During pregnancy the thyroid should adapt itself to the availability of the least quantities of iodides necessary to synthesis hormones and to several other possible modifications such as a rise in the thyroxine-binding globulin and the thyroid stimulating effect of beta-hCG. An increase in size of the thyroid gland is very common. The interpretation of the parameters used to diagnose abnormalities of thyroid function can be carried out. Although the development of the fetal thyroid can take place independently of the maternal thyroid behaviour, an abnormal thyroid function in the mother can not occur without affecting the pregnancy. Grave's disease can cause either fetal or neonatal hyperthyroidism due to a transplacental transfer of thyroid stimulating immunoglobulins or hypothyroidism secondary to the use of too large doses of synthetic antithyroid products. Pregnancy itself favours hyperthyroidism. Maternal hypothyroidism which has not been treated is rarer because of a lack of fertility. It can cause repercussions on the fetus that have probably been over estimated. When pregnancy occurs in a hypothyroid woman who is being treated the dosages of drugs that she is being given should be increased by 20-30%. Providing a good knowledge of the thyroid parameters and keeping the patient preferably euthyroid in cases where thyroid dysfunction can occur, the pregnancy can continue normally whatever the state of the mother thyroid function was. The risks to the fetus are minimal. In women who are at risk it is very important to keep controlling the thyroid state after delivery when there is an immunological rebound which may lead to a relapse in Grave's disease and to post-partum thyroiditis.