Hypothyroidism during pregnancy occurs in 1/1600-2000 deliveries, according to the most recent publications. The most common causes are chronic autoimmune thyroid disease, radiodine-131 treatment, or surgical removal. The diagnosis is difficult to make on clinical grounds alone, even in advanced cases, and a high index of suspicion is needed. Some women are at high risk of developing hypothyroidism, and they should be screened. These women may have had previous treatment for hyperthyroidism; high-dose neck irradiation, evidence of thyroid autoimmunity, amiodarone therapy, suspected hypopituitarism, and type I diabetics. The best laboratory test is the serum TSH, followed, if elevated, by a free T4 index and a TPO-ab titer. Thyroid antibodies have been associated with an increased (double) risk of miscarriage and postpartum thyroiditis. Frequent (22-44%) pregnancy-induced hypertension leading to preterm delivery, and prematurity is the main complication observed in those still hypothyroid near term. Proper therapy eliminates or reduces the risk. No congenital anomalies have been reported in the most recent studies, and the data available shows that both physical and mental development have been normal until children are 10 years old. However, one study reported lower IQs in children of euthyroid women with positive TPO-ab than in children of TPO-ab negative mothers. Levothyroxine is the treatment of choice. Euthyroidism must be reached and maintained in a timely fashion. Many women need more thyroxine during pregnancy, and surveillance of thyroid function is needed throughout gestation to make dose adjustments when needed. During the postpartum periods the thyroxine requirements decrease to preconception levels.