Hypothyroidism in Pregnancy
WHAT ARE THE NORMAL CHANGES IN THYROID FUNCTION ASSOCIATED WITH PREGNANCY?
HORMONE CHANGES. Thyroid function tests change during normal pregnancy due to the influence of two main hormones: human chorionic gonadotropin (hCG) and estrogen. Because hCG can weakly stimulate the thyroid, the high circulating hCG levels in the first trimester may result in a low TSH that returns to normal throughout the duration of pregnancy. Estrogen increases the amount of thyroid hormone binding proteins, and this increases the total thyroid hormone levels but the “Free” hormone (the amount that is not bound and can be active for use) usually remains normal. The thyroid is functioning normally if the TSH and Free T4 remain in the trimester-specific normal ranges throughout pregnancy.
THYROID SIZE CHANGES. The thyroid gland can increase in size during pregnancy (enlarged thyroid = goiter). However, pregnancy-associated goiters occur much more frequently in iodine-deficient areas of the world. It is relatively uncommon in the United States. If very sensitive imaging techniques (ultrasound) are used, it is possible to detect an increase in thyroid volume in some women. This is usually only a 10-15% increase in size and is not typically apparent on physical examination by the physician. However, sometimes a significant goiter may develop and prompt the doctor to measure tests of thyroid function (see Thyroid Function Test Brochure).
Hypothroidism in Pregnancy FAQs
The thyroid gland is a butterfly-shaped endocrine gland that is normally located in the lower front of the neck. The thyroid’s job is to make thyroid hormones, which are secreted into the blood and then carried to every tissue in the body. Thyroid hormones help the body use energy, stay warm and keep the brain, heart, muscles, and other organs working as they should.
For the first 18-20 weeks of pregnancy, the baby is completely dependent on the mother for the production of thyroid hormone. By mid-pregnancy, the baby’s thyroid begins to produce thyroid hormone on its own. The baby, however, remains dependent on the mother for ingestion of adequate amounts of iodine, which is essential to make the thyroid hormones. The World Health Organization recommends iodine intake of 250 micrograms/day during pregnancy to maintain adequate thyroid hormone production. Because iodine intakes in pregnancy are currently low in the United States, the ATA recommends that US women who are planning to become pregnant, who are pregnant, or breastfeeding, should take a daily supplement containing 150 mcg of iodine.
HYPOTHYROIDISM & PREGNANCY
WHAT ARE THE MOST COMMON CAUSES OF HYPOTHYROIDISM DURING PREGNANCY?
Overall, the most common cause of hypothyroidism is the autoimmune disorder known as Hashimoto’s thyroiditis (see Hypothyroidism brochure). Hypothyroidism can occur during pregnancy due to the initial presentation of Hashimoto’s thyroiditis, inadequate treatment of a woman already known to have hypothyroidism from a variety of causes, or over-treatment of a hyperthyroid woman with anti-thyroid medications. Approximately, 2.5% of women will have a TSH of greater than 6 mIU/L (slightly elevated) and 0.4% will have a TSH greater than 10 mIU/L during pregnancy.
Untreated, or inadequately treated, hypothyroidism has increased risk of miscarriage, and has been associated with maternal anemia, myopathy (muscle pain, weakness), congestive heart failure, pre-eclampsia, placental abnormalities, and postpartum hemorrhage (bleeding). These complications are more likely to occur in women with severe hypothyroidism. Some risks also appear to be higher in women with antibodies against thyroid peroxidase (TPO). Women with mild hypothyroidism may have no symptoms or attribute symptoms they have to the pregnancy.
Thyroid hormone is critical for brain development in the baby. Children born with congenital hypothyroidism (no thyroid function at birth) can have severe cognitive, neurological and developmental abnormalities if the condition is not recognized and treated promptly. With early treatment, these developmental abnormalities largely can be prevented. Consequently, all newborn babies in the United States are screened for congenital hypothyroidism so they can be treated with thyroid hormone replacement therapy as soon as possible.
Untreated severe hypothyroidism in the mother can lead to impaired brain development in the baby. Recent studies have suggested that mild developmental brain abnormalities also may be present in children born to women who had mild untreated hypothyroidism during pregnancy. At this time, there is no general consensus of opinion regarding screening all women for hypothyroidism during pregnancy. However, the ATA recommends checking a woman’s TSH as soon as pregnancy is confirmed in women at high risk for thyroid disease, such as those with prior treatment for hyper- or hypothyroidism, a family history of thyroid disease, a personal history of autoimmune disease, and those with a goiter.
Women with established hypothyroidism should have a TSH test as soon as pregnancy is confirmed. They also should immediately increase their levothyroxine dose, because thyroid hormone requirements increase during pregnancy. (See below for specific dosing recommendations.) If new onset hypothyroidism has been detected, the woman should be treated with levothyroxine to normalize her TSH values (see Hypothyroidism brochure).
Women found to have a TSH level greater than 10 mIU/L in the first trimester of pregnancy should be treated for hypothyroidism. Conversely, women with a TSH of 2.5 or less, do not need levothyroxine treatment. For women with TSH measured between these (2.5-10), ATA recommendations for treatment vary and may depend on whether or not the mother has TPO antibodies. When TPO antibodies are positive, treatment is recommended when the TSH is above 4 and should be considered when the TSH is between 2.5-4.0. However, when there are no TPO antibodies (i.e. negative), current ATA recommendations are less strong and suggest that treatment ‘may be considered’ when TSH is between 2.5-10.0 mIU/L. These recommendations are based on the degree of evidence that exists that treatment with levothyroxine would be beneficial.
The goal of treating hypothyroidism in a pregnant woman is adequate replacement of thyroid hormone. Ideally, hypothyroid women should have their levothyroxine dose optimized prior to becoming pregnant. Levothyroxine requirements frequently increase during pregnancy, usually by 25 to 50 percent. Hypothyroid women taking levothyroxine should independently increase their dose by 20%–30% as soon as pregnancy is diagnosed and should notify their doctor for prompt testing and further evaluation. One means of accomplishing the dose increase is to take two additional tablets weekly of their usual daily levothyroxine dosage. Thyroid function tests should be checked approximately every 4 weeks during the first half of pregnancy to ensure that the woman has normal thyroid function throughout pregnancy. As soon as delivery of the child occurs, the woman may go back to her usual prepregnancy dose of levothyroxine. It is also important to recognize that prenatal vitamins contain iron and calcium that can impair the absorption of thyroid hormone from the gastrointestinal tract. Consequently, levothyroxine and prenatal vitamins should not be taken at the same time and should be separated by at least 4 hours.
In addition to the dosing and testing considerations explained in this brochure, women with a history of Graves’ disease who were treated with radioiodine (RAI) or surgical thyroidectomy should also have Graves’ antibodies (TRAb) tested early in pregnancy to assess the risk of passing antibodies on to the fetus. If antibodies are elevated, follow-up testing is recommended at weeks 18- 22, and if antibodies are still elevated, additional follow-up is recommended at weeks 30-34 to evaluate the need for fetal and neonatal monitoring.