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Etomidate: a selective adrenocortical 11 beta-hydroxylase inhibitor
Klinische Wochenschrift
|November 2, 1984
Summary
Etomidate anesthetic specifically blocks adrenal steroid 11 beta-hydroxylation, causing reversible adrenocortical suppression. This leads to elevated intermediate steroids and reduced cortisol levels during treatment.
Area of Science:
- Endocrinology
- Pharmacology
- Biochemistry
Background:
- Etomidate is an anesthetic known to cause adrenocortical suppression.
- Investigating the precise mechanism of etomidate-induced adrenal suppression is crucial for patient management.
Observation:
- In a patient requiring continuous etomidate infusion for seizures, plasma steroid levels were measured before and after ACTH stimulation.
- Etomidate therapy resulted in elevated 11-deoxycorticosterone (DOC) and 11-deoxycortisol (S), with decreased cortisol (F) and cortisone (E).
- ACTH stimulation during etomidate infusion showed blunted responses for corticosterone (B), aldosterone (Aldo), cortisol (F), and cortisone (E), but increased DOC and S.
Findings:
- Etomidate significantly decreased the ratios of corticosterone/DOC and cortisol/11-deoxycortisol, indicating inhibition of 11 beta-hydroxylase activity.
- The ratios reflecting 21-hydroxylase activity remained elevated, suggesting this pathway is unaffected.
- Discontinuation of etomidate normalized the steroidogenic response to ACTH stimulation.
Implications:
- Etomidate induces a specific, reversible blockade of adrenal steroid 11 beta-hydroxylation.
- Understanding this mechanism is vital for managing patients on long-term etomidate, particularly regarding potential adrenal insufficiency.
- This study clarifies the biochemical basis of etomidate's endocrine side effects.