Neonatal Graves' disease with sustained hypothyroxinaemia post cessation of antithyroid medication.

Objective: This is a case series of two infants with neonatal Graves' disease with prolonged hypothyroxinaemia unrelated to initial treatment for neonatal hyperthyroidism. The mothers of both infants had Graves' disease with previous thyroidectomy and high circulating thyroid stimulating hormone receptor (TSHR) antibodies during the pregnancy. Method(s): Neonatal Graves' disease was diagnosed based on significant elevation of free thyroxine (FT4) on screening thyroid function tests and strongly positive TSH receptor antibodies. In one patient, intermittent tachycardia was noted on cardiac monitoring but otherwise no other overt symptoms of hyperthyroidism were noted. Result(s): After initial treatment with carbimazole, monitoring of thyroid function tests revealed ongoing suppression of TSH and sustained low FT4 levels more than 1-month post carbimazole cessation. This prompted commencement of thyroxine replacement with subsequent normalisation of FT4 levels. Conclusion(s): In neonatal Graves', delayed recovery of TSH is postulated to be due to suppression of the pituitary-thyroid axis by fetal hyperthyroxinaemia. Possible mechanisms to explain ongoing hypothyroidism without recovery after cessation of carbimazole could include the concept of 'switching' between hyperthyroidism and hypothyroidism in the setting of persistently suppressed TSH. The use of antithyroid medication in reducing thyroid stimulating antibodies along with disappearance of transplacentally transferred maternal antibodies over time may result in the increased synthesis of thyroid blocking antibodies. However persistently suppressed TSH may also be explained by the lack of normal feedback regulation, hence the subsequent development of hypothyroidism in both of these patients. This case series highlights the importance of ongoing screening thyroid function monitoring in infants with neonatal Graves' disease.