Ideally, women in the childbearing period with severe disease should have definitive therapy with 131I or subtotal thyroidectomy prior to pregnancy in order to avoid an acute exacerbation of the disease during pregnancy or following delivery. If thyrotoxicosis does develop during pregnancy, RAI is contraindicated because it crosses the placenta and may injure the fetal thyroid. Propylthiouracil (fewer teratogenic risks than methimazole) can be given in the first trimester, and then methimazole can be given for the remainder of the pregnancy in order to avoid potential liver damage. The dosage of propylthiouracil must be kept to the minimum necessary for control of the disease (ie, <300 mg/d), because it may affect the function of the fetal thyroid gland. Alternatively, a subtotal thyroidectomy can be safely performed during the mid trimester. It is essential to give the patient a thyroid supplement during the balance of the pregnancy.
Graves’ disease may occur in the newborn infant, due either to passage of maternal TSH-R Ab [stim] through the placenta, stimulating the thyroid gland of the neonate, or to genetic transmission of the trait to the fetus. Laboratory studies reveal an elevated free T4, a markedly elevated T3, and a low TSH—in contrast to the normal infant, in whom TSH is elevated at birth. TSH-R Ab [stim] is usually found in the serum of both the child and the mother.
If caused by maternal TSH-R Ab [stim], the disease is usually self-limited and subsides over a period of 4–12 weeks, coinciding with the fall in the infant’s TSH-R Ab [stim] level. However, treatment is necessary because of the severe metabolic stress the infant experiences. Therapy includes propylthiouracil at a dosage of 5–10 mg/kg daily in divided doses at 8-hour intervals; Lugol’s solution (8 mg of iodide per drop), 1 drop every 8 hours; and propranolol, 2 mg/kg daily in divided doses. Careful supportive therapy is essential. If the infant is very ill, oral prednisone, 2 mg/ kg daily in divided doses, will help block conversion of T4 to T3. These medications are gradually reduced as the clinical picture improves and can be discontinued by 6–12 weeks.
Subclinical hyperthyroidism is defined as a suppressed TSH level (below the normal range) in conjunction with normal thyroid hormone levels. Cardiac toxicity (eg, atrial fibrillation), especially in older persons and those with underlying cardiac disease, is of greatest concern. The consensus of thyroid experts concluded that hyperthyroidism treatment is appropriate in those with TSH less than 0.1 mIU/L, while close monitoring of the TSH level is appropriate for those with less TSH suppression.
In addition to those patients who develop hypothyroidism caused by amiodarone, approximately 3% of patients receiving this drug will develop hyperthyroidism instead. Two types of amiodaroneinduced thyrotoxicosis have been reported: iodine-induced (type I), which often occurs in persons with underlying thyroid disease (eg, multinodular goiter, Graves’ disease); and an inflammatory thyroiditis (type II) that occurs in patients without thyroid disease due to leakage of thyroid hormone into the circulation. Treatment of type I requires therapy with thioamides, while type II responds best to glucocorticoids. Since it is not always possible to differentiate between the two types, thioamides and glucocorticoids are often administered together. If possible, amiodarone should be discontinued; however, rapid improvement does not occur due to its long half-life.