Pregnancy affects thyroid physiology in many ways: (a) The renal iodide clearance rate is increased, hence iodine requirements increase. (b) The fetal requirements for thyroid hormones and iodide are an additional problem. (c) Serum thyroxine-binding globulin increases, thus producing an increase in the levels of total T4 and T3. (d) Chorionic gonadotropin has a thyroid-stimulating activity. This may be compensated for by a decrease in TSH, but in some cases gestational thyrotoxicosis occurs. (e) Thyroid autoimmunity usually subsides during pregnancy, but may rebound a few months after parturition, and postpartum thyroiditis may occur. Because maternal antithyroid autoantibodies cross the placenta readily, fetal and neonatal hyperthyroidism (or hypothyroidism) may develop. Pre-existing thyroid diseases are influenced. Nontoxic goiter increases in size. Iodine and/or thyroxine may be required. Graves' disease may remit. If present, antithyroid drugs should be given in small doses, and quite often they may be stopped altogether. Hypothyroid patients may require a larger T4 dose.