There is a lot of controversy about whether reverse T3 (rT3) should be measured to assess hypothyroidism. The normal thyroid gland secretes T4 (an inactive precursor), T3 (the active hormone), and reverse T3, a biologically inactive form of T3 that may block T3 from binding to the thyroid hormone receptor. Most of the circulating T3 is derived from 5′-deiodination of circulating T4 in the peripheral tissues by type 1 deiodinase. Deiodination of T4 can occur at the outer ring (5′- deiodination), producing T3 (3,5,3′-triiodothyronine), or at the inner ring, producing reverse T3 (3,3,5′-triiodothyronine) by type 3 deiodinase. Type 2 deiodinase in the pituitary also converts T4 to T3 and is regulated differently from type 1 deiodinase.
Many years ago, endocrinologists realized that in severe illnesses, type 3 deiodinase increases and rT3 is often high and T3 is often low. Endocrinologists termed this “sick euthyroid syndrome” and noted that it was common in many types of chronic illnesses, especially in patients hospitalized in intensive care units. It was usually recommended that these patients not be treated with thyroid hormone and in most cases, the elevated rT3 resolved when the patients' health returned.
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Many years ago, endocrinologists realized that in severe illnesses, type 3 deiodinase increases and rT3 is often high and T3 is often low. Endocrinologists termed this “sick euthyroid syndrome” and noted that it was common in many types of chronic illnesses, especially in patients hospitalized in intensive care units. It was usually recommended that these patients not be treated with thyroid hormone and in most cases, the elevated rT3 resolved when the patients' health returned.
MORE HERE
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