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Related Experiment Videos

Tissue thyroid hormone levels in critical illness.

Robin P Peeters1, Serge van der Geyten, Pieter J Wouters

  • 1Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands.

The Journal of Clinical Endocrinology and Metabolism
|September 22, 2005
PubMed
Summary

During critical illness, reduced serum triiodothyronine (T3) correlates with lower T3 levels in liver and muscle tissues. This suggests tissue-specific mechanisms contribute to decreased bioactive thyroid hormone supply.

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Area of Science:

  • Endocrinology
  • Critical Care Medicine
  • Molecular Biology

Background:

  • Critical illness causes significant changes in serum thyroid hormones, with decreased triiodothyronine (T3) and increased reverse triiodothyronine (rT3).
  • The relationship between altered serum thyroid hormone levels and actual tissue concentrations, impacting thyroid hormone bioactivity, remains unclear.

Purpose of the Study:

  • To investigate whether serum thyroid hormone levels reflect tissue levels in liver and muscle of critically ill patients.
  • To examine the correlation between tissue thyroid hormone levels, deiodinase activities, and monocarboxylate transporter 8 expression.

Main Methods:

  • Analysis of serum and tissue (liver, muscle) iodothyronine levels in 79 non-surviving intensive care patients.
  • Assessment of deiodinase activities and monocarboxylate transporter 8 expression in relation to thyroid hormone levels.

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Main Results:

  • Tissue iodothyronine levels, including T3, were positively correlated with serum levels.
  • Thyroid hormone treatment in patients led to higher liver and muscle T3 concentrations, indicating tissue-specific regulation.
  • Tissue rT3 and the T3/rT3 ratio correlated with deiodinase activities, but monocarboxylate transporter 8 expression did not correlate with serum/tissue iodothyronine ratios.

Conclusions:

  • Serum thyroid hormone levels generally correspond to tissue levels in critically ill patients.
  • Tissue-specific mechanisms, beyond hypothalamic-pituitary-thyroid axis changes, contribute to reduced bioactive thyroid hormone availability during critical illness.