WordNet

suggestive of a thyroid disorder; "thyroid personality"
of or relating to the thyroid gland; "thyroid deficiency"; "thyroidal uptake" (同)thyroidal
the secretion of an endocrine gland that is transmitted by the blood to the tissue on which it has a specific effect (同)endocrine, internal_secretion
rousing or quickening activity or the senses; "a stimulating discussion"

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甲状腺 / 甲状腺の
ホルモン
刺激する;激励する,元気づける

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/08/20 17:30:08」(JST)

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Thyroid-stimulating hormone (also known as thyrotropin, TSH, or hTSH for human TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T₄), and then triiodothyronine (T₃) which stimulates the metabolism of almost every tissue in the body.^[1] It is a glycoprotein hormone synthesized and secreted by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.^[2]^[3]

Physiology

The system of the thyroid hormones T₃ and T₄.^[4]

Hormone levels

TSH (with a half life of about an hour) stimulates the thyroid gland to secrete the hormone thyroxine (T₄), which has only a slight effect on metabolism. T₄ is converted to triiodothyronine (T₃), which is the active hormone that stimulates metabolism. About 80% of this conversion is in the liver and other organs, and 20% in the thyroid itself.^[1]

TSH is secreted throughout life but particularly reaches high levels during the periods of rapid growth and development.

The hypothalamus, in the base of the brain, produces thyrotropin-releasing hormone (TRH). TRH stimulates the pituitary gland to produce TSH.

Somatostatin is also produced by the hypothalamus, and has an opposite effect on the pituitary production of TSH, decreasing or inhibiting its release.

The concentration of thyroid hormones (T₃ and T₄) in the blood regulates the pituitary release of TSH; when T₃ and T₄ concentrations are low, the production of TSH is increased, and, conversely, when T₃ and T₄ concentrations are high, TSH production is decreased. This is an example of a negative feedback loop.^[5] Any inappropriateness of measured values, for instance a low-normal TSH together with a low-normal T₄ may signal tertiary (central) disease and a TSH to TRH pathology. Elevated reverse T₃ (RT₃) together with low-normal TSH and low-normal T₃, T₄ values, which is regarded as indicative for euthyroid sick syndrome, may also have to be investigated for chronic subacute thyroiditis (SAT) with output of subpotent hormones. Absence of antibodies in patients with diagnoses of an autoimmune thyroid in their past would always be suspicious for development to SAT even in the presence of a normal TSH because there is no known recovery from autoimmunity.

Subunits

TSH is a glycoprotein and consists of two subunits, the alpha and the beta subunit.

The α (alpha) subunit (i.e., chorionic gonadotropin alpha) is nearly identical to that of human chorionic gonadotropin (hCG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). The α subunit is thought to be the effector region responsible for stimulation of adenylate cyclase (involved the generation of cAMP).^[6] The α chain has a 92-amino acid sequence.
The β (beta) subunit (TSHB) is unique to TSH, and therefore determines its receptor specificity.^[7] The β chain has a 118-amino acid sequence.

The TSH receptor

The TSH receptor is found mainly on thyroid follicular cells.^[8] Stimulation of the receptor increases T₃ and T₄ production and secretion. Stimulating antibodies to this receptor mimic TSH and cause Graves' disease. In addition, hCG shows some cross-reactivity to the TSH receptor and therefore can stimulate production of thyroid hormones. In pregnancy, prolonged high concentrations of hCG can produce a transient condition termed gestational hyperthyroidism.^[9] This is also the mechanism of trophoblastic tumors increasing the production of thyroid hormones.

Applications

Diagnostics

Reference ranges for TSH may vary slightly, depending on the method of analysis, and do not necessarily equate to cut-offs for diagnosing thyroid dysfunction. In the UK, guidelines issued by the Association for Clinical Biochemistry suggest a reference range of 0.4-4.5 µIU/mL.^[10] The National Academy of Clinical Biochemistry (NACB) stated that it expected the reference range for adults to be reduced to 0.4–2.5 µIU/mL, because research had shown that adults with an initially measured TSH level of over 2.0 µIU/mL had "an increased odds ratio of developing hypothyroidism over the [following] 20 years, especially if thyroid antibodies were elevated".^[11]

TSH concentrations in children are normally higher than in adults. In 2002, the NACB recommended age-related reference limits starting from about 1.3 to 19 µIU/mL for normal-term infants at birth, dropping to 0.6–10 µIU/mL at 10 weeks old, 0.4–7.0 µIU/mL at 14 months and gradually dropping during childhood and puberty to adult levels, 0.3–3.0 µIU/mL.^[12]^{:Section 2}

Diagnosis of disease

TSH concentrations are measured as part of a thyroid function test in patients suspected of having an excess (hyperthyroidism) or deficiency (hypothyroidism) of thyroid hormones. Interpretation of the results depends on both the TSH and T₄ concentrations. In some situations measurement of T₃ may also be useful.

Source of pathology	TSH level	Thyroid hormone level	Disease causing conditions
Hypothalamus/pituitary	High	High	Benign tumor of the pituitary (adenoma) or thyroid hormone resistance
Hypothalamus/pituitary	Low	Low	Secondary hypothyroidism or "central" hypothyroidism
Hyperthyroidism	Low	High	Primary hyperthyroidism i.e. Graves' disease
Hypothyroidism	High	Low	Congenital hypothyroidism (cretinism), Primary hypothyroidism i.e. Hashimoto's thyroiditis

A TSH assay is now also the recommended screening tool for thyroid disease. Recent advances in increasing the sensitivity of the TSH assay make it a better screening tool than free T₄.^[3]

Monitoring

The therapeutic target range TSH level for patients on treatment ranges between 0.3 to 3.0 μIU/mL.^[12]

For hypothyroid patients on thyroxine, measurement of TSH alone is generally considered sufficient. An increase in TSH above the normal range indicates under-replacement or poor compliance with therapy. A significant reduction in TSH suggests over-treatment. In both cases, a change in dose may be required. A low or low-normal TSH value may also signal pituitary disease. TSH measurements could not be applied any more, however, treatment would have to be continued.

For hyperthyroid patients, both TSH and T₄ are usually monitored.

Therapeutic

A synthetic drug called recombinant human TSH alpha (rhTSHα or simply rhTSH, trade name Thyrogen) is manufactured by Genzyme Corp. The rhTSH is used to treat thyroid cancer.^[13]

References

^ ^a ^b Merck Manual of Diagnosis and Therapy, Thyroid gland disorders.
^ The American Heritage Dictionary of the English Language, Fourth Edition. Houghton Mifflin Company. 2006. ISBN 0-395-82517-2.
^ ^a ^b Sacher R, Richard A. McPherson (2000). Widmann's Clinical Interpretation of Laboratory Tests, 11th ed. F.A. Davis Company. ISBN 0-8036-0270-7.
^ References used in image are found in image article in Commons:Commons:File:Thyroid system.png#References.
^ Estrada JM, Soldin D, Buckey TM, Burman KD, Soldin OP (2014). "Thyrotropin isoforms: implications for thyrotropin analysis and clinical practice". Thyroid 24 (3): 411–23. doi:10.1089/thy.2013.0119. PMID 24073798.
^ Lalli E, Sassone-Corsi P (Oct 1995). "Thyroid-stimulating hormone (TSH)-directed induction of the CREM gene in the thyroid gland participates in the long-term desensitization of the TSH receptor" (PDF). Proceedings of the National Academy of Sciences of the United States of America 92 (21): 9633–7. doi:10.1073/pnas.92.21.9633. PMC 40856. PMID 7568187.
^ Porcellini A, Messina S, De Gregorio G, Feliciello A, Carlucci A, Barone M, Picascia A, De Blasi A, Avvedimento EV (Oct 2003). "The expression of the thyroid-stimulating hormone (TSH) receptor and the cAMP-dependent protein kinase RII beta regulatory subunit confers TSH-cAMP-dependent growth to mouse fibroblasts". The Journal of Biological Chemistry 278 (42): 40621–30. doi:10.1074/jbc.M307501200. PMID 12902333.
^ Parmentier M, Libert F, Maenhaut C, Lefort A, Gérard C, Perret J, Van Sande J, Dumont JE, Vassart G (Dec 1989). "Molecular cloning of the thyrotropin receptor". Science 246 (4937): 1620–2. doi:10.1126/science.2556796. PMID 2556796.
^ Fantz CR, Dagogo-Jack S, Ladenson JH, Gronowski AM (Dec 1999). "Thyroid function during pregnancy". Clinical Chemistry 45 (12): 2250–8. PMID 10585360.
^ Use of thyroid function tests: guidelines development group (2006-06-01). "UK Guidelines for the Use of Thyroid Function Tests" (pdf). Retrieved 2014-01-14.
^ Baloch Z, Carayon P, Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA, Niccoli-Sire P, John R, Ruf J, Smyth PP, Spencer CA, Stockigt JR (Jan 2003). "Laboratory medicine practice guidelines. Laboratory support for the diagnosis and monitoring of thyroid disease". Thyroid 13 (1): 3–126. doi:10.1089/105072503321086962. PMID 12625976.
^ ^a ^b Baskin HJ, Cobin RH, Duick DS, Gharib H, Guttler RB, Kaplan MM, Segal RL (2002). "American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism" (PDF). Endocr Pract 8 (6): 457–69. PMID 15260011.
^ Duntas LH, Tsakalakos N, Grab-Duntas B, Kalarritou M, Papadodima E (2003). "The use of recombinant human thyrotropin (Thyrogen) in the diagnosis and treatment of thyroid cancer". Hormones 2 (3): 169–74. doi:10.14310/horm.2002.1197. PMID 17003018.

External links

TSH at Lab Tests Online
MedlinePlus Encyclopedia 003684
Thyrotropin at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

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1. 甲状腺機能の臨床検査評価 laboratory assessment of thyroid function
2. 甲状腺刺激ホルモンおよび甲状腺刺激ホルモン放出ホルモンに対する抵抗性 resistance to thyrotropin and thyrotropin releasing hormone
3. TSH-secreting pituitary adenomas
4. 妊娠していない成人における甲状腺機能低下症の診断およびスクリーニング diagnosis of and screening for hypothyroidism in nonpregnant adults
5. 甲状腺機能亢進症の診断 diagnosis of hyperthyroidism

English Journal

BRCA1-Mediated Inflammation and Growth Activated & Inhibited Transition Mechanisms Between No-Tumor Hepatitis/Cirrhotic Tissues and HCC.

Diao H, Wang L, Huang J, Jiang M, Zhou H, Li X, Chen Q, Jiang Z, Feng H.Author information Bioinformatics Center, School of Electronic Engineering, Beijing University of Posts and Telecommunications, Beijing, 100876, China; State key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.AbstractTo understand breast cancer 1 early onset (BRCA1)-mediated inflammation and growth activated and inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and human hepatocellular carcinoma (HCC), BRCA1-activated different complete (all no positive correlation, Pearson correlation coefficient <0.25) and uncomplete (partly no positive correlation except BRCA1, Pearson <0.25) networks were identified in higher HCC compared with lower no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) from the corresponding BRCA1-stimulated (Pearson ≥0.25) or inhibited (Pearson ≤-0.25) overlapping molecules of Pearson and GRNInfer, respectively. This result was verified by the corresponding scatter matrix. As visualized by GO, KEGG, GenMAPP, BioCarta, and disease database integration, we proposed mainly that BRCA1-stimulated different complete network was involved in BRCA1 activation with integral to membrane killer cell lectin-like receptor C to nucleus interferon regulatory factor 5-induced inflammation, whereas the corresponding inhibited network participated in BRCA1 repression with matrix roundabout axon guidance receptor homolog 1 to plasma membrane versican-induced growth in lower no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). However, BRCA1-stimulated network contained BRCA1 activation with endothelium-specific to lysosomal transmembrane and carbamoyl synthetase to tastin, histone cluster and cyclin-induced growth, whereas the corresponding inhibited different complete network included BRCA1 repression with ovalbumin, thyroid stimulating hormone beta and Hu antigen C to cytochrome P450 to transducin-induced inflammation in higher HCC. Our BRCA1 different networks were verified by BRCA1-activated or -inhibited complete and uncomplete networks within and between no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) or (and) HCC. J. Cell. Biochem. 115: 641-650, 2014. © 2013 Wiley Periodicals, Inc.
Journal of cellular biochemistry.J Cell Biochem.2014 Apr;115(4):641-50. doi: 10.1002/jcb.24699.
To understand breast cancer 1 early onset (BRCA1)-mediated inflammation and growth activated and inhibited transition mechanisms between no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and human hepatocellular carcinoma (HCC), BRCA1-activated different complete (all no positive correlati
PMID 24151232

Systematic analysis of the relationship between standardized biological levels of polychlorinated biphenyls and thyroid function in pregnant women and newborns.

El Majidi N1, Bouchard M2, Carrier G1.Author information 1Département de Santé Environnementale et Santé au Travail, Chaire d'analyse et de Gestion des Risques Toxicologiques and Institut de Recherche en Santé Publique de l'Université de Montréal (IRSPUM), Faculty of Medicine, Université de Montréal, P.O. Box 6128, Main Station, Montreal, Quebec H3C 3J7, Canada.2Département de Santé Environnementale et Santé au Travail, Chaire d'analyse et de Gestion des Risques Toxicologiques and Institut de Recherche en Santé Publique de l'Université de Montréal (IRSPUM), Faculty of Medicine, Université de Montréal, P.O. Box 6128, Main Station, Montreal, Quebec H3C 3J7, Canada. Electronic address: michele.bouchard@umontreal.ca.AbstractThe impact polychlorinated biphenyl (PCB) exposure on thyroid status in pregnant women and newborns was investigated in various epidemiological studies, but findings show inconsistencies, and differences in biological indicators of exposure between studies limits comparison of results. The aim of this research was to use a procedure previously developed to standardize PCB biological concentration data between published studies to perform a systematic analysis of associations between PCB exposure and thyroid hormones (THs) (total and free T3 and T4) or thyroid stimulating hormone (TSH) in pregnant women and newborns. Biological concentrations from nineteen studies were expressed in total PCB equivalent per kg of lipids in maternal plasma (μgPCBMPEQkg(-1) lipids). Systematic analysis of the "standardized biological concentration-thyroid parameters" relationship was conducted through the application of methodological criteria in both pregnant women and newborns. Standardization of PCB levels and application of methodological criteria led to assign higher confidence to ten of the reviewed studies. Among the retained studies in pregnant women, only one reported a significant association between PCBs and total T3 levels, but no association were observed when circulating TSH and free T4 levels were used to assess thyroid function. Regarding the association between prenatal PCB exposure and thyroid status in newborns, a lack of significant association was consistently obtained in the retained studies assigned an overall high confidence. The weight of evidence of a significant impact of PCB exposure on TSH and TH levels at the described biological levels in pregnant women and newborns (mean<1000μgPCBMPEQkg(-1) lipids) appears low according to this systematical analysis.
Chemosphere.Chemosphere.2014 Mar;98:1-17. doi: 10.1016/j.chemosphere.2013.10.006. Epub 2013 Nov 5.
The impact polychlorinated biphenyl (PCB) exposure on thyroid status in pregnant women and newborns was investigated in various epidemiological studies, but findings show inconsistencies, and differences in biological indicators of exposure between studies limits comparison of results. The aim of th
PMID 24200047

Mild iodine deficiency in women after spontaneous abortions living in an iodine-sufficient area of Czech Republic: prevalence and impact on reproductive health.

Jiskra J, Fait T, Bílek R, Krátký J, Bartáková J, Lukáš J, Límanová Z, Telička Z, Zamrazil V, Potluková E.Author information 3rd Department of Medicine, 1st Faculty of Medicine, General University Hospital, Charles University, Prague, Czech Republic.AbstractOBJECTIVE: Iodine deficiency is associated with thyroid dysfunction and adverse pregnancy outcomes. The aim of our study was to investigate the status of iodine saturation in women after spontaneous abortion (SpA) residing in an iodine-sufficient area and to evaluate their subsequent reproductive health.
Clinical endocrinology.Clin Endocrinol (Oxf).2014 Mar;80(3):452-8. doi: 10.1111/cen.12298. Epub 2013 Aug 21.
OBJECTIVE: Iodine deficiency is associated with thyroid dysfunction and adverse pregnancy outcomes. The aim of our study was to investigate the status of iodine saturation in women after spontaneous abortion (SpA) residing in an iodine-sufficient area and to evaluate their subsequent reproductive he
PMID 23889327

Japanese Journal

ダイオキシン母体曝露による発達児の甲状腺ホルモンへの影響 (油症とPCB及びダイオキシン関連化合物に関する研究報告集(第25集))

服部友紀子,武田知起,田浦順樹 [他],黒木広明,石井祐次,山田英之
福岡医学雑誌 = Fukuoka acta medica 106(5), 127-134, 2015-05-25
… Previous studies have suggested that lactational exposure to 2,3,7,8-tetrachlorodizenzo-p-dioxin (TCDD) reduces the pup level of thyroid hormone after weaning, leading to the damage to their development including neural maturation. … However, the specificity for age and dioxin congeners as well as dose dependency in terms of a reduction in pup thyroid hormone remains to be clarified. …
NAID 120005624038

著明な精神症状を呈したバセドウ病の1例

久能芙美,岡田洋右,新生忠司,黒住旭,田中良哉
産業医科大学雑誌 37(1), 49-53, 2015-03-01
… 症例は42歳女性.動悸・発汗過多・手指振戦のため2011年3月に来院.甲状腺刺激ホルモン(thyroid stimulating hormone; …
NAID 110009924218

先天性甲状腺機能低下症のスクリーニングにおいて指標とする甲状腺刺激ホルモン値に影響を及ぼす採血日齢について

廣田美和,安片恭子,稲田佳美 [他]
調査研究ジャーナル = Chiba survey research journal 4(1), 22-26, 2015
NAID 40020481450

Related Pictures

★リンクテーブル★

リンク元	「下垂体前葉ホルモン」「甲状腺刺激ホルモン」
拡張検索	「thyroid-stimulating hormone receptor」「thyroid-stimulating hormone beta」「thyroid-stimulating hormone receptor antibody」
関連記事	「thyroid」「stimulating」

「下垂体前葉ホルモン」

Thyroid-stimulating hormone, beta
Identifiers
Symbol	TSHB
Entrez	7252
HUGO	12372
OMIM	188540
RefSeq	NM_000549
UniProt	P01222
Other data
Locus	Chr. 1 p13

Thyroid-stimulating hormone, alpha
Identifiers
Symbol	CGA
Alt. symbols	HCG, GPHa, GPHA1
Entrez	1081
HUGO	1885
OMIM	118850
RefSeq	NM_000735
UniProt	P01215
Other data
Locus	Chr. 6 q14-q21

　　[★]

英: anterior pituitary hormone
関: 下垂体前葉、下垂体、下垂体ホルモン、ホルモン

分泌されるホルモン

単純ペプチドホルモン

糖タンパク質ホルモン

GOO. chapter 55

名称		構造	分泌細胞	下垂体前葉細胞全細胞に対する産生細胞の割合	染色性		サブユニット	残基数 (aa.)	分子量 (kDa)	その他
成長ホルモン	GH	ペプチド	somatotroph	40-50%	好酸性		1	191	22
プロラクチン	PRL		mammotroph	10-25%	好酸性		1	199	23
副腎皮質刺激ホルモン	ACTH		corticotroph	0.1	好塩基性	嫌色素性	1	39	4.5	POMC由来
甲状腺刺激ホルモン	TSH	糖タンパク	thyrotroph	0.05	好塩基性		2	α: 92, β:118	28	αサブユニットは共通
卵胞刺激ホルモン	FSH		gonadotroph	10-15%	好塩基性		2	α: 92, β:111	32.6
黄体形成ホルモン	LH		gonadotroph	10-15%	好塩基性		2	α: 92, β:121	29.4

HIM.2196

Table 333-1 Anterior Pituitary Hormone Expression and Regulation
Cell	corticotrope	somatotrope	lactotrope	thyrotrope	gonadotrope
Tissue-specific transcription factor	T-Pit	Prop-1, Pit-1	Prop-1, Pit-1	Prop-1, Pit-1, TEF	SF-1, DAX-1
Fetal appearance	6 weeks	8 weeks	12 weeks	12 weeks	12 weeks
Hormone	POMC	GH	PRL	TSH	FSH LH
Chromosomal locus	2p	17q	6	－6q; －1p	－11p; －19q
Protein	ポリペプチド			糖タンパク
Amino acids	266 (ACTH 1–39)	191	199	211	210 204
Stimulators	CRH, AVP, gp-130 cytokines	GHRH, ghrelin, bromocriptine⁽¹⁾	estrogen, TRH, VIP	TRH	GnRH, activins, estrogen
Inhibitors	glucocorticoids	somatostatin, IGF-I	dopamine	T3, T4, dopamine, somatostatin, glucocorticoids	sex steroids, inhibin
Target gland	adrenal	liver, other tissues	breast, other tissues	thyroid	ovary, testis
Trophic effect	steroid production	IGF-I production, growth induction, insulin antagonism	milk production	T4 synthesis and secretion	sex steroid production, follicle growth, germ cell maturation