Many of symptoms of hyperthyroidism such as tachycardia, tremor, warm and moist skin, and systolic murmur may be present in normal pregnancy. In the first trimester of gestation, the normal elevation in TT4 and TT3, due to estrogen-induced increase in TBG concentration, and hCG thyroid stimulation with suppression of serum TSH, may pause difficulties in the diagnosis of maternal hyperthyroidism [16].
Management of hyperthyroidism during pregnancy requires special considerations because maternal thyroid disease could have adverse effects on the mother, fetus, and neonate.
Poorly treated or untreated maternal overt hyperthyroidism may affect pregnancy outcome, mainly as a result of complications such as preeclampsia, preterm delivery, intrauterine growth restriction, low birth weight, fetal hydrops, and stillbirths [17–19]. Other complications include congestive heart failure, thyroid storm, and postpartum bleeding. Inappropriate doses of antithyroid drugs and their crossing from the placenta could be the cause of fetal hypothyroidism with or without fetal goiter. [20]. Frequent determination of maternal thyroid hormones, with the target to keep the serum FT4 or TT4 in the 1/3 upper limit of reference range, is the most effective way to prevent such complications [1, 21]. In addition, the transplacental passage of maternal TRAb may cause fetal or neonatal Graves’ disease [22]. If the mother remains hyperthyroid during most of the pregnancy, high maternal thyroxine values, crossing the placenta may produce neonatal central hypothyroidism [23].
Postpartum thyrotoxicosis due to Graves’ disease may be treated with radioiodine but it requires radiation safety measurements for infant and is contraindicated if the mother is breast-feeding. Antithyroid drugs are the mainstay of the treatment of postpartum thyrotoxicosis due to Graves’ disease [24]. Recent investigations conclude that neither PTU up to 300 mg nor MMI up to 30 mg daily cause any alterations in thyroid function and physical and mental development of infants breast-fed by lactating thyrotoxic mothers [25–28]. However, MMI is the preferred drug, because of the potential necrosis of the liver in either mother or child.
Management of hyperthyroidism during pregnancy and lactation requires special considerations and should be meticulously implemented to provide best care to pregnant woman and prevent any adverse effects on the mother, fetus, or neonate. A comparison of recommendations of the American Thyroid Association (2011) and the Endocrine Society (2012) on various aspects of diagnosis and treatment of hyperthyroidism in pregnancy does not reveal any disagreement or controversy. Almost all the information given by one organization could be found in the text or recommendations of the other. Although the authors of both guidelines should be applauded for their ability to synthesize complex data into high quality guidelines, the presence of two guidelines in a time distance of only 10 months by 2 prestigious organizations may perplex clinicians to select one guideline or the other for management of their patients. In the opinion of the authors of this paper either of the two guidelines may be used for appropriate and up-to-date management of thyrotoxic pregnant women.