“…Studies have demonstrated that etomidate directly inhibits adrenal steroidogenesis [32,33] and the primary mode of action is thought to be inhibition of 11β-hydroxylation of gluco- and mineralocorticoids [6,34,35]. These studies, in patients and adrenal cell lines, consistently show a rise in 11-deoxycortisol and 11-deoxycorticosterone associated with a decrease in cortisol and corticosterone concentrations after low-dose etomidate administration [6,16,34,35,36,37,38,39,40]. However, higher concentrations of etomidate result in a reduction in 17α-OH-progesterone and progesterone concentrations, suggesting inhibition of other cytochrome P450-dependent enzymes, e.g.…”