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This version published online on May 15, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2007-0510
A more recent version of this article appeared on August 1, 2007
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Submitted on March 6, 2007
Accepted on May 7, 2007

The Type II Iodothyronine Deiodinase is Upregulated in Skeletal Muscle During Prolonged Critical Illness

Liese Mebis, Lies Langouche, Theo J. Visser, and Greet Van den Berghe*

Department of Intensive Care Medicine, Katholieke Universiteit Leuven, B-3000 Leuven, Belgium; Department of Internal Medicine, Erasmus University Medical Center, 3015 GE Rotterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: greet.vandenberghe{at}med.kuleuven.be.

Context. Critical illness is associated with the ‘low T3 syndrome’. It remains unclear whether altered type II deiodinase activity (D2) in skeletal muscle contributes to this syndrome.

Objective. To study D2 expression and activity in skeletal muscle of acute and prolonged critically ill patients.

Design. A clinical observational study in acute and prolonged critical illness with comparison to healthy controls.

Setting. A university hospital surgical intensive care unit and a university animal laboratory.

Patients. Sixty-three prolonged critically ill patients who died in ICU, 21 acutely ill patients and 38 controls matched for age, gender and BMI.

Results. Elevated expression of the D2 gene and D2 activity in skeletal muscle of prolonged, but not acute, critically ill patients were observed in the face of low circulating thyroid hormone levels.

Conclusions. Reduced D2 activity does not appear to play a role in the pathogenesis of the low T3 syndrome of critical illness.




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J Kwakkel, O Chassande, H C van Beeren, W M Wiersinga, and A Boelen
Lacking thyroid hormone receptor {beta} gene does not influence alterations in peripheral thyroid hormone metabolism during acute illness
J. Endocrinol., April 1, 2008; 197(1): 151 - 158.
[Abstract] [Full Text] [PDF]


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