To further characterize the adrenocortical response to acute illness, we measured basal and adrenocorticotropic hormone (ACTH)-stimulated 11-deoxycortisol, androstenedione, and dehydroepiandrosterone sulfate (DHEAS). Acutely ill patients had higher ACTH-stimulated 11-deoxycortisol and androstenedione, and decreased basal and ACTH-stimulated androstenedione/ Cortisol and DHEAS/cortisol ratios. Our data suggest that a shift away from androgen synthesis toward the glucocorticoid pathway occurs in acute illness.