The thyroid gland is located anteriorly in the neck and consists of two lobes joined by the isthmus. The thyroid plays an important role in fetal development, childhood development, and adult metabolism. Thyroid dysfunction in pregnancy can be associated with significant maternal and fetal morbidity.1 Therefore, an understanding of thyroid physiology changes in pregnancy and evaluation and treatment of thyroid dysfunction is essential in ensuring both maternal and child health.
The thyroid gland functions mainly in synthesizing and releasing thyroid hormones into the blood stream. Starting in the hypothalamic neurons, thyroid-releasing hormone (TRH) is synthesized and exerts its effect on the anterior pituitary thyrotrophs.2 Under this effect, thyroid-stimulating hormone (TSH) is synthesized by the anterior pituitary and released into the blood. The main target of TSH is the thyroid gland where activation of the TSH receptor promotes growth of thyroid cells and synthesis and release of thyroid hormones. Both TRH synthesis and TSH levels are regulated by negative feedback of the thyroid hormones on the hypothalamus and pituitary.2
Circulating TSH binds to the TSH receptor on the cell membrane of thyroid cells. Activation of the TSH receptor results in increased uptake of iodine in the thyroid. Iodide is oxidized by thyroid peroxidase (TPO) and is coupled to tyrosine on thyroglobulin to form mono-iodotyrosine (MIT) and di-iodotyrosine (DIT).3 These are stored in the glycoprotein thyroglobulin within the thyroid follicle. Thyroxine (T4) is synthesized when two DIT molecules are coupled together and tri-iodothyronine (T3) is synthesized when one MIT and one DIT molecules are joined. More than 99% of thyroid hormone molecules circulate in blood bound to proteins with the largest fraction bound to thyroid-binding globulin (TBG). The concentration of free T4 is higher than that of free T3 but T3 is more potent than T4.3
In peripheral tissues, thyroid hormones exert their effects by binding to receptors in the nucleus of the cell and exerting their effects on DNA transcription. In the kidney and the liver, T4 is de-iodinated by deiodinases to T3, which is more active than T4. T4 is also de-iodinated by different deiodinases to make reverse T3, which has no cellular activity.4 More than 80% of the T3 levels come from peripheral conversion of T4. The half-life of T3 is 1 day, whereas that of T4 is 1 week. The long half-life of T4 coupled with its storage in the thyroid explains the length of time required to detect hormone level changes following adjustment of thyroid medication.
CHANGES IN THYROID PHYSIOLOGY IN PREGNANCY
Several changes occur in thyroid physiology in pregnancy, which alter the level of thyroid hormones. Understanding these changes is important in the medical management of thyroid disease as normal ranges of thyroid function tests used outside of pregnancy are not valid during pregnancy. One of the changes observed in ...