. (1975). Archives of Disease in Childhood, 50, 40. Thyroid function during exchange transfusion. The changes in plasma thyroid hormone concentration were studied during exchange transfusion performed for haemolytic disease. 24 transfusions were performed using blood preserved with acid-citrate and dextrose and in 11 cases 10 or 50 ,ug glucagon was added to the donor blood. Plasma tri-iodothyronine (T3), thyroxine (T4), thyrotropin (TSH), thyroid hormone binding capacity, and free thyroxine index were measured in the donor blood and in the infant at the start and at intervals during the transfusion. Before transfusion the plasma TSH levels of the infants fell as postnatal age increased and plasma T3 and T4 were correlated with one another. In 20 transfusions the mean infant/donor ratio of TSH was approximately 10, of T4 3, and of T3 2. During these transfusions there was a progressive fall in the infant's plasma TSH, T4, and T3 concentration. In 3 transfusions in which the donor plasma TSH was greater than that of the infant, plasma TSH levels rose during the transfusion and in 2 cases this was associated with a late rise in plasma T3 levels. The addition of glucagon to donor blood had no effect on thyroid hormone levels.It is concluded that erythroblastotic infants have normal thyroid function and that they became biochemically hypothyroid during transfusion. Acute changes in plasma thyroid hormone and glucagon concentration do not induce TSH responses by the neonatal pituitary during the period of the exchange transfusion.In the minutes after birth there is a dramatic rise in plasma thyrotropin (TSH) concentration which then falls slowly to regain values characteristic of the adult in the second half of the first week of life (Fisher and Odell, 1969;Czernichow et al., 1971;Lemarchand-Beraud et al., 1972). The serum thyroxine (T1) and tri-iodothyronine (T3) levels rise in response to the increase in TSH concentration to reach a maximum at the age of 24 hours (Erenberg et al., 1974). The rise in T4 and T3 is in both the total and free concentration of the hormones, thus making the infant chemically thyrotoxic.The control of pituitary-thyroid function at this stage of development is poorly understood, in part because of ethical difficulties in the direct study of the normal infant. In the present work we have taken advantage of the experimental situation occurring during exchange transfusion to study the changes in plasma TSH and in total T4 and T3