• 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.

• The Korean Journal of Zoology
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• v.3 no.1
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• pp.19-23
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• 1960

A method for determination of thyroid secretion rate in rabbit by means of radioactive iodine presented. After injection of radioactive iodine, in vivo determination so f radioactivity in thyroid gland were made during a 19 day-experimental period. In the same period blood samples were drawn and analyzed for protein-bound iodine (PBI) and for protein-bound radioactive iodine(PBI181). A rate constant for secretion of thyroid hormone was calculated from the disappearance rate of radioactive iodine in thyroid gland. The secretion rate of radioactive hormone iodine was calculated by multiplying this rate constant by the amount of radioactive iodine present in thyroid gland. Assuming that the specific radioactiveness of the circulating thyroid hormone and of the hormone just secreted were identical , thyroid secretion rate was calculated by the equation. {{{{ { Secreted hormone-iodine , gamma /hr} over { Secreted hormone-I^131, % dose/hr }= { PBI, ${\gamma}$/ml.Serum} over { PBI^131 , % dose/ml . Serum } }} The method presented consisted of measurements for series of independent criteria on thyroid function, and the resulting thyroid secretion rate was calculated by combination of those.

• 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.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.2
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• pp.275-281
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• 2009

Modification of thyroid hormone levels has a profound effect on skeletal muscle differentiation, predominantly through direct regulation involving thyroid hormone receptors. Nevertheless, little is known about the regulation of myostatin gene expression in skeletal muscle due to altered concentrations of thyroid hormone. Thus, the goal of our study was to find out whether altered thyroid states could change the gene expression of myostatin, the most powerful inhibitor of skeletal muscle development. A hyperthyroid state was induced in rats by daily injections of L-thyroxine 20 mg/100 g body weight for 14 days, while a hypothyroid state was induced in another group of rats by administering methimazole (0.04%) in drinking water for 14 days. After a period of 14 days of L-thyroxine treatment we observed a significant increase of myostatin expression both in mRNA and protein level. However, decreased expression of myostatin mRNA and protein were observed in hypothyroid rats. Furthermore, our studies demonstrated that the upregulation of myostatin gene expression might be responsible for the loss of body weight induced by altered thyroid hormone levels. We concluded that myostatin played a role in a metabolic process in muscle that was regulated by thyroid hormone.

• 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 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.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.

• International Journal of Advanced Culture Technology
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• v.11 no.2
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• pp.276-283
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• 2023

Purpose: We aimed to determine the differences in the levels of serum thyroid hormone (free T4 [FT4]) and thyroid stimulating hormone [TSH]) as biomarkers for hepatitis B virus (HBV) infection status, with respect to age and sex. Methods: We retrospectively analyzed serum samples from 200 patients who underwent HBV testing from August 2022 to September 2022. Serum samples were collected from patients suspected of having HBV infection who visited this hospital. Thyroid hormone levels were measured, and patients were grouped according to age and sex. Results: Differences in TSH and FT4 levels in the serum of patients in the HBV-positive and -negative groups were not significant. Among the HBV-positive patients in the younger age group (<60 years), TSH and FT4 levels were 1.78 ± 0.09 µIU/mL (normal: 0.4-5.0 µIU/mL) and 1.24 ± 0.02 ng/mL (normal: 0.8-1.9 ng/mL), respectively, whereas among the HBV-positive patients in the older age group (≥60 years), TSH and FT4 levels were 2.22 ± 0.17 µIU/mL and 1.24 ± 0.07 ng/mL, respectively. Conclusions: The presence of HBV did not markedly affect serum thyroid hormone levels. Our findings shed light on the conflicting evidence on the association between thyroid hormone levels and HBV infection. We, Hyeokjun Yun and Bo Kyeung Jung are co-first authors which made substantial contribution equally to the conception and designed of this work. Jae Kyung Kim, In soo Rheem and Kap No Lee made significant contributions to the acquisition and analysis of the data.

• Animal cells and systems
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• v.2 no.4
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• pp.489-493
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• 1998

Various heterodimers of the thyroid hormone receptor (TR) with other nuclear hormone receptors confer a wide range of transcriptional activities on thyroid hormone response elements (TREs) in the presence of the thyroid hormone ($T_3$). The present study analyzed the potential roles of retinoid X receptor (RXR) isoforms $\alpha$ and $\beta$ in $T_3$-mediated transcription on a well characterized TRE, a direct repeat of AGGTCA separated by four nucleo-tides (DR4), using electrophoretic mobility shift assays and transient transfection in CV-1 cells. We demonstrated that RXR$\alpha$ supressed liganded $TR_{\alpha}$-induced transcription while $RXR_{\beta}$ did not although both $TR_{\alpha}/RXR_{\alpha}$ and $TR_{\alpha}/RXR_{\beta}$ heterodimers were the predominant forms bound to the TRE-DR4 in the presence of $T_3$. We further demonstrated using Scatchard analysis that the two heterodimers had similar affinities for the TRE-DR4. All these observations suggest that the TRE-DR4 accomodates different types of TR/RXR heterodimers for a more finely tuned transcriptional response to $T_3$.

• 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.