SummaryProlactin levels were measured in cord blood by radioimmunoassay in 57 premature infants between 26 and 36 weeks of gestation. The level of prolactin was in the range of 20 to 600 ng/ ml. Twenty-three of the infants subsequently developed respiratory distress syndrome (RDS). The mean cord prolactin in the infants with RDS was 140 + 30.7 ng/ml, whereas in the healthy infants it was 276.4 + 26.4 ng/ml. Cord prolactin levels less than 140 ng/ml were associated with a high incidence of RDS: of 25 infants with prolactin levels of less than 140 ng/ml, 19(76%) had RDS. Of the 34 healthy infants, 28(82%) had prolactin levels above 140 ng/ml. The highest levels (500 ng/ml) of prolactin in the group of infants with RDS were in two infants of diabetic mothers. The data suggest that prolactin might have a role in lung maturation in the human fetus.
SpeculationProlactin is the latest hormone to be added to the list of hormones affecting lung maturation. Three groups have now reported a significant correlation between low cord prolactin levels and respiratory distress syndrome. The relative importance and mode of action of prolactin is unclear at present. Prolactin is present in very high concentration in amniotic fluid, and prolactin receptors are present in lung preparations. Prolactin might act as a direct trigger of lecithin synthesis or in a "chain reaction" along the hypothalamic-pituitary-adrenal axis. It could also be only an indicator of the degree of lung maturation. However, it is rapidly becoming clear that prolactin has a major role not only in lactation but also in fat metabolism, ion transport, and probably lung maturation.Survival of the newborn infant depends primarily on its ability to establish effective ventilation. This ventilation is directly related to the presence of pulmonary surfactant in sufficient quantity to ensure alveolar stability (2). The precise mechanism that regulates fetal lung maturation is not clear at Dresent. Acceleration of -~ ~ U surfactant synthesis by corticosteroids and thyroxine has been demonstrated both in ex~erimental animals (6. 17) and human subjects (5, 13). ow eve;, studies by ~e s h e r ' k t a i (14) suggest that cortisol is not a natural trigger of surfactant synthesis.We have shown that administration of prolactin to fetal rabbits in utero leads within two days to a 67% increase in lung lecithin content (1 I), and we have suggested, therefore, that prolactin may be a physiological trigger of surfactant synthesis and lung maturation. Ballard et al. (3) have been unable to repeat our findings in rabbit fetuses. However, first Hauth et al. (12) then we (15) and Gluckrnan et al. (9,10) have confirmed independently an association between incidence of respiratory distress syndrome (RDS) and low cord prolactin levels in premature infants. In this paper, we present our observations and compare the results with the other reports.
MATERIALS AND METHODSThe subjects of this study were 57 premature infants admitted to the neonatal intensive care units of Georgetown Medical C...