Up to 20% of treated hypothyroid patients have residual hypothyroid complaints despite normalized thyroid-stimulating hormone (TSH) and free thyroxine (FT4) levels. The pathophysiological mechanism behind these persistent complaints is one of the major unresolved questions in thyroidology. In euthyroid individuals, ~20% of serum triiodothyronine (T3) results from direct thyroidal secretion, with the remainder derived from extrathyroidal conversion of T4 to T3 by type 1 and 2 deiodinase (D1 and D2). The vast majority of hypothyroid patients are treated with levothyroxine (LT4) monotherapy, and their serum T3 levels are therefore fully dependent on extrathyroidal T3 production. Thus, patients receiving LT4 monotherapy generally have higher T4/T3 ratios than euthyroid individuals. Some patients with normalized TSH levels will have serum T3 levels at the lower end or even less than the reference range, with high FT4 levels. D2 accounts for ～70% of circulating serum T3 levels in humans,...
展开▼
