This is the active thyroid hormone, triiodothyronine (T3). This conversion takes place primarily at the cellular level within tissues; only 20% of circulating T3 is generated by conversion of T4 within the thyroid gland itself.
Desyodinases: are the gatekeepers of intracellular thyroid hormone bioavailability.
This system not only controls the relative amounts of active and inactive hormone in the cell, but also has the effect of conserving iodine, which has multiple intracellular functions (in the thyroid gland, iodine is recycled for the synthesis of more thyroxine).
Since its description in the 1970s, it has been described that the thyroid profile shows decreased serum triiodothyronine (T3) levels and increased serum reverse triiodothyronine (T3r) levels in patients with acute illness with no history of thyroid disease.
Because of these changes, this entity is also known as «low T3 syndrome» or «sick thyroid».
Various disease states and some drugs alter the expression of individual desyodases and thus change the relative concentrations of circulating hormones.
In normal adults, rT3 circulates at approximately 40 times the level of free T3 (the reference range in normal adults for rT3 is about 9-25 ng/dL, whereas for free T3 it is 2.5-6.5 pg/mL, i.e. 0.25-0.65 ng/dL).
The relative levels of rT3 and T3 are affected by factors that stimulate or inhibit the activities of desyodases, as described below.
What is reverse T3:
Reverse T3 (3,3 ‘, 5’-triiodothyronine, rT3) is a biologically inactive metabolite of thyroxine (T4) formed by selective disiodination; the active thyroid hormone T3 is formed by removal of an iodine atom on the outer ring of T4, whereas rT3 is formed by removal of an iodine atom on the inner ring of T4.
The relative amounts of each are determined by the activity of the respective desyodase enzymes, which are regulated by hormonal and nutritional factors and physiological conditions.
-Changes in fasting or malnutrition states are secondary to an adaptive response (increased catabolic state), caloric restriction is recognized as a D1 inhibitory factor, with decreased serum T3 concentrations and increased T3r.
– No benefit has been demonstrated with the use of exogenous thyroid hormones in hospitalized patients, critically ill patients in intensive care units, burned individuals, persons with acute renal disease or those undergoing kidney transplantation.
-In patients with a history of trauma or sepsis, D2 expression in the hypothalamus is increased, with a consequent increase in T3 supply, which suppresses TRH production.
– In patients undergoing cardiac bypass, decreased serum levels of T4 and T3 and increased T3r are found in the first 30 minutes after the start of the procedure and persist for several days, there is no strong evidence that hormonal treatment with T3 has a favorable effect.
-In cases of organ donors, specifically heart donors with associated brain death, the administration of four hormones is recommended for maintenance: vasopressin, methylprednisolone, insulin and T3, in patients with left ventricular ejection fraction < 45% and/or hemodynamic instability. -Most of the studies performed so far have not found that hormone replacement therapy improves patient prognosis, but neither have they shown a deleterious effect. Finally, there is no evidence to indicate pharmacological treatment with the aim of improving serum thyroid hormone levels in the context of sick euthyroid syndrome. Pathologies that should be included in the differential diagnosis of sick euthyroid syndrome are Hashimoto's thyroiditis, primary and secondary hyperthyroidism, thyrotoxicosis, panhypopituitarism and thyroid hormone dysfunction secondary to amiodarone treatment. -References: -Van den Berghe G. Non-thyroidal illness in the ICU: a syndrome with different faces.Thyroid. 2014; 24 (10): 1456-1465. -Krysiak R, Kędzia A, Kowalcze K, Okopień B. Euthyroid sick syndrome: an important clinical problem. 2017; 70 (2 pt 2): 376-385.