Thyroid's secretory capacity

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Thyroid's secretory capacity
Reference ranges for TSH, FT4, JTI and SPINA-GT.svg
Reference ranges for SPINA-GT and other thyroid function tests
Synonyms SPINA-GT, GT, T4 output, thyroid hormone output, thyroid's incretory capacity, functional thyroid capacity [1]
Reference range 1.41–8.67 pmol/s
Test ofMaximum amount of T4 produced by the thyroid in one second
MeSH D013960
LOINC 82368-2

Thyroid's secretory capacity (GT, also referred to as thyroid's incretory capacity, maximum thyroid hormone output, T4 output or, if calculated from serum levels of thyrotropin and thyroxine, as SPINA-GT [a] ) is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit (e.g. one second). [2] [3]

Contents

How to determine GT

Experimentally, GT can be determined by stimulating the thyroid with a high thyrotropin concentration (e.g. by means of rhTSH, i.e. recombinant human thyrotropin) and measuring its output in terms of T4 production, or by measuring the serum concentration of protein-bound iodine-131 after administration of radioiodine. [4] These approaches are, however, costly and accompanied by significant exposure to radiation. [5]

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

or

[TSH]: Serum thyrotropin concentration (in mIU/L or μIU/mL)
[FT4]: Serum free T4 concentration (in pmol/L)
[TT4]: Serum total T4 concentration (in nmol/L)
: Theoretical (apparent) secretory capacity (SPINA-GT)
: Dilution factor for T4 (reciprocal of apparent volume of distribution, 0.1 L−1)
: Clearance exponent for T4 (1.1e-6 sec−1), i. e., reaction rate constant for degradation
K41: Binding constant T4-TBG (2e10 L/mol)
K42: Binding constant T4-TBPA (2e8 L/mol)
DT: EC50 for TSH (2.75 mU/L) [2] [6]

The method is based on mathematical models of thyroid homeostasis. [2] [3] Calculating the secretory capacity with one of these equations is an inverse problem. Therefore, certain conditions (e.g. stationarity) have to be fulfilled to deliver a reliable result.

Specific secretory capacity

The ratio of SPINA-GT and thyroid volume VT (as determined e.g. by ultrasonography)

,

i.e.

or

is referred to as specific thyroid capacity (SPINA-GTs). [7] It is a measure for how much one millilitre of thyroid tissue can produce under conditions of maximum stimulation. Thereby, SPINA-GTs is an estimate for the endocrine quality of thyroid tissue.[ citation needed ]

Reference Range

Percentiles for thyroid's secretory capacity (SPINA-GT) along with reference ranges for Jostel's TSH index (TSHI or JTI) and univariable reference ranges for thyrotropin (TSH) and free thyroxine (FT4), shown in the two-dimensional phase plane defined by serum concentrations of TSH and FT4. SPINA-GT percentiles.svg
Percentiles for thyroid's secretory capacity (SPINA-GT) along with reference ranges for Jostel's TSH index (TSHI or JTI) and univariable reference ranges for thyrotropin (TSH) and free thyroxine (FT4), shown in the two-dimensional phase plane defined by serum concentrations of TSH and FT4.
Lower limitUpper limitUnit
1.41 [2] 8.67 [2] 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. [2]

Clinical significance

Validity

SPINA-GT is elevated in primary hyperthyroidism [8] [9] and reduced in both primary hypothyroidism [10] [11] [12] [9] and untreated autoimmune thyroiditis. [13] It has been observed to correlate (with positive direction) to resting energy expenditure, [14] resting heart rate, [15] the colour Doppler ultrasound pattern [16] and thyroid volume, [2] [7] and (with negative direction) to thyroid autoantibody titres, which reflect organ destruction due to autoimmunity. [17] Elevated SPINA-GT in Graves' disease is reversible with antithyroid treatment. [14] While SPINA-GT is significantly altered in primary thyroid disorders, it is insensitive to disorders of secondary nature (e.g. pure pituitary diseases). [3]

Reliability

In silico experiments with Monte Carlo simulations demonstrated that both SPINA-GT and SPINA-GD can be estimated with sufficient reliability, even if laboratory assays have limited accuracy. [3] This was confirmed by longitudinal in vivo studies that showed that GT has lower intraindividual variation (i.e. higher reliability) than TSH, FT4 or FT3. [18]

Clinical utility

In clinical trials SPINA-GT was significantly elevated in patients with Graves' disease and toxic adenoma compared to normal subjects. [2] [8] [19] It is also elevated in diffuse and nodular goiters, and reduced in untreated autoimmune thyroiditis. [2] [13] In patients with toxic adenoma it has higher specificity and positive likelihood ratio for diagnosis of thyrotoxicosis than serum concentrations of thyrotropin, free T4 or free T3. [2] GT's specificity is also high in thyroid disorders of secondary or tertiary origin. [3]

Calculating SPINA-GT has proved to be useful in challenging clinical situations, e.g. for differential diagnosis of subclinical hypothyroidism and elevated TSH concentration due to type 2 allostatic load (as it is typical for obesity and certain psychiatric diseases). [20] For this purpose, its usage has been recommended in sociomedical assessment. [21]

Pathophysiological and therapeutic implications

In patients suffering from toxic adenoma, toxic multinodular goitre and Graves’ disease radioiodine therapy leads to a significant decrease of the initially elevated SPINA-GT. [19]

Correlation of SPINA-GT with creatinine clearance suggests a negative influence of uremic toxins on thyroid biology. [22] [23] In the initial phase of major non-thyroidal illness syndrome (NTIS) SPINA-GT may be temporarily elevated. [24] [25] In chronic NTIS [26] as well as in certain non-critical chronic diseases, e.g. chronic fatigue syndrome [27] [28] or asthma [29] SPINA-GT is slightly reduced.

According to the results of a community-based study in China it was associated to sleep duration and exercise habits. [30] With respect to iodine supply, it showed a complex U-shaped pattern, being reduced in subjects consuming iodine-rich food, but elevated in situations of iodine excess. [30] In two other studies from China, SPINA-GT correlated with negative direction to markers of obesity including body mass index, waist circumference and waist to hip ratio. [31] [32] This doesn't seem to be the case, however, in Western populations. [33]

In women, therapy with Metformin results in increased SPINA-GT, in parallel to improved insulin sensitivity. [34] [35] This observation was reproducible in men with hypogonadism, but not in men with normal testosterone concentrations,. [36] In postmenopausal women this effect was only observed in subjects on oestradiol replacement therapy. [37] Therefore, the described phenomenon seems to depend on an interaction of metformin with sex hormones. [36] [38] In hyperthyroid [8] men both SPINA-GT and SPINA-GD negatively correlate to erectile function, intercourse satisfaction, orgasmic function and sexual desire. Likewise, in women with thyrotoxicosis elevated thyroid's secretory capacity predicts depression and sexual dysfunction. [39] Conversely, in androgen-deficient men with concomitant autoimmune thyroiditis, substitution therapy with testosterone leads to a decrease in thyroid autoantibody titres and an increase in SPINA-GT. [40] In a large study from mainland China, SPINA-GT was elevated in certain psychiatric diseases including bipolar disorder and schizophrenia. [41] In bipolar disorder with manic or mixed episodes it was higher than in cases with depressive episodes. [41]

SPINA-GT is reduced in persons suffering from hidradenitis suppurativa compared to healthy controls with the same sex and age distribution. [42] This phenomenon has been ascribed to B-cell-mediated hypothyroidism, i.e. hypothyroid Graves' disease due to inhibiting TSH receptor autoantibodies (iTRAb). [42]

In patients with autoimmune thyroiditis a gluten-free diet results in increased SPINA-GT (in parallel to sinking autoantibody titres). [43] Statin therapy has the same effect, but only if supply with vitamin D is sufficient. [44] Accordingly, substitution therapy with 25-hydroxyvitamin D leads to rising secretory capacity. [45] [46] [47] [48] This effect is potentiated by substitution therapy with myo-inositol [49] and selenomethionine [45] [46] [50] or, in women, with dehydroepiandrosterone, [51] but impaired in males with early-onset androgenic alopecia. [52] The effects of vitamin D and selenomethionine are attenuated in hyperprolactinaemia, suggesting an inhibitory effect of prolactin. [53] Although both vitamin D supplementation and gluten-free diet result in increased SPINA-GT, there seems to be a complex interaction between both therapeutic measures, since vitamin D treatment is only able to elevate the thyroid's secretory capacity in subjects not following any dietary recommendation. [54]

On the other hand, men treated with spironolactone are faced with decreasing SPINA-GT (in addition to rising thyroid antibody titres). [55] It has, therefore, been concluded that spironolactone may aggravate thyroid autoimmunity in men. [55]

In subjects with type 2 diabetes, treatment with beta blockers resulted in decreased SPINA-GT, suggesting sympathetic innervation to contribute to the control of thyroid function. [56] In diabetic women, but not in men, SPINA-GT shows a positive correlation to the β-C-terminal cross-linked telopeptides of type I collagen (β-CTX), a marker of bone resorption. [57] In both diabetic and non-diabetic persons it correlates (negatively) with age and (positively) with the concentrations of troponin T and HbA1c. [58]

SPINA-GT correlates to mechanical pain sensitivity (MPS) in quantitative sensory testing (QST) and to measures of respiratory arrhythmia in the analysis of heart rate variability, indicating a potential link to both sensorimotor and autonomic neuropathy. [59]

A study in euthyroid subjects with structural heart disease found that increased SPINA-GT predicts the risk of malignant arrhythmia including ventricular fibrillation and ventricular tachycardia. [60] This applies to both incidence and event-free survival. [60] Likewise, SPINA-GT is elevated in a significant subgroup of patients with takotsubo syndrome, [61] especially in non-survivors. [62] A stress-mediated effect on SPINA-GT is also suggested by the observation that it is increased in persons with a history of psychological trauma. [63] On the other hand, two studies found negative correlation between SPINA-GT and markers of dispersion in cardiac repolarisation, including Tp-e interval, JT interval, Tp-e/ QT ratio and Tp-e/QTc ratio. These results suggest that reduced thyroid function may trigger cardiovascular mortality as well. [64] [9]

Among subjects with Parkinson's disease, SPINA-GT is significantly elevated in tremor-dominant and mixed subtypes compared to the akinetic-rigid type. [65]

Specific secretory capacity (SPINA-GTs) is reduced in obesity [2] and autoimmune thyroiditis. [7] [66]

Endocrine disruptors may affect stimulated thyroid output, as demonstrated by a positive correlation of SPINA-GT with exposure to 2-hydroxynaphthalene (2-NAP), [67] urinary mercury concentration [68] and the excretion of certain phthalate metabolites, [69] and negative correlation with combined exposure to polycyclic aromatic hydrocarbons (PAHs) [67] and nickel. [70] Additionally, SPINA-GT is altered in persons exposed to butylparaben and propylparaben. [71] [72]

In a longitudinal evaluation of a large sample of the general US population over 10 years, reduced SPINA-GT significantly predicted all-cause mortality. [73]

See also

Notes

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

References

  1. ↑ Hoermann R, Midgley J, Larisch R, Dietrich JW (4 August 2021). "Treatment options for subclinical hypothyroidism". European Journal of Endocrinology. 185 (3): L5 –L6. doi: 10.1530/EJE-20-1405 . PMID   34243143.
  2. 1 2 3 4 5 6 7 8 9 10 11 Dietrich, J. W. (2002). Der Hypophysen-Schilddrüsen-Regelkreis. Berlin, Germany: Logos-Verlag Berlin. ISBN   978-3-89722-850-4. OCLC   50451543. OL   24586469M.
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  4. ↑ Bierich JR (1964). "Endokrinologie". In H. Wiesener (ed.). Einführung in die Entwicklungsphysiologie des Kindes. Springer. p. 310. ISBN   978-3-642-86507-7.{{cite book}}: ISBN / Date incompatibility (help)
  5. ↑ Thompson MA (June 2001). "Radiation safety precautions in the management of the hospitalized (131)I therapy patient". Journal of Nuclear Medicine Technology. 29 (2): 61–6, test 74–5. PMID   11376097.
  6. ↑ 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 Endocrine Disorders. 8 (1): 13. doi: 10.1186/1472-6823-8-13 . PMC   2576461 . PMID   18851740.
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