Context: Critical illness is associated with the low T3syndrome. It remains unclear whether altered type II deiodinase activity (D2) in skeletal muscle contributes to this syndrome. Objective: Our objective was to study D2 expression and activity in skeletal muscle of acute and prolonged critically ill patients. Design and Setting: We conducted a clinical observational study in acute and prolonged critical illness with comparison with healthy controls at a university hospital surgical intensive care unit. Patients: Subjects included 63 prolonged critically ill patients who died in the intensive care unit, 21 acutely ill patients, and 38 controls matched for age, gender, and body mass index. 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 T3syndrome of critical illness. Copyright,
Journal of Clinical Endocrinology and Metabolism
Erasmus MC: University Medical Center Rotterdam

Mebis, L., Langouche, L., Visser, T., & van den Berghe, G. (2007). Brief report: The type II iodothyronine deiodinase is up-regulated in skeletal muscle during prolonged critical illness. Journal of Clinical Endocrinology and Metabolism, 92(8), 3330–3333. doi:10.1210/jc.2007-0510