• 제목/요약/키워드: Thyroid stimulating hormone

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준임상적 갑상선기능저하증;논란이 되는 주제들 (Subclinical Hypothyroidism;Controversial Subjects and Therapeutic Regimen)

  • 박지훈;김호준;이명종
    • 한방비만학회지
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    • 제6권2호
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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.

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Resistance to Thyroid Hormone Syndrome Mutation in THRB and THRA: A Review

  • Jung Eun Moon
    • Journal of Interdisciplinary Genomics
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    • 제5권2호
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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.

Enhancement of Osteogenic Differentiation by Combination Treatment with 5-azacytidine and Thyroid-Stimulating Hormone in Human Osteoblast Cells

  • Sun, Hyun Jin;Song, Young Shin;Cho, Sun Wook;Park, Young Joo
    • International journal of thyroidology
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    • 제10권2호
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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.

울트라마라톤이 뇌하수체 전엽 및 갑상선 호르몬에 미치는 영향 (Effect of Ultramarathon on the Anterior Pituitary and Thyroid Hormones)

  • 신경아;김영주
    • 대한스포츠의학회지
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    • 제36권4호
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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.

Expression of Endoplasmic Reticulum Membrane Kinases by Thyroid Stimulating Hormone in the FRTL-5 Cells

  • ;;;;권오유
    • 대한의생명과학회지
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    • 제14권1호
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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.

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갑상선기능이 정상인 성인에서 골다공증과 갑상선호르몬의 관련성 (The association of Osteoporosis and Thyroid Hormone in euthyroid adults)

  • 윤현;류은진
    • 한국산학기술학회논문지
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    • 제16권2호
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    • pp.1137-1144
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    • 2015
  • 본 연구는 일부 종합검진 수검자들을 대상으로 골다공증이 갑상선호르몬에 미치는 영향을 검토하고자 2012년 1월부터 12월까지 G시의 일개 종합병원 건강검진센터에서 종합건강검진을 받았던 20세 이상의 지역주민 1,117명(남자 636, 여자 481)을 분석대상으로 하였다. 연구결과에서 연령과 성별을 보정하였을 때, 갑상선자극호르몬(thyroid stimulating hormone)에 대한 평균값은 정상군(${\geq}-1g/cm^2$)이 $1.61{\pm}0.07{\mu}IU/m{\ell}$, 골감소증군(-1 >, ${\geq}-2.5g/cm^2$)이 $1.82{\pm}0.08{\mu}IU/m{\ell}$, 골다공증군(< $-2.5g/cm^2$)이 $3.14{\pm}0.27{\mu}IU/m{\ell}$로 T-score가 감소할수록 증가하였다(p<0.001). 또한 성별과 FBS를 보정하였을 때, 유리타이록신(free thyroxine)에 대한 평균값은 정상군이 $1.30{\pm}0.01ng/d{\ell}$, 골감소증군이 $1.22{\pm}0.01ng/d{\ell}$, 골다공증군이 $1.13{\pm}0.04ng/d{\ell}$로 T-score가 감소할수록 감소하였다(p<0.001). 결론적으로 갑상선기능이 정상인 성인에서 T-score의 감소는 갑상선 자극호르몬(thyroid stimulating hormone)를 증가시키고, 유리 타이록신(free thyroxine)를 감소시킨다.

Thyroid dysfunction and subfertility

  • Cho, Moon Kyoung
    • Clinical and Experimental Reproductive Medicine
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    • 제42권4호
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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.

갑상선호르몬 수용체 베타 유전자 돌연변이(H435Y)가 확인된 갑상선호르몬 저항성 증후군 1례 (Identification of a de novo mutation (H435Y) in the THRB gene in a Korean patient with resistance to thyroid hormone)

  • 신진영;기창석;김진경
    • Clinical and Experimental Pediatrics
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    • 제50권6호
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    • pp.576-579
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    • 2007
  • 갑상선 호르몬 저항성 증후군은 갑상선 호르몬에 대한 조직의 반응이 감소되어 나타나는 드문 유전 질환이다. 대부분은 갑상선 호르몬 수용체 (TR) 유전자의 돌연변이로 인한 갑상선 호르몬 수용체의 결함에 의한다. TR 유전자의 변이는 일반적으로 이형접합성이며 상염색체 우성 유전 양상을 보인다. 혈청 갑상선 호르몬 수치가 증가되어 있음에도 불구하고 혈청 갑상선 자극호르몬 수치가 억제되지 않으며, 임상 양상은 다양하다. 본 증례는 경미한 갑상선종, 총 및 유리 $T_4$, $T_3$의 증가, 정상 범위의 TSH 소견을 보이는 4세 여아로서 TR 유전자 분석에서 과오돌연변이(H435Y)를 확인하였다. 부모에서는 돌연변이가 관찰되지 않았으며, 갑상선 기능도 정상이었다. 특별한 투약 없이 추적 관찰 중에 갑상선종의 증가나 다른 증상의 악화는 없는 상태이다.

조현병 입원 환자에서의 갑상샘 기능이상과 증상 심각도, 치료 반응과의 관계 (Association between Thyroid Dysfunction and Severity, Treatment Response in Schizophrenic Inpatients)

  • 정미줄;황현국;서영은;최종혁
    • 생물정신의학
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    • 제26권1호
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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.

Changes in the thyroid hormone profiles in children with nephrotic syndrome

  • Jung, Sun Hee;Lee, Jeong Eun;Chung, Woo Yeong
    • Clinical and Experimental Pediatrics
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    • 제62권3호
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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.