Altered adrenal steroid production in term infants having respiratory acidosis.

Prior studies have provided evidence for reduced fetal adrenal production of dehydroepiandrosterone sulfate and normal or increased production of cortisol in association with pregnancy complications believed to result in fetal stress. In the present study, we sought to determine the status of adrenal steroidogenesis in 36 term infants having respiratory acidosis and to compare acidotic infants to (i) non-acidotic infants matched for pregnancy complications, gestational age, and method and indications for delivery (control infants), and (ii) non-acidotic infants of non-complicated pregnancies who were also matched for gestational age and delivery method (normal infants). Umbilical cord serum levels of dehydroepiandrosterone sulfate were lowest in acidotic infants, intermediate in the condition matched control infants and highest in the non-acidotic infants of normal pregnancies. On the other hand, cortisol levels were highest in acidotic infants, intermediate in control infants and lowest in the normal infants. These data suggest that various pregnancy complications give rise to significant alterations in adrenal steroidogenesis (decreased dehydroepiandrosterone sulfate and increased cortisol). Intrauterine deterioration during labor with resultant respiratory acidosis has an additional effect on fetal adrenal function.

Investigation of the effect of interleukin-1 beta on steroidogenesis in the human fetal adrenal gland.

Interleukin-1 beta (IL-1 beta) has been shown by several investigators to be a stimulator of adrenal glucocorticoid production in vivo. However, little evidence exists for direct actions of IL-1 beta on the adrenal gland. We sought to elucidate the direct effects, if any, of IL-1 beta on human fetal adrenal steroidogenesis in the presence and absence of ACTH in both cell and organ cultures. We studied the effects of several doses of recombinant human IL-1 beta (0.05, 0.5, and 5 U/ml), in the presence and absence of two doses of ACTH (0.1 and 1 microgram/ml). With all doses of IL-1 beta, we were unable to demonstrate alterations in basal adrenal steroidogenesis as measured by dehydroepiandrosterone sulfate and cortisol production. Whereas both doses of ACTH induced significant increases in steroid production over control values (P less than 0.05), there was no additional effect on steroidogenesis when IL-1 beta was added to cultures containing ACTH. We conclude that although IL-1 beta may act in conjunction with other products of the immune system to modulate adrenal cortisol production, IL-1 beta alone does not directly influence human fetal adrenal steroidogenesis. Rather, it is likely that this cytokine acts via stimulation of pituitary ACTH production.