Thyroid hormones are produced by the fetus from 11 weeks gestation 1 and are essential for normal fetal and neonatal development. Maternal autoimmune thyroid disease (Graves' disease) or its treatment may adversely affect this normal development by causing hypo-or hyperthyroidism in utero and/or in the early neonatal period. This case demonstrates that the fetus/ infant may be susceptible to both mechanisms of disruption of thyroid function.A 35-year-old woman in her fifth pregnancy with known Graves' disease presented with thyrotoxicosis at 7 weeks gestation (thyroid stimulating hormone (TSH) 0.01 mIU/L (0.3-4), fT 3 50 pmol/L (3.5-6.5), fT4 95.3 pmol/L (10-23)) with positive thyroid antibodies (anti-thyroid peroxidase antibodies 190 IU/mL (<10) and thyroid stimulating immunoglobulin (TSI) >40 U/L (0-1). She was transferred from carbimazole to propylthiouracil (PTU) daily dose 150 mg. This was reduced to 100 mg by the end of the first trimester. Low TSH and high fT3 levels persisted throughout the second trimester (fT3 8.2-29.3 pmol/L) but levels of fT4 returned to the normal range.On ultrasound at 26 weeks gestation, a fetal goitre was identified. The goitre appeared to have a uniform increase in vascularity, fetal growth, heart rate and skeletal ossification appeared normal. By 31 weeks, maternal thyroid function remained unchanged but the fetal goitre had enlarged with a circumference of 9.4 cm, >95th centile (95th centile by biparietal diameter 6.5 cm and by gestational age 5.2 cm).2 Referral was made to a tertiary fetal therapy unit for fetal blood sampling (FBS) to determine fetal thyroid function and to assess the potential obstructive effect of the fetal neck mass and possible need for ex utero intrapartum treatment procedure.The trachea appeared patent, fetal swallowing was observed and liquor volume was normal, and there was no significant change in the size of the goitre (Fig. 1). FBS revealed fT3 3.5 pmol/L (3.9-6.8), fT4 6.7 pmol/L (12-22) and TSH of >100 mIU/L (0.3-4), confirming severe fetal hypothyroidism. Treatment with 60 mcg intra-amniotic tri-iodothyronine (Liothyronine sodium, Goldshield Pharmaceuticals, Croydon UK) was given and maternal PTU decreased to 50 mg daily. By 35 +3 weeks, maternal clinical and biochemical status was increasingly thyrotoxic (TSH 0.01 mU/L, fT3 19.1 pmol/L and fT4 22.9 pmol/L). Despite administration of propanolol, the woman was increasingly symptomatic and so a decision was made to proceed with delivery. A healthy male infant weighing 2850 g (63rd customised birthweight centile) was delivered by an uncomplicated lower segment caesaren section. There were no concerns with the neonate's airway and no palpable goitre. On day one, the infant's thyroid function was normal (TSH 11 mIU/L (0.01-10.5), fT3 5.5 pmol/L (3.4-7.2), fT4 15.3 pmol/L (10-40)). However, from day 10, the infant was thyrotoxic (TSH 0.09 mIU/L, fT4 61.1 pmol/L, fT3 14.7 pmol/L) with TSI level >40 U/L (0-1). Carbimazole (1.25 mg bd) and propranolol (1 mg tds) were commenced due to tachycardia and fre...