During illness changes in thyroid hormone metabolism occur, collectively known as the non-thyroidal illness syndrome (NTIS). NTIS is characterized by low serum thyroid hormone levels, while TSH and TRH expression do not increase, indicating a disturbance of the normal thyroid hormone feedback regulation.
Although the common view was that NTIS results in overall downregulation of metabolism in order to save energy, recent work has shown that genes involved in thyroid hormone (TH) metabolism show remarkably variable, illness-induced changes in key metabolic organs such as liver, muscle and adipose tissue, ranging from inhibition to activation. That illness-induced changes in peripheral organs appear to be very different during acute or chronic inflammation adds an additional level of complexity. Organ- and timing-specific changes in the TH deiodinating enzymes (deiodinase type 1, 2 and 3) highlight deiodinases as proactive players in the response to illness. Furthermore, the granulocyte is a novel and potentially important cell type involved in NTIS during bacterial infection. Finally, complex changes in thyroid hormone metabolism occur in muscle during critical illness that may be relevant for the pathogenesis of respiratory failure. Although acute NTIS may represent an adaptive response to support the immune response, NTIS may turn disadvantageous when critical illness enters a chronic phase necessitating prolonged mechanical ventilation, dialysis and inotropic support.
In sum, NTIS appears to be a timing-related and organ-specific response to illness, occurring independently from the decrease in serum thyroid hormone levels and potentially relevant for disease course.
30 Apr - 04 May 2011
European Society of Endocrinology