(see Thyroid Disorders.)
Thyroid disorders may predate or develop during pregnancy. Pregnancy does not change the symptoms of hypothyroidism and hyperthyroidism or the normal values and ranges of free serum thyroxine (T4) and thyroid-stimulating hormone (TSH).
Fetal effects vary with the disorder and the drugs used for treatment. But generally, hyperthyroidism causes fetal growth restriction and stillbirth, and hypothyroidism causes intellectual deficits in offspring and miscarriage. 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 the offspring. Goiters and thyroid nodules discovered during pregnancy should be evaluated as they are in other patients.
Maternal Graves disease is monitored clinically and with free T4 and high-sensitivity TSH assays.
Treatment varies. Usually, pregnant women are given the lowest possible dose of oral propylthiouracil (50 to 100 mg q 8 h). Therapeutic response occurs over 3 to 4 wk; 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 po once/day), beginning 24 h later.
Radioactive iodine (diagnostic or therapeutic) and iodide solutions are contraindicated during pregnancy because of adverse effects on the fetal thyroid gland. β-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.
Congenital Graves disease:
If pregnant women have taken propylthiouracil, congenital Graves disease in the fetus may be masked until 7 to 10 days after birth, when the drug's effect subsides.
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 at 0.1 mg po once/day.
Maternal immune suppression during pregnancy often ameliorates this disorder; however, hypothyroidism or hyperthyroidism that requires treatment sometimes develops.
Acute (subacute) thyroiditis:
Common during pregnancy, this disorder usually produces a tender goiter during or after a respiratory infection. Transient, symptomatic hyperthyroidism with elevated T4 can occur, often resulting in misdiagnosis as Graves disease. Usually, treatment is unnecessary.
Postpartum maternal thyroid dysfunction:
Hypothyroid or hyperthyroid dysfunction occurs in 4 to 7% of women during the first 6 mo 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.
Last full review/revision June 2013 by Lara A. Friel, MD, PhD
Content last modified October 2013