Thyroid's secretory capacity

Thyroid's secretory capacity (GT, also referred to as thyroid's incretory capacity, maximum thyroid hormone output, T4 output or, if calculated from levels of thyroid hormones, as SPINA-GT) is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit (e.g. one second).[1]

How to determine GT

Experimentally, GT can be determined by stimulating the thyroid with high a thyrotropin concentration (e.g. by means of rhTSH, i.e. recombinant human thyrotropin) and measuring its output in terms of T4 production.

In vivo, GT can also be estimated from equilibrium levels of TSH and T4 or free T4. In this case it is calculated with

\hat G_T  = {{\beta _T (D_T  + [TSH])(1 + K_{41} [TBG] + K_{42} [TBPA])[FT_4 ]} \over {\alpha _T [TSH]}}

or

\hat G_T  = {{\beta _T (D_T  + [TSH])[TT_4 ]} \over {\alpha _T [TSH]}}

\hat G_T : Theoretical (apparent) secretory capacity (SPINA-GT)
\alpha _T: Dilution factor for T4 (reciprocal of apparent volume of distribution, 0.1 l−1)
\beta _T: Clearance exponent for T4 (1.1e-6 sec−1)
K41: Dissociation constant T4-TBG (2e10 l/mol)
K42: Dissociation constant T4-TBPA (2e8 l/mol)
DT: EC50 for TSH (2.75 mU/l)[1][2]

Reference Range

Lower limitUpper limitUnit
1.41[1] 8.67[1] pmol/s

The equations and their parameters are calibrated for adult humans with a body mass of 70 kg and a plasma volume of ca. 2.5 l.[1]

Clinical significance

GT is elevated in primary hyperthyroidism and reduced in primary hypothyroidism,[3][4][5] and it has been observed to correlate with thyroid volume.[1] In longitudinal evaluation GT shows lower intraindividual variation than TSH, FT4 or FT3.[6] Correlation of SPINA-GT with creatinine clearance suggested a negative influence of uremic toxins on thyroid biology.[7] In the initial phase of major non-thyroidal illness SPINA-GT may be temporarily elevated.[8]

See also

External links

References

  1. 1 2 3 4 5 6 Dietrich, J. W. (2002). Der Hypophysen-Schilddrüsen-Regelkreis. Berlin, Germany: Logos-Verlag Berlin. ISBN 978-3-89722-850-4. OCLC 50451543. 3897228505
  2. Dietrich JW, Stachon A, Antic B, Klein HH, Hering S (Oct 2008). "The AQUA-FONTIS study: protocol of a multidisciplinary, cross-sectional and prospective longitudinal study for developing standardized diagnostics and classification of non-thyroidal illness syndrome". BMC Endocr Disord 8 (1): 13. doi:10.1186/1472-6823-8-13. PMC 2576461. PMID 18851740.
  3. Dietrich, J., M. Fischer, J. Jauch, E. Pantke, R. Gärtner und C. R. Pickardt (1999). "SPINA-THYR: A Novel Systems Theoretic Approach to Determine the Secretion Capacity of the Thyroid Gland." European Journal of Internal Medicine 1999; 10(Suppl. 1): S34.
  4. Dietrich JW (Sep 2012). "Thyroid storm". Med Klin Intensivmed Notfmed 107 (6): 448–53. doi:10.1007/s00063-012-0113-2. PMID 22878518.
  5. Wang, X; Liu, H; Chen, J; Huang, Y; Li, L; Rampersad, S; Qu, S (21 April 2016). "Metabolic Characteristics in Obese Patients Complicated by Mild Thyroid Hormone Deficiency.". Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. PMID 27101096.
  6. Dietrich JW, Landgrafe G, Fotiadou EH (2012). "TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis". Journal of Thyroid Research 2012: 351864. doi:10.1155/2012/351864. PMC 3544290. PMID 23365787.
  7. Rosolowska-Huszcz D, Kozlowska L, Rydzewski A (Aug 2005). "Influence of low protein diet on nonthyroidal illness syndrome in chronic renal failure". Endocrine 27 (3): 283–8. doi:10.1385/endo:27:3:283. PMID 16230785.
  8. Liu S, Ren J, Zhao Y, Han G, Hong Z, Yan D, Chen J, Gu G, Wang G, Wang X, Fan C, Li J (2013). "Nonthyroidal Illness Syndrome: ist it Far Away From Crohn's Disease?". J Clin Gastroenterol. 47 (2): 153–9. doi:10.1097/MCG.0b013e318254ea8a. PMID 22874844.
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