Hypothalamic–pituitary–adrenal axis multiple and organ dysfunction syndrome in critical illness: A special focus on arginine-vasopressin and apelin

Gallo‐Payet, Nicole; Roussy, Jean-François; Chagnon, Frédéric; Roberge, Claude; Lesur, Olivier

doi:10.1080/17471060802339711

Cited by 5 publications

(8 citation statements)

References 153 publications

(134 reference statements)

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“…In this respect, starting CS before or during AVP infusion did not alter the potential benefit of this combination in the current study [7]. Another putative mechanism is a V1 receptorindependent effect through the resolution of inflammatory processes, including the pleiotropic anti-inflammatory activities of CS and the immunomodulatory properties of AVP on microbial-induced inflammation [20,21].…”

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confidence: 76%

Arginine–vasopressin and corticosteroids in septic shock: engaged but not yet married!

Lauzier

Lesur

2011

Intensive Care Med

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Considerable efforts have been made to spare excessive catecholamine exposure and avoid side effects when treating patients with refractory septic shock. Until recently, physiological replacement of arginine-vasopressin (AVP) and corticosteroid (CS) deficits was considered promising but equivocal to improve end-organ function [1], reduce new-onset tachyarrhythmias [2], shorten duration of shock [3], and improve survival [4]. However, two large multicenter randomized controlled trials failed to demonstrate mortality reduction when using physiological doses of AVP [5] and CS [6] and hampered the initial enthusiasm for their widespread use.In this issue of Intensive Care Medicine, Torgersen et al. [7] evaluate the effect on mortality of adding CS to AVP in 159 patients with severe septic shock. Patients included in this single-center retrospective study were relatively ill, as outlined by high baseline sepsis-related organ failure assessment (SOFA) score (median score 15), frequent requirement of continuous renal replacement therapy (99/159, 62.3%), and overall intensive care unit (ICU) mortality (97/159, 61.0%). This sample is not fully representative of the severe sepsis population currently encountered in ICUs [8]. Because treatment assignment was not randomized, the authors used three different statistical analyses to account for baseline characteristics imbalance: multivariate logistic regression, Cox proportional hazard model, and Cox model stratified to matched pairs based on propensity score. Both adjusted analyses and propensity score determination were based on covariables such as age, year of admission, baseline SOFA score, and initial AVP dose, and ignored potentially significant confounders or cointerventions like fluid resuscitation or early effective antimicrobial therapy. Improved survival at 28 days was demonstrated with the Cox proportional hazard model, but not with other statistical analyses, maybe due to lack of power. These results should be cautiously interpreted and must not lead to hasty conclusions regarding the benefits of combining AVP and CS.Two previous studies using retrospective design and prone to similar biases reported consistent results [9,10]. Bauer et al. [9] compared 21 patients receiving AVP and CS with 21 patients infused with AVP without CS. Patients were matched for age, sex, acute physiology score component of the acute physiology and chronic health evaluation (APACHE), number of vasopressors, and primary ICU service [9]. Patients receiving CS were more likely to be alive and weaned off vasopressors at day 7 (80.9 vs. 47.6%, p = 0.02), although the 28-day and hospital mortality were not statistically different. In another retrospective analysis of 778 patients with septic shock enrolled in a multicenter randomized controlled

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confidence: 76%

Arginine–vasopressin and corticosteroids in septic shock: engaged but not yet married!

Lauzier

Lesur

2011

Intensive Care Med

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“…These actions require the specific apelin receptor, APJ, to be expressed in the central nervous system, cardiovascular system, hypothalamus, pituitary gland, and adipoinsular axis. 38 APJ shares great homology with the angiotensin II receptor, AT1R, although it does not bind angiotensin II. 39 The daily production of cortisol is 55 mmol/d, and reaches its physiologic nadir in the morning.…”

Section: Hypothalamic-pituitary-adrenal Axis Physiologymentioning

confidence: 99%

Adrenal Insufficiency in Septic Shock

Maxime

Lesur

Annane

2009

Clinics in Chest Medicine

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“…For example, VIP, which levels increase during experimental endotoxemia in adrenal medulla, was found to stimulate DHEA, testosterone, androstenedione, cortisol, and aldosterone secretion in adrenocortical cells (48–52). Among other mediators found in adrenal medulla, which may influence GC production during sepsis, are angiotensin, AVP, CRH, ACTH, and apelin (53–55). Although direct stimulatory effects of angiotensin 2, CRH, and ACTH on adrenal hormone production are well described, the degree to which each of these peptides contributes to hormone production during sepsis conditions has not been fully elucidated yet (2, 56).…”

Section: Adrenal Gland Microenvironmentmentioning

confidence: 99%

“…Apelin is a neurohormone, which acts through its receptor APJ expressed in various organs including hypothalamic neurons, anterior pituitary, and adrenal gland. It was recently found to modulate neuroendocrine response to stress through stimulation of secretion of both ACTH and corticosterone directly and via AVP- and CRH-dependent pathways (54, 55, 57). …”

Section: Adrenal Gland Microenvironmentmentioning

confidence: 99%

Adrenal Gland Microenvironment and Its Involvement in the Regulation of Stress-Induced Hormone Secretion during Sepsis

2016

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Survival of all living organisms depends on maintenance of a steady state of homeostasis, which process relies on its ability to react and adapt to various physical and emotional threats. The defense against stress is executed by the hypothalamic–pituitary–adrenal axis and the sympathetic–adrenal medullary system. Adrenal gland is a major effector organ of stress system. During stress, adrenal gland rapidly responds with increased secretion of glucocorticoids (GCs) and catecholamines into circulation, which hormones, in turn, affect metabolism, to provide acutely energy, vasculature to increase blood pressure, and the immune system to prevent it from extensive activation. Sepsis resulting from microbial infections is a sustained and extreme example of stress situation. In many critical ill patients, levels of both corticotropin-releasing hormone and adrenocorticotropin, the two major regulators of adrenal hormone production, are suppressed. Levels of GCs, however, remain normal or are elevated in these patients, suggesting a shift from central to local intra-adrenal regulation of adrenal stress response. Among many mechanisms potentially involved in this process, reduced GC metabolism and activation of intra-adrenal cellular systems composed of adrenocortical and adrenomedullary cells, endothelial cells, and resident and recruited immune cells play a key role. Hence, dysregulated function of any of these cells and cellular compartments can ultimately affect adrenal stress response. The purpose of this mini review is to highlight recent insights into our understanding of the adrenal gland microenvironment and its role in coordination of stress-induced hormone secretion.

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Hypothalamic–pituitary–adrenal axis multiple and organ dysfunction syndrome in critical illness: A special focus on arginine-vasopressin and apelin

Cited by 5 publications

References 153 publications

Arginine–vasopressin and corticosteroids in septic shock: engaged but not yet married!

Arginine–vasopressin and corticosteroids in septic shock: engaged but not yet married!

Adrenal Insufficiency in Septic Shock

Adrenal Gland Microenvironment and Its Involvement in the Regulation of Stress-Induced Hormone Secretion during Sepsis

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