Endocrine Abstracts

Clinical fetal thyrotoxicosis is a rare disease occurring in 1-5% of pregnancies with Graves disease. Although transplacental passage of maternal TSH receptor stimulating autoantibodies (TRab) to the fetus does occur early in gestation, the fetal concentration is low until the end of second trimester, but reaches maternal levels in the last period of pregnancy. The mortality of fetal thyrotoxicosis is 12–20% mainly due to heart failure. We present a case of fetal and neonatal thyrotoxicosis with favorable development and evolution in a 37-year-old woman, known with Graves disease with ophthalmopathy and thyroidectomy performed 12 years ago, with hypothyroidism and post-surgical hypoparathyroidism, in substitution treatment, which has in history a complicated pregnancy with fetal anasarca, premature birth and neonatal death. Pregnancy begins with euthyroid status and persistently increased TRAb (40 IU/l), whose value reaches 101 IU/l at 20 weeks gestational age, decreases rapidly within 1 month to 7.5 IU/l at the same time with the installation of fetal tachycardia in the absence of any other signs of fetal thyrotoxicosis, rapidly remitted under methymazole 20 mg/day. The patient gives birth by cesarean section at 37 weeks gestational age to a live, male fetus, 2530 g with mild congenital hyperthyroidism (fT4 = 3.46 ng/dl. fT3 = 7 pg/ml), TRAb titer 18.6 UI/l, which gradually disappears under methymazole (0.5 to 2 mg/kg body weight/day) and propranolol within 8 weeks postpartum. In conclusion, monitoring for signs of fetal thyrotoxicosis by periodically assessing fetal growth, heart rate, and constant monitoring of maternal anti-TSH antibody titer to detect massive decline through massive transplacental passage may successfully guide the progression of pregnancy associated with Graves disease.