摘要：In an average adult, the thyroid gland produces around 80 mcg of thyroxine (T4) and 20 mcg of triiodothyronine (T3) per day to match the body’s metabolic demands. Thus, the activation of the prohormone T4 to the active hormone T3 mainly occurs at peripheral organs, a process fine-tuned by the deiodinases type 1 (D1) and 2 (D2) enzymes accordingly to specific tissue needs. The physiological background and the fact that some patients remain symptomatic regardless of normal thyrotropin (TSH) levels under levothyroxine (LT4) replacement has fuelled the interest in the potential theoretical advantages of adding liothyronine (LT3) to LT4 as a therapeutic strategy. Given that D2 activates approximately 60% of circulating T3 and that some genetic variants of D2, like the D2-Thr92Ala polymorphism, are associated with impaired enzyme activation of T4 into T3, patients homozygotic for the D2-Ala92 genotype might comprise a group that could benefit from combined LT4 + LT3 therapy (3-5). Notwithstanding, despite some preliminary studies had indicated that this might be the case, these findings remain to be confirmed in larger studies before being routinely incorporated in clinical practice.
