![]() The fall in serum albumin level in euthyroid sick syndrome enhances the activity of different competitors of T4 on thyroid-binding globulin. Serum albumin binds to fatty acids, which displaces thyroid hormones from the thyroid-binding globulin. Several other mechanisms can contribute to the inhibition of 5'-monodeiodination, causing a decrease in the concentration of serum total T3 levels in patients with a nonthyroidal illness, such as high serum cortisol and the use of exogenous corticosteroid therapy, as well as other medications like amiodarone and propranolol. The peripheral deiodinase activity type 1 is downregulated, and the central type 2 and type 3 deiodinase activities are up-regulated in critically ill patients. Cytokines were also thought to reduce the activity of type 1 deiodinase and decrease the binding capacity of the T3 nuclear receptors. The euthyroid sick syndrome is also caused by cytokines such as interleukin 1, interleukin 6, tumor necrosis factor-alpha, and interferon-beta affecting the hypothalamus and pituitary glands, thus inhibiting TSH, thyroid-releasing hormone (TRH), thyroglobulin (TG), T3, and the thyroid-binding globulins (TBG) production. One cause suggested is when the presence of thyroid-binding hormone inhibitors in the serum and different body tissues inhibits the binding of the thyroid hormone to the thyroid-binding protein. There are many proposed mechanisms regarding the pathogenesis of euthyroid sick syndrome.
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