The role of thyroid stimulating immunoglobulins of Graves's disease in neonatal thyrotoxicosis.

Abstract

SummaryGraves's disease is characterized by hyperthyroidism, a diffuse, uniform enlargement of the thyroid gland and marked eye signs. It is now widely believed that the thyroid overactivity of Graves's disease is a result of the presence in the circulation of abnormal thyroid stimulating immunoglobulins (TSIg). TSIg are transferred from mother to fetus and cause neonatal thyrotoxicosis in around 1 per cent of babies born to mothers who have a history of Graves's disease. Because TSIg may persist in the maternal circulation after successful treatment of Graves's disease by partial thyroidectomy, neonatal thyrotoxicosis may occur in babies born to mothers who have been euthyroid throughout pregnancy. In our study, 9 of 12 examples of neonatal thyrotoxicosis encountered in 96 pregnancies occurred in babies born to mothers who were thought to be thyrotoxic at some stage during the pregnancy. Two main categories of TSIg are recognized: the long‐acting thyroid stimulator (LATS) and LATS‐protector (LATS‐P) both of which were assayed in maternal serum samples withdrawn during the third trimester. Levels in maternal and cord blood were similar. The critical level of TSIg causing neonatal thyrotoxicosis appeared to be 10 units/ml and above 20 units/ml the babies were always thyrotoxic at birth.