Adrenal Insufficiency Due to Inhaled Etomidate in Electronic Cigarettes

A 33-year-old female presented with recurrent fainting. There was no hyperpigmentation, hirsutism, virilization, or oligomenorrhoea. She had not used antifungal medications, mitotane, metyrapone, or exogenous steroids. Her blood pressure was 135/83 mmHg when supine and 84/62 mmHg on standing. She was afebrile (36.8 °C) and her pulse rate was 81/min. Investigations showed: serum potassium 3.9 mmol/L (3.3 – 5.1), bicarbonate 25 mmol/L (21 – 32 mmol/L), peak cortisol on 250 mcg adrenocorticotropic hormone stimulation test 36 nmol/L, adrenocorticotropic hormone 29.7 pmol/L (1.6 – 13.9), 17-alpha-hydroxyprogesterone 3.6 nmol/L (0.3 – 3.3), dehydroepiandrosterone sulphate 2.6 umol/L (2.6 – 13.9), plasma aldosterone concentration 152 pmol/L (83 – 731), plasma renin activity 0.97 ng/ml/h (0.40 – 6.38), undetectable 21-hydroxylase antibody, and absence of adrenal hyperplasia or atrophy on computed tomography. Primary adrenal insufficiency was diagnosed. She was treated with hydrocortisone and dehydroepiandrosterone. Two months later, she admitted to using electronic cigarettes containing etomidate. Adrenocortical suppression by inhaled etomidate presents variably. Most cases had glucocorticoid deficiency. More than half had mineralocorticoid excess. Two cases had hyperandrogenism. Our patient had low dehydroepiandrosterone sulphate which was not expected from 11-beta-hydroxylase inhibition by etomidate. Recovery from adrenocortical suppression was reported in 4 cases while 1 case had persistent adrenal insufficiency 5 months after abstinence. Adrenal insufficiency resolved after 8 months in our patient. Inhaled etomidate misuse is increasingly common and should be suspected in patients with unexplained adrenal insufficiency. Adrenocortical suppression by inhaled etomidate mimics rare forms of congenital adrenal hyperplasia and hypokalaemic periodic paralysis.