Introduction: Regulation of thyroid function undergoes important alterations to maintain euthyroidism during pregnancy. During normal pregnancy, increased estrogen production from the placenta causes an increase in TBG and total T4 and increase in hCG stimulates the thyroid gland and decreases serum TSH concentration in addition, thyroxine metabolism and urinary iodine excretion are also increased. Women residing in iodine deficient regions present with goiter and hypothyroxinemia during pregnancy, with overt thyroid dysfunction occuring in 2-3% of pregnancies, and subclinical dysfunction in 10% of pregnancies. Hyperthyroidism is exacerbated during the first trimester, with relative amelioration in the second and third trimesters, and accelerates again during the postpartum period. Transfer of TSH receptor antibodies from placenta may cause neonatal hyperthyroidism with tachycardia, accelerated bone growth and delayed intra-uterine growth. Unrecognized thyroid dysfunction during pregnancy may cause irreversible alterations in pregnancy outcomes and physical and mental development of fetus and neonate. Therefore, proper evaluation, diagnosis and treatment of thyroid deranagements during pregnancy are of outmost importance.