Impact of betamethasone load given to pregnant women on endocrine balance of fetoplacental unit.

Corticosteroid administration to pregnant women for attempted prevention of the respiratory distress syndrome in infants (IRDS) involves the hazard of seriously altering the endocrine status in the fetoplacental unit. The effect of a betamethasone load (12 mg. daily for three days) to 19 pregnant women in the last trimester was studied, and a comparison was made with 13 control subjects. Amniocentesis was performed twice in most patients. There was a sharp reduction of cortisol in maternal serum and a significant decrease in cortisol concentration in amniotic fluid (p less than 0.05) after betamethasone treatment. Maternal urinary estriol excretion decreased; this was strongly correlated to the basal estriol excretion (r equals 0.945). A residual fraction of estriol excretion, not less than 2 mg. per 24 hour urine specimen, remained despite the high corticosteroid dose. The origin of the nondepressed part of urinary estriol might be multifactorial, e.g., nonadrenal production of estriol precursors and functional inhomogeneity of the fetal adrenal in response to adrenocorticotropic hormone stimulation. The corticosteroid treatment for prevention of IRDS transiently excludes the use of urinary estriol for assessment of fetoplacental integrity but does not influence the plasma level of human chorionic somatomammotropin.