Thyroid disorders may predate or develop during pregnancy. Pregnancy does not change the symptoms of hypothyroidism and hyperthyroidism.
Fetal effects vary with the disorder and the drugs used for treatment. But generally, untreated or inadequately treated hyperthyroidism can result in
Untreated hypothyroidism can cause
The most common causes of maternal hypothyroidism are Hashimoto thyroiditis and treatment of Graves disease.
If women have or have had a thyroid disorder, thyroid status should be closely monitored during and after pregnancy in the women and in their offspring. Goiters and thyroid nodules discovered during pregnancy should be evaluated as they are in other patients (see Approach to the Patient With a Thyroid Nodule and Simple Nontoxic Goiter/Diagnosis).
Maternal Graves disease is monitored clinically and with free T4 and high-sensitivity thyroid-stimulating hormone (TSH) assays.
Treatment of Graves disease varies. Usually, pregnant women are given the lowest possible dose of oral propylthiouracil (50 to 100 mg every 8 hours). Therapeutic response occurs over 3 to 4 weeks; then the dose is changed if needed. Propylthiouracil crosses the placenta and may cause goiter and hypothyroidism in the fetus. Simultaneous use of L-thyroxine or L-triiodothyronine is contraindicated because these hormones may mask the effects of excessive propylthiouracil in pregnant women and result in hypothyroidism in the fetus. Methimazole is an alternative to propylthiouracil. Graves disease commonly abates during the 3rd trimester, often allowing dose reduction or discontinuation of the drug.
In centers with experienced thyroid surgeons, a 2nd-trimester thyroidectomy, although very uncommon, may be considered after drug treatment restores euthyroidism. After thyroidectomy, women are given full replacement of L-thyroxine (0.15 to 0.2 mg orally once a day), beginning 24 hours later.
Radioactive iodine (diagnostic or therapeutic) and iodide solutions are contraindicated during pregnancy because of adverse effects on the fetal thyroid gland. Beta-blockers are used only for thyroid storm or severe maternal symptoms.
If pregnant women have or have had Graves disease, fetal hyperthyroidism may develop. Whether these women are clinically euthyroid, hyperthyroid, or hypothyroid, thyroid-stimulating immunoglobulins (Igs) and thyroid-blocking Igs (if present) cross the placenta. Fetal thyroid function reflects the relative fetal levels of these stimulating and blocking Igs. Hyperthyroidism can cause fetal tachycardia (> 160 beats/min), growth restriction, and goiter; rarely, goiter leads to decreased fetal swallowing, polyhydramnios, and preterm labor. Ultrasonography is used to evaluate fetal growth, thyroid gland, and heart.
Women with mild to moderate hypothyroidism frequently have normal menstrual cycles and can become pregnant.
During pregnancy, the usual dose of L-thyroxine is continued. As pregnancy progresses, minor dose adjustments may be necessary, ideally based on TSH measurement after several weeks.
If hypothyroidism is first diagnosed during pregnancy, L-thyroxine is started; dosing is based on weight. Usually, pregnant women require a higher dose than nonpregnant women.
Maternal immune suppression during pregnancy often ameliorates Hashimoto thyroiditis; however, hypothyroidism or hyperthyroidism that requires treatment sometimes develops.
Hypothyroid or hyperthyroid dysfunction occurs in 4 to 7% of women during the first 6 months after delivery. Incidence seems to be higher among pregnant women with any of the following:
In women with any of these risk factors, TSH and free serum T4 levels should be checked during the 1st trimester and postpartum. Dysfunction is usually transient but may require treatment. After delivery, Graves disease may recur transiently or persistently.
Painless thyroiditis with transient hyperthyroidism is a recently recognized postpartum, probably autoimmune disorder. It occurs abruptly in the first few weeks postpartum, results in a low radioactive iodine uptake, and is characterized by lymphocytic infiltration. Diagnosis is based on symptoms, thyroid function tests, and exclusion of other conditions. This disorder may persist, recur transiently, or progress.