Non-Thyroidal Illness Syndrome

Abstract

Patients admitted to the intensive care unit with lifethreatening diseases may develop low T3 syndrome including low T3, normal or low T4, increased rT3, and the absence of increase in the thyroid stimulating hormone (TSH) levels. The pathophysiology of low T3 syndrome is still imperfectly understood. The intensity of biological alterations seems correlated to the disease severity. Decrease in T4 appears as a possible prognosticator, with a 50%-mortality rate if T4 is less than 4 μg/dl and 80%-mortality rate if less than 2 μg/dl. However, all the biological alterations are reversible as soon as the underlying disease has been treated. In the acute phase, the low T3 syndrome appears to be beneficial as an adaptive mechanism in response to the aggression-induced hypercatabolism, explained by several mechanisms like abnormal transport and increased peripheral uptake of thyroid hormones and altered expression and activity of type 1 and 3 desiodinase enzymes. During the chronic phase of patient’s care, low T3 syndrome is more related to the hypothalamic–pituitary–thyroid axis dysfunction, characterized by a decrease in thyrotropin releasing hormone (TRH), TSH and T3-T4 hormones. Whether these changes should be considered as related to an adaptive mechanism or not, even their role in the lack of recovery from the syndrome is unknown. Accordingly, the absence of anabolism contributes to muscle atrophy, prolonging the patient’s dependence on the ventilator. The prescription of thyroid hormones or TSH does not improve the final prognosis. A possible benefit of TRH infusion in combination with the growth hormone (GH) in the chronic phase needs to be confirmed.