Clinical hyperthyroidism affects 0.1% to 0.4% of pregnancies. Gestational thyrotoxicosis is due to homology of the structure of TSH and HCG, which weakly stimulates the TSH receptor. Graves’ disease (GD) most commonly causes clinically significant hyperthyroidism. Given concerns for teratogenicity from antithyroid drugs, these may be discontinued in low-risk GD patients. High-risk patients are treated with propylthiouracil in the first trimester then may transition to methimazole. Surgery is reserved for special circumstances; radioactive iodine is contraindicated. In late pregnancy, GD may remit; postpartum relapse is common. Measurement of serum thyrotropin receptor antibodies identifies pregnancies at-risk for fetal and neonatal hyperthyroidism.