Introduction

Abstract

Thyroid hormones are unique in that they are formed from the coupling and iodination of a nonessential amino acid, tyrosine. The thyroid almost exclusively produces thyroxine (T4), a precursor of the active hormone, triiodothyronine (T3). T3 is largely derived from deiodination of T4 in peripheral tissues, a still partially understood method for regionally regulating T3 levels. The thyroid also secretes a small amount of T3, but the physiological relevance of this is unclear. Upon binding with its ubiquitous nuclear receptors, T3 facilitates or activates transcription of a great variety of genes throughout almost all organ systems [1]. It is therefore not surprising that lack of thyroid hormones affects several physiologic pathways. Since T4, (after being deiodinated in the tyrotroph to T3) is largely predominant in the regulation of TSH production at the pituitary-hypothalamic levels and since TSH is the only natural regulator of T4 production, serum TSH levels are very tightly correlated to serum T4 levels. However changes in T4 result in TSH changes on a logarithmic scale. As a consequence, when the hypothalamic-pituitary-thyroid axis feedback mechanism is preserved, thyroid function can be effectively tested through TSH measurements.