ABSTRACT
Hypothyroidism is a condition in which the thyroid gland produces amounts of thyroid hormones that are insufficient to satisfy the requirements of peripheral tissues. The normal thyroid gland secretes both thyroxine (T4) and triiodothyronine (T3). T4 is converted to T3 in peripheral tissues by the enzyme 5’ deiodinase (1); 85% of circulating T3 is produced by peripheral conversion from T4, whereas 15% is directly secreted from the thyroid gland (2,3). Both T4 and T3 are transported across target cell membranes to enter the cytoplasm and later the nucleus where they bind to specific thyroid hormone receptors. T3 binds to these receptors with about 10-fold higher affinity than does T4. The thyroid hormone-receptor complex then binds with other cofactors to the regulatory regions of thyroid hormone responsive genes, where it governs the production of various proteins that mediate thyroid hormone effects (4-7). Receptors for thyroid hormones are located in multiple tissues throughout the body, being most abundant in pituitary, brain, liver, kidney, heart, muscle, bone, and skin cells (6,7). The multitude of thyroid hormone responsive tissues throughout the body underlies the diverse array of clinical features that may be seen in patients experiencing thyroid hormone deficiency.
