Sum activity of peripheral deiodinases
SynonymsSPINA-GD, GD, deiodination capacity, total deiodinase activity
Reference range20–40 nmol/s
Test ofMaximum amount of T3 produced from T4 by peripheral deiodinases
MeSHD013960
LOINC82367-4

The sum activity of peripheral deiodinases (GD, also referred to as deiodination capacity, total deiodinase activity or, if calculated from levels of thyroid hormones, as SPINA-GD[lower-alpha 1]) is the maximum amount of triiodothyronine produced per time-unit under conditions of substrate saturation.[1] It is assumed to reflect the activity of deiodinases outside the central nervous system and other isolated compartments. GD is therefore expected to reflect predominantly the activity of type I deiodinase.

How to determine GD

GD can be determined experimentally by exposing a cell culture system to saturating concentrations of T4 and measuring the T3 production. Whole body deiodination activity can be assessed by measuring production of radioactive iodine after loading the organism with marked thyroxine.[2]

However, both approaches are faced with draw-backs. Measuring deiodination in cell culture delivers little, if any, information on total deiodination activity. Using marked thyroxine exposes the body to thyrotoxicosis and radioactivity. Additionally, it is not possible to differentiate step-up reactions resulting in T3 production from the step-down reaction catalyzed by type 3 deiodination, which mediates production of reverse T3. Distinguishing the contribution of distinct deiodinases is possible, however, by sequential approaches using deiodinase-specific blocking agents, but this approach is cumbersome and time-consuming.[2]

In vivo, it may therefore be beneficial to estimate GD from equilibrium levels of T4 and T3. It is obtained with

or

[FT4]: Serum free T4 concentration (in pmol/L)
[FT3]: Serum free T3 concentration (in pmol/L)
[TT3]: Serum total T3 concentration (in nmol/L)
: Dilution factor for T3 (reciprocal of apparent volume of distribution, 0.026 L−1)
: Clearance exponent for T3 (8e-6 sec−1) (i. e., reaction rate constant for degradation)
KM1: Binding constant of type-1-deiodinase (5e-7 mol/L)
K30: Binding constant T3-TBG (2e9 L/mol)[3]

The method is based on mathematical models of thyroid homeostasis.[1][3] Calculating deiodinase activity with one of these equations is an inverse problem. Therefore, certain conditions (e.g. stationarity) have to be fulfilled to deliver a reliable result.

The product of SPINA-GD times the urinary iodine excretion can be used to assess iodine-independent factors affecting deiodinase activity, e.g. selenium deficiency.[4]

Reference range

Lower limitUpper limitUnit
20[3]40[3]nmol/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.[3]

Clinical significance

Validity

SPINA-GD correlates to the T4-T3 conversion rate in slow tissue pools, as determined with isotope-based measurements in healthy volunteers.[1] It was also shown that GD correlates with resting energy expenditure,[5] body mass index[3][6][7] and thyrotropin levels in humans,[8][9] and that it is reduced in nonthyroidal illness with hypodeiodination.[6][10][11][12][13] Multiple studies demonstrated SPINA-GD to rise after initiation of substitution therapy with selenium, a trace element that is essential for the synthesis of deiodinases.[14][15][16][17][18] Conversely, it was observed that SPINA-GD is reduced in persons positive for autoantibodies to selenoprotein P, which is assumed to be involved in transport and storage of selenium.[4]

Clinical utility

Compared to both healthy volunteers and subjects with hypothyroidism and hyperthyroidism, SPINA-GD is reduced in subacute thyroiditis. In this condition, it has a higher specificity, positive and negative likelihood ratio than serum concentrations of thyrotropin, free T4 or free T3.[3] These measures of diagnostic utility are also high in nodular goitre, where SPINA-GD is elevated.[3] Among subjects with subclinical thyrotoxicosis, calculated deiodinase activity is significantly lower in exogenous thyrotoxicosis (resulting from therapy with levothyroxine) than in true hyperthyroidism (ensuing from toxic adenoma, toxic multinodular goitre or Graves' disease).[19] SPINA-GD may therefore be an effective biomarker for the differential diagnosis of thyrotoxicosis.[20][21]

Compared to healthy subjects, SPINA-GD is significantly reduced in euthyroid sick syndrome.[22]

Pathophysiological and therapeutic implications

Recent research revealed total deiodinase activity to be higher in untreated hypothyroid patients as long as thyroid tissue is still present.[9] This effect may ensue from the existence of an effective TSH-deiodinase axis or TSH-T3 shunt. After total thyroidectomy or high-dose radioiodine therapy (e.g. in treated thyroid cancer) as well as after initiation of substitution therapy with levothyroxine the activity of step-up deiodinases decreases[23][24] and the correlation of SPINA-GD to thyrotropin concentration is lost.[25]

SPINA-GD is elevated in obesity. This applies to both the metabolically healthy obese (MHO) or metabolically unhealthy obese (MUO) phenotypes.[26] In two large population-based cohorts within the Study of Health in Pomerania SPINA-GD was positively correlated to some markers of body composition including body mass index (BMI), waist circumference, fat-free mass and body cell mass,[27] confirming observations in the NHANES dataset[28] and in a Chinese study.[29] This positive association was age-dependent and with respect to BMI significant in young subjects only, but with respect to body cell mass stronger in elderly persons.[27] Generally, SPINA-GD seems to be upregulated in metabolic syndrome, as demonstrated by a significant correlation to the triglyceride-glucose index, a marker of insulin resistance.[30]

SPINA-GD is reduced in low-T3 syndrome[31] and certain chronic diseases, e.g. chronic fatigue syndrome,[32][4] chronic kidney disease,[33][34] short bowel syndrome[35] or geriatric asthma.[36] In Graves' disease, SPINA-GD is initially elevated but decreases with antithyroid treatment in parallel to declining TSH receptor autoantibody titres.[5] Although takotsubo syndrome (TTS) results in most cases from psychosocial stressors, thereby reflecting type 2 allostatic load, SPINA-GD has been described to be reduced in TTS.[37] This may result from concomitant non-thyroidal illness syndrome, so that the clinical phenotype represents overlapping type 1 and type 2 allostatic response.

In hyperthyroid[38] men both SPINA-GT and SPINA-GD negatively correlate to erectile function, intercourse satisfaction, orgasmic function and sexual desire. Substitution with selenomethionine results in increased SPINA-GD in subjects with autoimmune thyroiditis.[14][15][16][17]

In subjects with diabetes mellitus SPINA-GD is positively correlated to several bone resorption markers including the N-mid fragment of osteocalcin and procollagen type I N-terminal propeptide (P1NP), as well as, however in men only, the β-C-terminal cross-linked telopeptides of type I collagen (β-CTX).[39] In the general population it is, however, positively associated with the bone mineral density of the femoral neck and with reduced risk of osteoporosis.[40] In both diabetic and non-diabetic subsjects it correlates (negatively) with age and concentrations of c-reactive protein, troponin T and B-type natriuretic peptide, and (positively) with the concentrations of total cholesterol, low-density lipoprotein and triglycerides.[41]

Deiodination capacity proved to be an independent predictor of substitution dose in several trials that included persons on replacement therapy with levothyroxine.[42][43]

Probably as a consequence of non-thyroidal illness syndrome, SPINA-GD predicts mortality in trauma[22] and postoperative atrial fibrillation in patients undergoing cardiac surgery.[12] The association to mortality is retained even after adjustment for other established risk factors, including age, APACHE II score and plasma protein binding of thyroid hormones.[22] Correlations were also shown to age, total atrial conduction time, and concentrations of 3,5-diiodothyronine and B-type natriuretic peptide.[12] In a population suffering from pyogenic liver abscess SPINA-GD correlated to markers of malnutrition, inflammation and liver failure.[31] A study on subjects with Parkinson's disease found SPINA-GD to be significantly decreased in tremor-dominant and mixed subtypes compared to the akinetic-rigid type.[44] Euthyroid sick syndrome may be the reason for variations of SPINA-GD in subjects treated with immune checkpoint inhibitors for cancer as well.[45]

Endocrine disruptors may have pronounced effects on step-up deiodinases, as suggested by positive correlation of SPINA-GD to combined exposure to polycyclic aromatic hydrocarbons (PAHs)[46] and urine concentrations of cadmium and phthalate metabolites[47][48][49] and negative correlation to paraben, mercury and bisphenol A concentration.[50][47][48] In a cohort of manganese-exposed workers, SPINA-GD responded to a tenfold increase in concentrations of titanium, nickel, selenium and strontium.[51]

See also

Notes

  1. ↑ SPINA is an acronym for "structure parameter inference approach".

References

  1. 1 2 3 Dietrich JW, Landgrafe-Mende G, Wiora E, Chatzitomaris A, Klein HH, Midgley JE, Hoermann R (9 June 2016). "Calculated Parameters of Thyroid Homeostasis: Emerging Tools for Differential Diagnosis and Clinical Research". Frontiers in Endocrinology. 7: 57. doi:10.3389/fendo.2016.00057. PMC 4899439. PMID 27375554. S2CID 14210899.
  2. 1 2 Bianco, AC; Anderson, G; Forrest, D; Galton, VA; Gereben, B; Kim, BW; Kopp, PA; Liao, XH; Obregon, MJ; Peeters, RP; Refetoff, S; Sharlin, DS; Simonides, WS; Weiss, RE; Williams, GR (January 2014). "American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models". Thyroid. 24 (1): 88–168. doi:10.1089/thy.2013.0109. PMC 3887458. PMID 24001133.
  3. 1 2 3 4 5 6 7 8 Dietrich JW (2002). Der Hypophysen-Schilddrüsen-Regelkreis. Berlin, Germany: Logos-Verlag Berlin. ISBN 978-3-89722-850-4. OCLC 50451543. OL 24586469M.
  4. 1 2 3 Sun, Q; Oltra, E; Dijck-Brouwer, DAJ; Chillon, TS; Seemann, P; Asaad, S; Demircan, K; Espejo-Oltra, JA; Sánchez-Fito, T; Martín-Martínez, E; Minich, WB; Muskiet, FAJ; Schomburg, L (3 July 2023). "Autoantibodies to selenoprotein P in chronic fatigue syndrome suggest selenium transport impairment and acquired resistance to thyroid hormone". Redox Biology. 65: 102796. doi:10.1016/j.redox.2023.102796. PMC 10338150. PMID 37423160.
  5. 1 2 Kim, Min Joo; Cho, Sun Wook; Choi, Sumin; Ju, Dal Lae; Park, Do Joon; Park, Young Joo (2018). "Changes in Body Compositions and Basal Metabolic Rates during Treatment of Graves' Disease". International Journal of Endocrinology. 2018: 9863050. doi:10.1155/2018/9863050. PMC 5960571. PMID 29853888. S2CID 44088904.
  6. 1 2 Liu S, Ren J, Zhao Y, Han G, Hong Z, Yan D, Chen J, Gu G, Wang G, Wang X, Fan C, Li J (February 2013). "Nonthyroidal illness syndrome: is it far away from Crohn's disease?". Journal of Clinical Gastroenterology. 47 (2): 153–9. doi:10.1097/MCG.0b013e318254ea8a. PMID 22874844. S2CID 35344744.
  7. ↑ Dietrich JW, Landgrafe G, Fotiadou EH (2012). "TSH and Thyrotropic Agonists: Key Actors in Thyroid Homeostasis". Journal of Thyroid Research. 2012: 1–29. doi:10.1155/2012/351864. PMC 3544290. PMID 23365787. S2CID 15996441.
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  10. ↑ Rosolowska-Huszcz D, Kozlowska L, Rydzewski A (August 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. S2CID 25630198.
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  12. 1 2 3 Dietrich JW, Müller P, Schiedat F, Schlömicher M, Strauch J, Chatzitomaris A, Klein HH, Mügge A, Köhrle J, Rijntjes E, Lehmphul I (June 2015). "Nonthyroidal Illness Syndrome in Cardiac Illness Involves Elevated Concentrations of 3,5-Diiodothyronine and Correlates with Atrial Remodeling". European Thyroid Journal. 4 (2): 129–37. doi:10.1159/000381543. PMC 4521060. PMID 26279999. S2CID 207639541.
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  15. 1 2 Krysiak, Robert; Kowalcze, Karolina; Okopień, Bogusław (December 2018). "Selenomethionine potentiates the impact of vitamin D on thyroid autoimmunity in euthyroid women with Hashimoto's thyroiditis and low vitamin D status". Pharmacological Reports. 71 (2): 367–73. doi:10.1016/j.pharep.2018.12.006. PMID 30844687. S2CID 73486105.
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  21. ↑ Pattarawongpaiboon, Chidchanok; Srisawat, Nattachai; Tungsanga, Kriang; Champunot, Ratapum; Somboonjun, Jukrin; Srichomkwun, Panudda (20 November 2023). "Clinical characteristics and outcomes of an exogenous thyrotoxicosis epidemic in prison". BMJ Nutrition, Prevention & Health: e000789. doi:10.1136/bmjnph-2023-000789.
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  42. ↑ Midgley JE, Larisch R, Dietrich JW, Hoermann R (December 2015). "Variation in the biochemical response to l-thyroxine therapy and relationship with peripheral thyroid hormone conversion efficiency". Endocrine Connections. 4 (4): 196–205. doi:10.1530/EC-15-0056. PMC 4557078. PMID 26335522.
  43. ↑ Le Moli, R; Malandrino, P; Russo, M; Tumino, D; Piticchio, T; Naselli, A; Rapicavoli, V; Belfiore, A; Frasca, F (March 2023). "Levothyroxine therapy, calculated deiodinases activity and basal metabolic rate in obese or nonobese patients after total thyroidectomy for differentiated thyroid cancer, results of a retrospective observational study". Endocrinology, Diabetes & Metabolism. 6 (2): e406. doi:10.1002/edm2.406. PMC 10000637. PMID 36722311.
  44. ↑ Tan, Y; Gao, L; Yin, Q; Sun, Z; Man, X; Du, Y; Chen, Y (April 2021). "Thyroid hormone levels and structural parameters of thyroid homeostasis are correlated with motor subtype and disease severity in euthyroid patients with Parkinson's disease". The International Journal of Neuroscience. 131 (4): 346–356. doi:10.1080/00207454.2020.1744595. PMID 32186220. S2CID 212752563.
  45. ↑ Verelst, FR; Beyens, MMJ; Vandenbroucke, E; Forceville, K; Th B Twickler, M (15 April 2022). "A decrease in peripheral thyroid hormone conversion efficiency in patients treated with immune checkpoint inhibitors and L-T3 as a possible alternative therapeutic escape option". European Journal of Clinical Investigation. 52 (7): e13790. doi:10.1111/eci.13790. PMID 35428986. S2CID 248203797.
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  47. 1 2 Choi, Sohyeon; Kim, Min Joo; Park, Young Joo; Kim, Sunmi; Choi, Kyungho; Cheon, Gi Jeong; Cho, Yoon Hee; Jeon, Hye Li; Yoo, Jiyoung; Park, Jeongim (July 2020). "Thyroxine-binding globulin, peripheral deiodinase activity, and thyroid autoantibody status in association of phthalates and phenolic compounds with thyroid hormones in adult population". Environment International. 140: 105783. doi:10.1016/j.envint.2020.105783. PMID 32464474.
  48. 1 2 Kim, Min Joo; Kim, Sunmi; Choi, Sohyeon; Lee, Inae; Moon, Min Kyong; Choi, Kyungho; Park, Young Joo; Cho, Yoon Hee; Kwon, Young Min; Yoo, Jiyoung; Cheon, Gi Jeong; Park, Jeongim (December 2020). "Association of exposure to polycyclic aromatic hydrocarbons and heavy metals with thyroid hormones in general adult population and potential mechanisms". Science of the Total Environment. 762: 144227. doi:10.1016/j.scitotenv.2020.144227. PMID 33373756. S2CID 229722026.
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  50. ↑ Huang, PC; Chen, HC; Leung, SH; Lin, YJ; Huang, HB; Chang, WT; Huang, HI; Chang, JW (1 December 2023). "Associations between paraben exposure, thyroid capacity, homeostasis and pituitary thyrotropic function in the general Taiwanese: Taiwan Environmental Survey for Toxicants (TEST) 2013". Environmental Science and Pollution Research. doi:10.1007/s11356-023-31277-y. PMID 38038926. S2CID 265514578.
  51. ↑ Ge, X; He, J; Lin, S; Bao, Y; Zheng, Y; Cheng, H; Cai, H; Feng, X; Yang, W; Hu, S; Wang, L; Liao, Q; Wang, F; Liu, C; Chen, X; Zou, Y; Yang, X (16 September 2023). "Associations of metal mixtures with thyroid function and potential interactions with iodine status: results from a cross-sectional study in MEWHC". Environmental Science and Pollution Research International. 30 (48): 105665–105674. Bibcode:2023ESPR...30j5665G. doi:10.1007/s11356-023-29682-4. PMID 37715904. S2CID 262013667.

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