Adrenocortical suppression and other endocrine effects of etomidate

Preziosi, P; Vacca, Michèle

doi:10.1016/0024-3205(88)90087-2

Cited by 41 publications

(10 citation statements)

References 61 publications

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“…In addition, this study did not control for effects that could have been due solely to etomidate or to RU486, ACTH, or any of the several precursor molecules that accumulate in plasma after etomidate use 21. However, we believe it unlikely that any observed effects in this study were due to etomidate alone, because the concentration of etomidate needed to suppress adrenocortical synthesis (0.2 μ M) is 1/50th the sedating concentration 22.…”

Section: Discussionmentioning

confidence: 89%

In Vivo Exposure to High or Low Cortisol Has Biphasic Effects on Inflammatory Response Pathways of Human Monocytes

Yeager¹,

Pioli²,

Wardwell³

et al. 2008

Anesthesia &Amp; Analgesia

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BACKGROUND Recent studies demonstrate that glucocorticoids (GCs) have both supportive (stimulatory) and suppressive effects on immune responses, depending upon the GC concentration. Since some GC effects on inflammation are stimulatory, we hypothesized that acute in vivo GC depletion would decrease inflammatory responses of human monocytes. METHODS Monocytes were isolated from healthy volunteer participants before and after in vivo treatment with; 1) IV saline, 2) IV high dose hydrocortisone (8 μg · kg−1 · min−1) followed by oral hydrocortisone overnight, and 3) oral RU486 (200 mg at 0400 and 1600 h) to block the intracellular GC receptor and IV etomidate (1.5 mg · kg−1 · h−1) for 12 h to prevent compensatory adrenal cortisol synthesis. Plasma adrenocorticotropic hormone, plasma, and salivary cortisol were measured serially. Monocytes were tested for; 1) cytokine responses, 2) expression of CD163, CD119, and CD54, and 3) mRNA levels of GC-responsive inflammatory mediators. All measurements were made with and without in vitro stimulation of monocytes by lipopolysaccharide. RESULTS Cortisol and adrenocorticotropic hormone measurements demonstrated effective manipulation of in vivo cortisol. In vivo hypercortisolemia and in vivo GC depletion had reciprocal effects on monocyte mRNA levels of 4 important GC-responsive molecules: 1) GC receptor, CD163, interleukin-10, and suppressor of the cytokine synthesis-3. Monocyte cytokine responses and protein expression were not affected by GC depletion. CD163 expression was increased by hypercortisolemia. CONCLUSIONS Short-term GC depletion affects mRNA levels of GC-responsive molecules but does not affect monocyte protein expression or cytokine responses.

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Section: Discussionmentioning

confidence: 89%

In Vivo Exposure to High or Low Cortisol Has Biphasic Effects on Inflammatory Response Pathways of Human Monocytes

Yeager¹,

Pioli²,

Wardwell³

et al. 2008

Anesthesia &Amp; Analgesia

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“…Injection pain may result from local irritation caused by etomidate, [19] and adrenal suppression may result from reversible inhibition of 11-β-hydroxylase, which converts 11-deoxycortisol into cortisol. [20] However, the explicit mechanism of myoclonus development remains unclear. [11,21,22] In our study, the incidence of myoclonus in the etomidate group was 48.6%, which was close to the rate of 50% to 80% reported by Doenicke et al [17] The slight difference might be because of the administration of 0.3 mg/kg lidocaine in this study, which could inhibit the myoclonus partially induced by etomidate.…”

Section: Discussionmentioning

confidence: 99%

Propofol decreases etomidate-related myoclonus in gastroscopy

Liu

Meng

et al. 2017

Medicine

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Objective:Myoclonus, a common complication during intravenous induction with etomidate, is bothersome to both anesthesiologists and patients. This study explored the preventive effect of pretreatment with propofol on etomidate-related myoclonus.Methods:This was a prospective, double-blind, clinical, randomized controlled study. Totally, 363 patients who were scheduled for a short-duration, painless gastrointestinal endoscopy were divided into 5 groups. Four groups received 0 mg/kg (E group), 0.25 mg/kg (LPE group), 0.50 mg/kg (MPE group), or 0.75 mg/kg (HPE group) propofol pretreatment before etomidate anesthesia. Another group only received 1 to 2 mg/kg of propofol (P group) as anesthesia. The incidence and severity of myoclonus, patient circulation and respiratory status, and intraoperative and postoperative complications were recorded.Results:The incidence of myoclonus in the LPE group (26.8%), MPE group (16.4%), HPE group (14.9%), and P group (0) was lower than the E group (48.6%, P < .05). The incidence of grade 1, 2, and 3 of myoclonus in the LPE group, MPE group, HPE group, and P group was significantly lower than the E group, and that in the P group was lower than the LPE group (P < .05). The incidence of hypoxemia in the P group was higher than the E group, and the incidence of adverse events in the HPE group and P group was lower than the E group (P < .05).Discussion:Pretreatment with propofol was feasible for preventing etomidate-related myoclonus. Furthermore, as propofol dosage increased, its effect on reducing the incidence and severity of myoclonic movements induced by etomidate increased.

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“…All patients in this study required rapid sequence intubation and were treated with a single dose of etomidate in the trauma bay. Therapeutic levels of etomidate inhibit 11β-hydroxylase, an enzyme that is required for aldosterone synthesis [27]. The use of etomidate in the critically injured clearly warrants further investigation, but is not likely to be the sole factor responsible for the high prevalence of MD observed in this study.…”

Section: Discussionmentioning

confidence: 90%

Mineralocorticoid deficiency in hemorrhagic shock

Tolstoy

Aized

McMonagle

et al. 2013

Journal of Surgical Research

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Background In the critically ill, mineralocorticoid deficiency (MD) is associated with greater disease severity, the development of acute renal insufficiency, and increased mortality. We hypothesized that severely injured trauma patients presenting with hemorrhagic shock would demonstrate a high degree of MD. We also hypothesized that MD in these patients would be associated with increased length of stay, hypotension, fluid requirements, and acute kidney injury (AKI). Materials and methods Thirty-two trauma patients in hemorrhagic shock on admission to the trauma bay (SBP <90 mm Hg × 2) were enrolled. Blood samples were obtained on ICU admission and 8, 16, 24, and 48 hours later. Plasma aldosterone (PA) and renin (PR) were assayed by radioimmunoassay. MD was defined as a ratio of PA/PR ≤2. Demographic data, injury severity score, ICU and hospital length of stay, fluid requirements, mean arterial pressure, serum sodium, hypotension, and risk for AKI were compared for patients with and without MD. Results At ICU admission, 48% of patients met criteria for MD. Patients with MD were significantly more likely to experience hypotension (MAP ≤60 mm Hg) during the study period. MD patients required significantly more units of blood in 48 h than non-MD patients (13 [7–22] versus 5 [2–7], P = 0.015) and had increased crystalloid requirements (18L [14–23] versus 9L [6–10], P < 0.001). MD patients were at higher risk for AKI according to RIFLE and AKIN criteria. Conclusions MD is a common entity in trauma patients presenting in hemorrhagic shock. Patients with MD required a more aggressive resuscitative effort, were more likely to experience hypotension, and had a higher risk of AKI than non-MD patients. Future studies are needed to fully understand the impact of MD following trauma and the potential role for hormonal replacement therapy.

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Adrenocortical suppression and other endocrine effects of etomidate

Cited by 41 publications

References 61 publications

In Vivo Exposure to High or Low Cortisol Has Biphasic Effects on Inflammatory Response Pathways of Human Monocytes

In Vivo Exposure to High or Low Cortisol Has Biphasic Effects on Inflammatory Response Pathways of Human Monocytes

Propofol decreases etomidate-related myoclonus in gastroscopy

Mineralocorticoid deficiency in hemorrhagic shock

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