scholarly journals IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells

2011 ◽  
Vol 121 (5) ◽  
pp. 1834-1845 ◽  
Author(s):  
Simone Magagnin Wajner ◽  
Iuri Martin Goemann ◽  
Ana Laura Bueno ◽  
P. Reed Larsen ◽  
Ana Luiza Maia
Keyword(s):  
Thyroid Hormone ◽  
Human Cells ◽  
Nonthyroidal Illness ◽  
Hormone Inactivation

Predictive value of thyroxine for prognosis in pediatric septic shock: a prospective observational study

2020 ◽  
Vol 33 (5) ◽  
pp. 653-659
Author(s):  
Jia Song ◽  
Yun Cui ◽  
Chunxia Wang ◽  
Jiaying Dou ◽  
Huijie Miao ◽  
...  
Keyword(s):  
Septic Shock ◽  
Thyroid Hormone ◽  
Observational Study ◽  
Hospital Mortality ◽  
Predictive Value ◽  
Prospective Observational Study ◽  
Threshold Value ◽  
Nonthyroidal Illness ◽  
Hormone Levels ◽  
Thyroid Hormone Levels

AbstractBackgroundThyroid hormone plays an important role in the adaptation of metabolic function to critically ill. The relationship between thyroid hormone levels and the outcomes of septic shock is still unclear. The aim of this study was to assess the predictive value of thyroid hormone for prognosis in pediatric septic shock.MethodsWe performed a prospective observational study in a pediatric intensive care unit (PICU). Patients with septic shock were enrolled from August 2017 to July 2019. Clinical and laboratory indexes were collected, and thyroid hormone levels were measured on PICU admission.ResultsNinety-three patients who fulfilled the inclusion criteria were enrolled in this study. The incidence of nonthyroidal illness syndrome (NTIS) was 87.09% (81/93) in patients with septic shock. Multivariate logistic regression analysis showed that T4 level was independently associated with in-hospital mortality in patients with septic shock (OR: 0.965, 95% CI: 0.937–0.993, p = 0.017). The area under receiver operating characteristic (ROC) curve (AUC) for T4 was 0.762 (95% CI: 0.655–0.869). The cutoff threshold value of 58.71 nmol/L for T4 offered a sensitivity of 61.54% and a specificity of 85.07%, and patients with T4 < 58.71 nmol/L showed high mortality (60.0%). Moreover, T4 levels were negatively associated with the pediatric risk of mortality III scores (PRISM III), lactate (Lac) level in septic shock children.ConclusionsNonthyroidal illness syndrome is common in pediatric septic shock. T4 is an independent predictor for in-hospital mortality, and patients with T4 < 58.71 nmol/L on PICU admission could be with a risk of hospital mortality.

Nonthyroidal illness

2011 ◽  
pp. 336-344
Author(s):  
R.P. Peeters
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Disease ◽  
Clinical Signs ◽  
Negative Energy ◽  
Nonthyroidal Illness ◽  
Hormone Levels ◽  
Euthyroid Sick Syndrome ◽  
Thyroid Hormone Levels ◽  
Low Levels ◽  
Save Energy

A few hours after the onset of acute illness, marked changes in serum thyroid hormone levels occur. This is referred to as nonthyroidal illness (NTI). The most characteristic and persistent abnormality is a low level of serum triiodothyronine (T3). Despite these low levels of serum T3, patients usually have no clinical signs of thyroid disease. Other terms for this disease state have been used, e.g. the low T3 syndrome and the euthyroid sick syndrome. In addition to nonthyroidal illness, a low T3 in euthyroid patients is seen during caloric deprivation and after the use of certain types of medication (see Chapter 3.1.4). Low levels of thyroid hormone in hypothyroidism are associated with a decreased metabolic rate. Both in nonthyroidal illness and in fasting there is a negative energy balance in the majority of cases. Therefore the low levels of T3 during nonthyroidal illness and starvation have been interpreted as an attempt to save energy expenditure, and intervention is not required. However, this remains controversial and has been a debate for many years. In this chapter, the changes in thyroid hormone levels, the pathophysiology behind these changes, the diagnosis of intrinsic thyroid disease, and the currently available evidence whether these changes should or should not be corrected will be discussed (Box 3.1.5.1).

scholarly journals Nonthyroidal Illness Syndrome and Thyroid Hormone Actions at Integrin αvβ3

2018 ◽  
Vol 103 (4) ◽  
pp. 1291-1295 ◽  
Author(s):  
Aleck Hercbergs ◽  
Shaker A Mousa ◽  
Paul J Davis
Keyword(s):  
Thyroid Hormone ◽  
Integrin Αvβ3 ◽  
Nonthyroidal Illness

scholarly journals Effects of Thyroid Hormone Treatment on Diaphragmatic Efficiency in Mechanically Ventilated Subjects With Nonthyroidal Illness Syndrome

2019 ◽  
Vol 64 (10) ◽  
pp. 1199-1207 ◽  
Author(s):  
Giuseppe Bello ◽  
Giorgia Spinazzola ◽  
Valentina Giammatteo ◽  
Luca Montini ◽  
Gennaro De Pascale ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Treatment ◽  
Nonthyroidal Illness ◽  
Mechanically Ventilated

scholarly journals Type 1 deiodinase is stimulated by iodothyronines and involved in thyroid hormone metabolism in human somatomammotroph GX cells

1999 ◽  
pp. 367-370 ◽  
Author(s):  
A Baur ◽  
J Kohrle
Keyword(s):  
Thyroid Hormone ◽  
Anterior Pituitary ◽  
Specific Activity ◽  
Thyroid Hormone Metabolism ◽  
Phenolic Ring ◽  
Liver Membranes ◽  
Significant Release ◽  
Hormone Inactivation ◽  
Serum Free Conditions

BACKGROUND: Local 5'-deiOdination of l-thyroxine (T4) to the active thyroid hormone, 3,3',5-tri-iodothyronine (T3) via two deiodinase isoenzymes (D1 and D2) has an important role for various T3-dependent functions in the anterior pituitary. However, no evidence has been presented yet for thyroid hormone inactivation via the 5-deiodinase (D3) in anterior pituitary models. METHODS: Using the human somatomammotroph cell line, GX, we analysed effects of T3 and its 5'-deiodination product, 3,5-di-iodothyronine (3,5-T2), on deiodinase activities, measuring release of iodide-125 (125I-) from phenolic-ring- or tyrosyl-ring-labelled substrates respectively. RESULTS: T3 and 3,5-T2 rapidly stimulated D1 activity in GX cells in the presence of serum in the culture medium, whereas D2 activity was not detectable under these conditions. However, when the cells were kept under serum-free conditions, specific activity of D2 reached levels similar to those of D1. With tyrosyl-ring labelled 3, 5-[125I]-,3'-T3 as substrate, a significant release of 125I- was observed in GX cell homogenates. This is comparable to the D1 activity of liver membranes, which preferentially catalyses 5'-deiodination, but to some extent also 5-deiodination, at the tyrosyl ring. CONCLUSIONS: D1 activity of human GX cells is increased by T3 and 3,5-T2. Inactivation of T3 in the anterior pituitary might occur by deiodination at the tyrosyl ring via D1, thus terminating the stimulatory thyroid hormone signal in human somatomammotroph cells.

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