Congenital neonatal thyrotoxicosis and previous maternal radioiodine therapy

The risk of congenital thyrotoxicosis may well be apparent when a pregnant woman has florid thyrotoxic Graves' disease (figure). A maternal history of Graves' disease, however, may be overlooked, especially if the mother is taking thyroxine replacement after radioablation or surgery. Maternal thyroid stimulating antibodies may persist,1 and consequently a woman's newborn infant is still at risk. Thyroid stimulating antibodies can be quantified by measuring the “thyroid stimulating hormone binding inhibiting immunoglobulin” (TBI) index.2 This competitive radioreceptor assay measures binding to a porcine thyroid stimulating hormone receptor of the patient's immunoglobulin, compared with labelled thyroid stimulating hormone. A high maternal TBI index is a useful measure to indicate increased likelihood of disease developing in the infant. Although certain prediction of an infant being affected is not possible antenatally,2 ^2-44 a maternal TBI index of more than 30 units predicts, and more than 70 units strongly predicts, that the infant will be more likely to be affected. Therefore all infants of mothers with a history of Graves' disease must be carefully monitored, both clinically and biochemically, for up to seven days postnatally.

Although Graves' disease complicates 0.1-0.2% of all pregnancies, congenital thyrotoxicosis is rare, occurring in 1 in 70 of these pregnancies, and its development may be irrespective of either maternal disease or antibody status alone. Congenital thyrotoxicosis is transient, lasting up to three months or more, and is due to the transplacental passage of the stimulating (infrequently inhibitory) maternal antibodies of the IgG class, which may cause substantial neonatal morbidity or …