• Journal of Korean Medicine for Obesity Research
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• v.6 no.2
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• pp.29-41
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• 2006

Subclinical hypothyroidism is defined as a normal serum free thyroxine level combined with an elevated thyroid stimulating hormone level. The causes of subclinical hypothyroidism are the same as those of overt hypothyroidism. There is good evidence that subclinical hypothyroidism is associated with progression to overt disease. The management of subclinical hypothyroidism is remains controversial. Patients with a serum thyroid stimulating hormone level greater than 10 mU/L have a higher incidence of elevated serum low-density lipoprotein cholesterol concentrations; however, evidence is lacking for other associations. There is insufficient evidence that hormone treatment of subclinical hypothyroidism is beneficial. The use of thyroid stimulating hormone level lone as a diagnostic and assessment tool for hypothyroidism is inadequate because this test cannot identify numerous conditions this sentence is unclear in its meaning. Using an expanded list of clinical signs and symptoms associated with dysfunction of the Hypothalamus-Pituitary-Thyroid axis, it is possible to hypothesize that subclinical hypothyroidism may be more common in a population of patients with early signs of age-related diseases than most practitioners realize. To improve thyroid function in subclinical hypothyroidism patients, practitioners should become familiar with foods and nutrients that can hinder or support thyroid function.

• Journal of Interdisciplinary Genomics
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• v.5 no.2
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• pp.32-34
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• 2023

Resistance to thyroid hormone syndrome (RTH) is a genetic disease caused by the mutation of either the thyroid hormone receptor-β (THRB) gene or the thyroid hormone receptor-α (THRA) gene. RTH caused by THRB mutations (RTH-β) is characterized by the target tissue's response to thyroid hormone, high levels of triiodothyronine and/or thyroxine, and inappropriate secretion of thyroid-stimulating hormone (TSH). THRA mutation is characterized by hypothyroidism that affects gastrointestinal, neurological, skeletal, and myocardial functions. Most patients do not require treatment, and some patients may benefit from medication therapy. These syndromes are characterized by decreased tissue sensitivity to thyroid hormones, generating various clinical manifestations. Thus, clinical changes of resistance to thyroid hormones must be recognized and differentiated, and an approach to the practice of personalized medicine through an interdisciplinary approach is needed.

• International journal of thyroidology
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• v.10 no.2
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• pp.71-76
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• 2017

Background and Objectives: The role of thyroid-stimulating hormone (TSH) signaling on osteoblastic differentiation is still undetermined. The aim of this study was to investigate the effects of 5-aza-2'-deoxycytidine (5-azacytidine) on TSH-mediated regulations of osteoblasts. Materials and Methods: MG63, a human osteoblastic cell-line, was treated with 5-azacytidine before inducing osteogenic differentiation using osteogenic medium (OM) containing L-ascorbic acid and ${\beta}$-glyceophosphate. Bovine TSH or monoclonal TSH receptor stimulating antibody (TSAb) was treated. Quantitative real-time PCR analyses or measurement of alkaline phosphatase activities were performed for evaluating osteoblastic differentiation. Results: Studies for osteogenic-related genes or alkaline phosphatase activity demonstrated that treatment of TSH or TSAb alone had no effects on osteoblastic differentiation in MG63 cells. However, treatment of 5-azacytidine, per se, significantly increased osteoblastic differentiation and combination treatment of 5-azacytidine and TSH or TSAb in the condition of OM showed further significant increase of osteoblastic differentiation. Conclusion: Stimulating TSH signaling has little effects on osteoblastic differentiation in vitro. However, in the condition of epigenetic modification using inhibitor of DNA methylation, TSH signaling positively affects osteoblastic differentiation in human osteoblasts.

• The Korean journal of sports medicine
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• v.36 no.4
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• pp.214-220
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• 2018

Purpose: The purpose of this research is to study changes in pituitary hormone in anterior lobe and thyroid hormone before, after, and during recovery time in severe 100 km ultramarathon. Methods: Healthy middle-aged runners (age, $52.0{\pm}4.8$ years) participated in the test. Grade exercise test is done, and then blood is taken from those participants before and after completing 100 km ultramarathon at the intervals of 24 hours (1 day), 72 hours (3 days), and 120 hours (5 days) to analyze their luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), and free thyroxine (Free T4). Results: For LH, it decreased more significantly at 100 km than pre-race. However, after 1 day result increased more than that of 100 km. At 3 days, it was significantly higher than pre-race and 100 km, recovering at 5 days. In terms of FSH, it decreased at 100 km, 1 day, and 3 days more than pre-race but recovered at 5 days. TSH was higher at 1 day and 5 days compared to pre-race. T3 was only higher at 100 km than pre-race. T4 was higher till 5 days at 100 km than pre-race. Free T4 increased more significantly at 100 km than pre-race. Conclusion: In terms of severe long distance running, LH and FSH which belong to hormone from anterior lobe as well as T3, T4, and Free T4 which belong to thyroid hormone showed their variation within the standard range. However, TSH showed abnormal increase from enhanced concentration of blood after marathon becoming hyper-activation even during the recovery period.

• Biomedical Science Letters
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• v.14 no.1
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• pp.59-62
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• 2008

This experiment was performed to study the effect of TSH (thyroid-stimulating hormone) on the expression of endoplasmic reticulum (ER) chaperones in the rat thyrocytes FRTL-5 cells. Although the expressions of ER membrane kinases (ATF6, IRE1 and PERK) were specially enhanced under absence of TSH, no remarkable up- or down regulations of ER chaperones (BiP, CHOP and Calnexin) were detected by TSH. We firstly report here that TSH by dose up-regulated expression of ER membrane kinases in FRTL-5 culture thyrocytes.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.16 no.2
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• pp.1137-1144
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• 2015

This study examined the impact of osteoporosis on thyroid hormone in health check-up examinees. The study subjects were 1,117 adults, 20 years and over (636 males, 481 females), who underwent a health package check-up at the general hospital G from January to December, 2011. After adjusting for factors, such as year and gender, the mean thyroid stimulating hormone increased with decreasing T-score (Normal[${\geq}-1g/cm^2$], $1.61{\pm}0.07{\mu}IU/m{\ell}$ and osteopenia[-1 >, ${\geq}-2.5g/cm^2$],$1.82{\pm}0.08{\mu}IU/m{\ell}$ and osteoporosis[< $-2.5g/cm^2$],$3.14{\pm}0.27{\mu}IU/m{\ell}$). After adjusting for factors, such as gender and FBS, the mean free thyroxine decreased with decreasing T-score(Normal, $1.30{\pm}0.01ng/d{\ell}$, and osteopenia, $1.22{\pm}0.01ng/d{\ell}$, and osteoporosis, $1.13{\pm}0.04ng/d{\ell}$). Conclusion. These results suggest that a decrease in T-score might increase the thyroid stimulating hormone and decrease the free thyroxine levelin euthyroid adults.

• Clinical and Experimental Reproductive Medicine
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• v.42 no.4
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• pp.131-135
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• 2015

The thyroid hormones act on nearly every cell in the body. Moreover, the thyroid gland continuously interacts with the ovaries, and the thyroid hormones are involved in almost all phases of reproduction. Thyroid dysfunctions are relatively common among women of reproductive age, and can affect fertility in various ways, resulting in anovulatory cycles, high prolactin levels, and sex hormone imbalances. Undiagnosed and untreated thyroid disease can be a cause of subfertility. Subclinical hypothyroidism (SCH), also known as mild thyroid failure, is diagnosed when peripheral thyroid hormone levels are within the normal reference laboratory range, but serum thyroid-stimulating hormone levels are mildly elevated. Thyroid autoimmunity (TAI) is characterized by the presence of anti-thyroid antibodies, which include anti-thyroperoxidase and anti-thyroglobulin antibodies. SCH and TAI may remain latent, asymptomatic, or even undiagnosed for an extended period. It has also been demonstrated that controlled ovarian hyperstimulation has a significant impact on thyroid function, particularly in women with TAI. In the current review, we describe the interactions between thyroid dysfunctions and subfertility, as well as the proper work-up and management of thyroid dysfunctions in subfertile women.

• Clinical and Experimental Pediatrics
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• v.50 no.6
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• pp.576-579
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• 2007

The syndrome of resistance to thyroid hormone (RTH) is characterized by reduced tissue sensitivity to thyroid hormone (TH). In the majority of subjects, RTH is caused by mutations in the thyroid hormone receptor beta ($TR{\beta}$) gene, located on the chromosome locus 3p24.3. RTH is inherited in an autosomal dominant manner. The clinical presentation of RTH is variable, but common features include elevated serum levels of thyroid hormone (TH), a normal or slightly increased thyrotropin (thyroid stimulating hormone, TSH) level that responds to thyrotropin releasing hormone (TRH), and goiter. We report a 4 year-old girl, who was clinically euthyroid in spite of high total and free $T_4$, and $T_3$ concentrations, while TSH was slightly increased. Sequence analysis of the thyroid hormone receptor beta gene (THRB) confirmed a heterozygous C to T change at nucleotide number 1303, resulting in a substitution of histidine by tyrosine at codon 435 (H435Y). Further analysis of her parents revealed that the H435Y variation was a de novo mutation since neither parents had the variation. Her parents' TH and TSH levels were within normal range.

• Korean Journal of Biological Psychiatry
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• v.26 no.1
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• pp.14-21
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• 2019

Objectives Thyroid hormone deficiency during the neurodevelopmental period can impair brain development and induce psychiatric symptoms. This study examined the association between thyroid dysfunction and the severity of symptoms in schizophrenia patients, and the treatment response of patients with schizophrenia. Methods Three hundred thirty-eight schizophrenia patients, with no prior history of thyroid disease or taking medication associated with it, were studied. We assessed the blood thyroid hormone level, the Brief Psychiatric Rating Scale (BPRS) scores on the day of admission and discharge, admission period, dose of administered antipsychotics, and the number of antipsychotic combinations. The collected data were subsequently analyzed using the Kruskal-Wallis test and Pearson's chi-square test. Results The percentage of schizophrenia patients who presented with abnormal thyroid hormone level was 24.6%. High total triiodothyronine (TT3) (p = 0.003), low TT3 (p = 0.001), and high free thyroxine (fT4) (p < 0.001) groups showed a higher BPRS score on admission than did the normal thyroid hormone group, while thyroid stimulating hormone (TSH) levels were not significantly correlated with the severity of symptoms. Furthermore, thyroid hormone was not associated with the treatment response assessed by the rate of BPRS score reduction, admission days, use of clozapine, and dose of antipsychotics. Conclusions The TT3 and fT4 hormone levels were significantly associated with the severity of symptoms in schizophrenia patients. These relations suggested that thyroid dysfunction may be associated with the severity of schizophrenia. And hence, further analysis of the results of the thyroid function test, which is commonly used in cases of psychiatric admission, is required.

• Clinical and Experimental Pediatrics
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• v.62 no.3
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• pp.85-89
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• 2019

Purpose: We compared thyroid hormone profiles in children with nephrotic syndrome (NS) during the nephrotic phase and after remission. Methods: This study included 31 pediatric NS patients. The thyroid hormone profiles included serum levels of triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), and free T4. Results: Of the 31 patients, 16 (51.6%) showed abnormal thyroid hormone profiles: 6 had overt hypothyroidism, 8 had subclinical hypothyroidism, and 2 had low T3 syndrome. The mean serum T3, T4, and free T4 levels in the nephrotic phase and after remission were $82.37{\pm}23.64$ and $117.88{\pm}29.49ng/dL$, $5.47{\pm}1.14$ and $7.91{\pm}1.56{\mu}g/dL$, and $1.02{\pm}0.26$ and $1.38{\pm}0.23ng/dL$, respectively; the levels were significantly lower in the NS nephrotic phase (P=0.0007, P<0.0001, and P=0.0002). The mean serum TSH levels during the nephrotic phase and after remission were $8.05{\pm}3.53$ and $4.08{\pm}2.05{\mu}IU/mL$, respectively; they were significantly higher in the nephrotic phase (P=0.0005). The urinary protein/creatinine ratio during the nephrotic phase was significantly correlated with serum T3, T4, and free T4 levels (r=-0.5995, P=0.0032; r=-0.5797, P=0.0047; r=-0.5513, P=0.0078) as well as with TSH levels (r=0.5022, P=0.0172). A significant correlation was found between serum albumin and serum T3 levels during the nephrotic phase (r=0.5385, P=0.0018) but not between serum albumin and T4, TSH, or free T4 levels. These significant correlations all disappeared after remission. Conclusion: Abnormal thyroid hormone profile findings were observed in 51.6% of pediatric patients with NS. Thyroid hormone levels normalized after remission, regardless of levothyroxine therapy.