Clinical, or overt, hypothyroidism complicates approximately 2 per 1000 pregnancies. Clinical hypothyroidism is diagnosed when an abnormally high serum thyrotropin (TSH) level is accompanied by an abnormally low free thyroxine (T4) level. The most common etiology is glandular destruction by autoantibodies or Hashimoto thyroiditis. Thyroid peroxidase (TPO) antibodies have been identified in 5 to 15 percent of pregnant women, up to half of whom later in life develop an autoimmune thyroiditis.
Overt hypothyroidism is associated with infertility. When pregnancy does occur, there are increased rates of maternal and fetal complications, to include preeclampsia, placental abruption, cardiac dysfunction, stillbirth, and prematurity. Fortunately, perinatal outcomes are usually normal with adequate treatment. Replacement therapy is with thyroxine, 50 to 100 μg daily. Serum TSH and free thyroxine levels are measured at 4- to 6-week intervals, and thyroxine adjusted by 25- to 50-μg increments until normal values are reached. Pregnancy is associated with an increase in thyroxine requirements of about a third; however, care should be individualized, as not all women require an adjustment in therapy.
Subclinical hypothyroidism is defined by an abnormally elevated TSH level with normal serum free T4 in an asymptomatic woman. The prevalence of subclinical hypothyroidism in pregnancy is approximately 2.3 percent. Approximately 2 to 5 percent of reproductive age women with subclinical disease per year progress to overt thyroid failure. Heredity is a potent risk factor. Other risk factors for thyroid failure include type-1 diabetes and thyroid peroxidase antibodies. Effects of subclinical hypothyroidism on pregnancy outcome are not clear. Pregnancies with subclinical hypothyroidism may be at increased risk for preterm birth or placental abruption.
EFFECT OF MATERNAL HYPOTHYROIDISM ON THE FETUS AND INFANT
Hypothyroidism—either overt or subclinical—has been reported to cause subnormal mental development. Elevated maternal TSH values have been associated with offspring who have diminished school performance, reading recognition, and intelligence quotient (IQ) scores as compared with matched controls. Some organizations have recommended prenatal screening and treatment for subclinical disease. However, the American College of Obstetricians and Gynecologists continues to recommend against routine screening. Randomized placebo-controlled trials to determine risks or benefits of detecting and treating subclinical thyroid dysfunction in pregnancy are in progress.
In the United States over the past 25 years, iodide fortification of table salt and bread products has diminished, and iodide deficiency has been identified in some of the population. Adequate iodide is requisite for normal fetal neurological development beginning soon after conception. The recommended daily intake during pregnancy is at least 220 μg/day. Severe deficiency is associated with endemic cretinism. Although not quantified, it is presumed that moderate deficiency has intermediate and variable effects on intellectual and psychomotor function. Although it is doubtful that mild deficiency causes intellectual impairment, supplementation prevents fetal goiter.
Congenital hypothyroidism is found in about 1 in 2500 infants. Because the clinical diagnosis of hypothyroidism in neonates is usually missed, newborn mass screening was introduced in the United States in 1974 and is now required by law. Early and aggressive thyroxine replacement is critical. Follow-up data from infants identified by screening programs who were treated promptly and adequately are encouraging. Most, if not all, sequelae of congenital hypothyroidism—including intellectual impairment—are typically preventable.
For further reading in Williams Obstetrics, 23rd ed.,
see Chapter 53, “Thyroid and Other Endocrine Disorders.”