thyroid activity. They used mice that were genetically modified to lack TET1 specifically in their thyroid glands. These mice showed signs of hyperthyroidism such as increased thyroid hormone levels and faster metabolism. The researchers found that TET1 normally helps suppress the activity of certain genes involved in thyroid hormone production by interacting with other proteins that modify DNA structure. This study suggests that TET1 plays a crucial role in regulating thyroid function and that its absence can lead to hyperthyroidism. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.

Abstract Purpose To investigate the importance of dietary selenium (Se) for hyperthyroidism. Methods We performed a more in-depth analysis of a large cross-sectional study of 6152 participants from two counties within the Shaanxi Province, China. These counties are characterized by different habitual Se intake. We investigated the effects of a different dietary Se supply (0.02, 0.18, 0.6, or 2.0 ppm Se) on disease development in a mouse model of Graves disease (GD). Results The cross-sectional study revealed a comparable prevalence of hyperthyroidism, irrespective of Se intake, in both counties. However, an unexpected sex-specific difference was noted, and Se deficiency might constitute a risk factor for hyperthyroidism, especially in males. In a mouse model, pathological thyroid morphology was affected, and greater Se intake exerted some protecting effects on the pathological distortion. Circulating thyroid hormone levels, malondialdehyde concentrations, total antioxidant capacity, and the titer of GD-causing TSH receptor autoantibodies were not affected by Se. Expression analysis of the transcripts in the spleen indicated regulatory effects on genes implicated in the immune response, erythropoiesis, and oxygen status. However, the humoral immune response, including the CD4/CD8 or T-helper 1/T-helper 2 cell ratio and the concentration of regulatory T cells, was similar between the experimental groups, despite the difference in Se intake. Conclusions Our data have highlighted a sexual dimorphism for the interaction of Se and thyroid disease risk in humans, with indications of a local protective effects of Se on thyroid gland integrity, which appears not to be reflected in the circulating biomarkers tested. An unexpected sex-specific difference was noted, and Se deficiency might constitute a risk factor for hyperthyroidism, especially in males from population and animal studies.

This study investigated the therapeutic effects of Radix Scrophulariae (RS) extract on hyperthyroidism and the associated mechanisms. A hyperthyroid cell model was established using thyrotropin receptor antibody and levothyroxine sodium tablets. FRTL-5 rat thyroid cells were treated with varying concentrations of RS-containing serum. Protein expression levels of Bcl-2, Caspase-3, PCNA, Cyclin D1, MST1, LC3-II/I, and ATG5 were assessed by Western blotting to determine the optimal concentration. Subsequent experiments included RS treatment with or without MST1 overexpression or the Hippo pathway inhibitor XMU-MP-1. Transmission electron microscopy was used to visualize secretory vesicles, and immunofluorescence analysis was performed to detect thyroid-stimulating hormone receptor (TSHR) expression. Protein levels of MST1, p-LATS1, p-YAP, PCNA, Cyclin D1, Bcl-2, Caspase-3, LC3-II/I, and ATG5 were further quantified by Western blotting. The hyperthyroid model exhibited elevated expression of TSHR, Bcl-2, PCNA, and Cyclin D1 ( P  < 0.05), and reduced levels of MST1, p-LATS1, p-YAP, Caspase-3, LC3-II/I, and ATG5 ( P  < 0.05). Secretory vesicles were rarely observed. Treatment with RS-containing serum significantly downregulated TSHR, Bcl-2, PCNA, and Cyclin D1 expression ( P  < 0.05), and upregulated MST1, p-LATS1, p-YAP, Caspase-3, LC3-II/I, and ATG5 ( P  < 0.05), with abundant bilayer membrane vesicles observed. The therapeutic effects of RS were attenuated by MST1 overexpression but were restored by co-treatment with XMU-MP-1 ( P  < 0.05). RS extract may attenuate hyperthyroidism by suppressing excessive thyroid cell proliferation, enhancing apoptosis and autophagy, and activating the MST1/Hippo signaling pathway in FRTL-5 cells.

In this work, the effect of thyroxine on energy and oxidative metabolism in the mitochondria of the rat heart was studied. Hyperthyroidism was observed in experimental animals after chronic administration of T4, which was accompanied by an increase in serum concentrations of free triiodothyronine (T3) and thyroxine (T4) by 1.8 and 3.4 times, respectively. The hyperthyroid rats (HR) had hypertrophy of the heart. In HR, there was a change in the oxygen consumption in the mitochondria of the heart, especially when using palmitoylcarnitine. The assay of respiratory chain enzymes revealed that the activities of complexes I, I + III, III, IV increased, whereas the activities of complexes II, II + III decreased in heart mitochondria of the experimental animals. It was shown that the level of respiratory complexes of the electron transport chain in hyperthyroid rats increased, except for complex V, the quantity of which was reduced. The development of oxidative stress in HR was observed: an increase in the hydrogen peroxide production rate, increase in lipid peroxidation and reduced glutathione. The activity of superoxide dismutase in the heart of HR was higher than in the control. At the same time, the activity of glutathione peroxidase decreased. The obtained data indicate that increased concentrations of thyroid hormones lead to changes in energy metabolism and the development of oxidative stress in the heart of rats, which in turn contributes to heart dysfunction.

Hyperthyroidism in cats can mask changes in renal function, including chronic kidney disease (CKD), because of hyperfiltration and muscle loss. Symmetric dimethylarginine (SDMA) has been shown to increase earlier than creatinine in cats with renal dysfunction, and, unlike creatinine, SDMA is not impacted by lean muscle mass. The aim of this study was to describe the relationship between SDMA, creatinine, body weight and TT4 over time during treatment of hyperthyroidism. Cats were retrospectively identified from the US IDEXX Reference Laboratories database where TT4, SDMA and creatinine were measured on the same cat at multiple time points. A hyperthyroid treated group was identified (TT4 ≤ 4.7 μg/dL and decreased by a minimum of 2.5 μg/dL) that had body weight and laboratory results available from more than one visit, and was used to evaluate body weight, creatinine, SDMA and TT4 pre-treatment and at 1-30, 31-60, 61-90, 91-120 days post-treatment. Creatinine significantly decreased with increasing concentrations of TT4 (Spearman's ρ = -0.37, P < 0.001), whereas SDMA did not. Body weight, SDMA and creatinine concentrations significantly increased during the immediate 1-30 day post-treatment period (P < 0.012, P < 0.001, P < 0.001, respectively). During treatment creatinine continued to increase as cats gained weight. In contrast, SDMA remained stable during treatment and was comparable to age-matched control cats. Therefore, SDMA may be a more reliable biomarker of renal function than creatinine in hyperthyroid cats before and during treatment.

The aim of this study was to review the course of persistent hyperthyrotropinaemia in well, term infants and to determine the risk of decompensation in this cohort of infants. Cody et al reported one of eight infants followed for 3 years decompensated and developed hypothyroidism at 1 year of age and continued to require thyroid replacement at 7 years of age.6 The strength of the study is our population selection of only well, term infants with hyperthyrotropinaemia. A limitation of the study was that it was a single centre with a moderate sample size and the selection of the study population enrolled only a group of infants with prolonged jaundice in whom thyroid function was evaluated.

The aim of the research is to explore the relationship between hyperthyroidism, iodine, antithyroid drugs (propylthiouracil) and vascular endothelial injury. In total, 136 SD rats were randomly allocated into the control group, the hyperthyroidism group, the hyperthyroidism propylthiouracil group, the hyperthyroidism low iodine group, the high iodine group, and the endothelial injury group. Rats were raised for 60 days. Afterward, indicators concerning endothelial damage were determined, including the von Willebrand Factor (vWF), thrombomodulin (TM), nitric oxide (NO), endothelin 1 (ET-1), and P-selectin, as well as the plant hemagglutinin sample type oxidized low-density lipoprotein receptor 1 (LOX-1) from the aorta and the number of endothelial progenitor cells (EPCs) in whole blood. The hyperthyroidism group had significantly higher values for vWF, TM, NO, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with the control group, similar to the LOX-1 expression in abdominal aorta. The hyperthyroidism low iodine group had significantly higher values for vWF, ET-1, and P-selectin in serum and a higher number of EPCs in whole blood compared with those of the control group, as was the case for LOX-1 expression in the abdominal aorta. The hyperthyroidism propylthiouracil group had significantly higher values for FT 4 in the serum compared with those in the control group. The electron microscope showed that hyperthyroidism caused a certain degree of endothelial injury to the abdominal aorta in rats. Hyperthyroidism can damage the vascular endothelium and is a high-risk factor for cardio-cerebrovascular disease. Propylthiouracil could be used in the treatment of hyperthyroidism, thus protecting endothelial cells from damage.