ADRENAL FUNCTION IN PREMATURE INFANTS

Abstract

The urinary formaldehydogenic steroid excretion was measured in 5 ACTH-treated premature infants and in 3 premature infants born of toxemic mothers. One of these toxemic mothers received no therapy, one received ACTH antepartum, and one cortisone antepartum. Na, K and N balance studies were conducted in three of the above infants. Steroid excretion rose during ACTH administration and fell 2 to 4 days after discontinuance of ACTH therapy. The fall was followed by a moderate rise, or rebound, in some cases. These findings indicate that the adrenals of young infants have a functional reserve and are capable of responding to either an increase or a decrease in the adrenocorticotrophic stimulus by a corresponding change in steroid production. This response resembles that seen in normal adults and is further evidence that this aspect of adrenal function is not impaired during involution of the fetal adrenal cortex. ACTH administration in one infant produced an increase in sodium excretion during the first 16 days of therapy. This response is the opposite of that usually found in normal adults, and confirms a similar previous finding reported by Klein. Under continued ACTH therapy, the infant ultimately retained Na as does the normal adult. The cause for this early abnormal response is unknown, but it resembles one seen in adults with Cushing's disease, in whom desoxycorticosterone induces a loss of sodium. The infant born of the cortisone-treated toxemic mother had normal postnatal urinary steroid values; the infant born of the ACTH-treated toxemic mother had unusually high postnatal values. These observations suggest that cortisone failed to cross the placenta in sufficient quantity to influence steroid excretion of the infant, but that ACTH administered to the mother reached the fetus and stimulated his adrenals.