Thyroid dysfunction is not uncommon in pregnancy and is associated with various maternal, foetal and neonatal complications. We report the occurrence of neonatal hyperthyroidism in two successive pregnancies in a post radio-ablation mother with Graves disease who is on thyroxine replacement.
Mother: A 30-year-old lady, treated for Graves thyrotoxicosis with radioiodine 10 years ago, was on thyroxine 100 mcg replacement for hypothyroidism. She was seen in antenatal clinic during the final trimester of her first pregnancy. Premature delivery occurred prior to initiation of foetal heart monitoring in her first pregnancy. She was biochemically euthyroid but with elevated Thyroid Blocking Inhibiting Immunoglobulin (TBII) levels (Table 1). During her second pregnancy she was treated with Propylthiouracil in the hope of preventing neonatal hyperthyroidism (thyroxine replacement was continued).
|MOTHER||BABY 1||BABY 2|
|Pregnancy 1||Pregnancy 2||Day 5||Day 8|
|FT4 pmol/l||17 (1023)||16||>100||74|
|TSH mIU/l||0.1 (0.45.5)||0.3||<0.05||<0.05|
|TBII Units||83 (015)||89||39||55|
Baby 1: Male infant had meconium staining at birth and cord around the neck which resulted in premature delivery at 34 weeks gestation and weighed 1.835 kg. He developed thyrotoxicosis postpartum (Table 1) and was treated with block-replace (Carbimazole+Thyroxine) and propranolol for 3 months.
Baby 2: Female infant was born at 39 weeks gestation and weighed 2.5 kg. She had neonatal hyperthyroidism (Table 1) and was treated with block and replacement akin to her brother.
Foetal problems caused by transplacental transfer of thyroid blocking (Inhibitory and Stimulating) Immunoglobulins could easily be missed in a euthyroid mother with treated Graves disease. The bioassay of TBII has been used to predict the occurrence of neonatal hyperthyroidism but early anticipation and recognition remains cornerstone of treatment.
01 - 05 Apr 2006
European Society of Endocrinology