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Thyroid-stimulating hormone


Thyroid-stimulating hormone

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

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 1
    • Hormone levels 1.1
    • Subunits 1.2
    • The TSH receptor 1.3
  • Applications 2
    • Diagnostics 2.1
      • Diagnosis of disease 2.1.1
      • Monitoring 2.1.2
    • Therapeutic 2.2
  • References 3
  • External links 4


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

External links

  1. ^ a b Merck Manual of Diagnosis and Therapy, Thyroid gland disorders.
  2. ^ The American Heritage Dictionary of the English Language, Fourth Edition. Houghton Mifflin Company. 2006.  
  3. ^ a b Sacher R, Richard A. McPherson (2000). Widmann's Clinical Interpretation of Laboratory Tests, 11th ed. F.A. Davis Company.  
  4. ^ References used in image are found in image article in Commons:.
  5. ^ 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.  
  6. ^ 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.  
  7. ^ 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.  
  8. ^ 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.  
  9. ^ Fantz CR, Dagogo-Jack S, Ladenson JH, Gronowski AM (Dec 1999). "Thyroid function during pregnancy". Clinical Chemistry 45 (12): 2250–8.  
  10. ^ 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. 
  11. ^ 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.  
  12. ^ 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.  
  13. ^ Baskin; et al. (2002). "AACE Medical Guidelines for Clinical Practice for Evaluation and Treatment of Hyperthyroidism and Hypothyroidism" (PDF). American Association of Clinical Endocrinologists. pp. 462, 465. 
  14. ^
  15. ^ 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.  


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.[15]


For hyperthyroid patients, both TSH and T4 are usually monitored. It must also be noted that in pregnancy, TSH measurements do not seem to be a good marker for the well-known association of maternal thyroid hormone availability with [14]offspring neurocognitive development.

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.

The therapeutic target range TSH level for patients on treatment ranges between 0.3 to 3.0 μIU/mL.[13]


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]

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

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.

Diagnosis of disease

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

[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]



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.

The TSH receptor

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


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.

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

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

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


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