| Prior to the mid twentieth century, serum thyroxine levels, measured as protein bound iodine (PBI), were found to be similar to maternal values, and it was believed that the placenta was freely permeable to thyroid hormones. During the late 1960’s and 1970’s, development of sensitive TSH and thyroid hormone radioimmunoassays (RIA) facilitated physiologic studies of fetal and perinatal thyroid function in animals and human species which showed that the placenta is impermeable to TSH, that maternal to fetal thyroid hormone transfer is limited, and that the fetal pituitary-thyroid system functions autonomously of the maternal system.4-8 Studies of thyroid function in the newborn infant characterized a state of physiological thyroidal hyperactivity secondary to an early extrauterine TSH surge stimulated by the acute cooling effect of exposure to the extrauterine environment.9-11With this information, several groups focused on approaches to newborn screening for CH.12 Dussault and Laberge adapted the T4 RIA to the filter paper blood spots collected at 48–72 hours in Quebec for phenylketonuria (PKU) screening.13 Klein et al measured TSH in cord blood14; Walfish compared cord blood T4 measurements to capillary blood spot screening.15; and Winkler et al proposed screening for serum TSH elevation at 5 days, at which time neonatal serum TSH levels are normally similar to adult values.16 The most practical approach proved to be utilization of the already existent infrastructure for newborn PKU screening. Using this approach Dussault and coworkers in Quebec reported the first mass population screening program in 1975.17 The TSH RIA adapted to filter paper samples was added for follow-up TSH measurements to increase screening specificity and decrease false positive results.18,19 |
