Total and unbound Cortisol‐, progesterone‐, oestrone‐ and transcortin‐binding activities in sera from patients with myocardial infarction: evidence for differential responses of good and bad prognostic cases

Zouaghi, H.; Savu, Lia; Guérot, C; Gryman, R; Coulon, A; Nunez, Emmanuel A.

doi:10.1111/j.1365-2362.1985.tb00286.x

Cited by 24 publications

(21 citation statements)

References 22 publications

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“…108 The production of cortisol in adrenocortical cells in response to ACTH occurs within minutes, and there is a shift towards an increase in glucocorticoid and away from mineralocorticoid and androgen production. 113 The CBG concentration in serum and the CBG binding affinity are both decreased 22,23,26,238 resulting in a dramatic increase in the biological active free cortisol concentration. In addition, the glucocorticoid receptor shows an increased affinity to free hormone during the acute phase of critical illness.…”

Section: Hpa (Dys)function In Human Sepsismentioning

confidence: 99%

“…18 Under basal conditions, 90-95% of plasma cortisol is bound to CBG, and it is generally believed that the fraction of CBG-bound cortisol has a limited access to target cells and, therefore, is biologically inactive. 19 CBG is a 'negative acute phase protein' and levels of CBG are reduced during stress, 20,21 inflammation 22,23 or infection/sepsis. [23][24][25][26] It has been proposed that during inflammation CBG is reduced through interactions of the steroid-bound CBG complex with serine proteases that are released by activated neutrophils.…”

Section: The Hpa Axismentioning

confidence: 99%

“…19 CBG is a 'negative acute phase protein' and levels of CBG are reduced during stress, 20,21 inflammation 22,23 or infection/sepsis. [23][24][25][26] It has been proposed that during inflammation CBG is reduced through interactions of the steroid-bound CBG complex with serine proteases that are released by activated neutrophils. 18,25,27 These enzymes cleave steroid from CBG, concentrating free steroid at the site of inflammation and, once cleaved, CBG's affinity for the steroid is reduced.…”

Section: The Hpa Axismentioning

confidence: 99%

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Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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Endotoxin is considered to be a systemic (immunological) stressor eliciting a prolonged activation of the hypothalamo-pituitary-adrenal (HPA) axis. The HPA-axis response after an endotoxin challenge is mainly due to released cytokines (IL-1, IL-6 and TNF-a) from stimulated peripheral immune cells, which in turn stimulate different levels of the HPA axis. Controversy exists regarding the main locus of action of endotoxin on glucocorticoid secretion, since the effect of endotoxin on this neuro-endocrine axis has been observed in intact animals and after ablation of the hypothalamus; however, a lack of LPS effect has been described at both pituitary and adrenocortical levels. The resulting increase in adrenal glucocorticoids has well-documented inhibitory effects on the inflammatory process and on inflammatory cytokine release. Therefore, immune activation of the adrenal gland by endotoxin is thought to occur by cytokine stimulation of corticosteroidreleasing hormone (CRH) production in the median eminence of the hypothalamus, which, in turn stimulates the secretion of ACTH from the pituitary. Acute administration of endotoxin stimulates ACTH and cortisol secretion and the release of CRH and vasopressin (AVP) in the hypophysial portal blood. During repeated endotoxemia, tolerance of both immune and HPA function develops, with a crucial role for glucocorticoids in the modulation of the HPA axis. A single exposure to a high dose of LPS can induce a long-lasting state of tolerance to a second exposure of LPS, affecting the response of plasma TNF-a and HPA hormones. Although there are gender differences in the HPA response to endotoxin and IL-1, these responses are enhanced by castration and attenuated by androgen and estrogen replacement. Estrogens attenuate the endotoxin-induced stimulation of IL-6, TNF-a and IL-1ra release and subsequent activation in postmenopausal women. There appears to be a temporal and functional relation between the HPA-axis response to endotoxin and nitric oxide formation in the neuro-endocrine hypothalamus, suggesting a stimulatory role for nitric oxide in modulating the HPA response to immune challenges. demonstrate higher plasma levels of IL-1 and TNF-a. Elevation of plasma glucocorticoids results in suppression of cytokines such as IL-1, IL-6, and TNF-a and in up-regulation of other cytokines, such as IL-4 and IL-10, and cytokine receptors. Thus, by regulation of cytokine production and action, the HPA axis contributes to modulation of the response to inflammation/infection. In addition, the role of HPA activation has been suggested to be a negative feedback system provided by the immunosuppressive activity of glucocorticoids, limiting inflammatory responses and preventing the immune system from over-reacting and causing tissue damage or autoimmunity.As early as 1957, Wexler et al. suggested that LPS could induce ACTH release since they found a depletion of ascorbic acid and cholesterol in the adrenal glands. 10 Moreover, LPS was not able to cause these changes in hypophysectomized rats. ...

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Section: Hpa (Dys)function In Human Sepsismentioning

confidence: 99%

Section: The Hpa Axismentioning

confidence: 99%

Section: The Hpa Axismentioning

confidence: 99%

See 1 more Smart Citation

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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“…A previous study of just 34 patients also reported a negative association between cortisol concentration and risk of death (4). By contrast, three small studies of between 22 and 70 patients with few deaths suggested increased risk of death among patients with high cortisol concentrations (5-7).…”

Section: Discussionmentioning

confidence: 93%

Low serum cortisol predicts early death after acute myocardial infarction

Reynolds

Walker

Haw

et al. 2010

Critical Care Medicine

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ObjectiveLow serum cortisol concentrations have been associated with adverse prognosis in critical illness of diverse aetiology. We aimed to determine whether low serum cortisol concentrations are associated with adverse prognosis in patients with acute myocardial infarction. DesignNested case-control study. SettingProspective cohort study of consecutive patients admitted with acute myocardial infarction to 9 Scottish hospitals.Patients 100 patients who survived 30 days (controls) and 100 patients who died within 30 days (cases). Measurements and Main ResultsAdmission cortisol concentrations were lower in patients who died than those who survived (median 1,189 versus 1,355 nmol/L, p<0.001). A cortisol concentration in the bottom quartile (<1,136 nmol/L) was a strong predictor of death within 30 days, and remained so after adjustment for age and cardiac troponin concentration (adjusted OR 8.78, 95% CI 3.09-24.96, p<0.001). ConclusionsPatients who mount a lesser cortisol stress response to acute myocardial infarction have a poorer early prognosis.2

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“…The HLE cleavage of CBG results in a ten-fold decrease in its binding affinity 21 , thus releasing cortisol 10 . In states of stress such as sepsis 22 , burns 23 and myocardial infarction 24 , the free cortisol percentage increases to up to 20%, due to the saturation of available CBG by increased cortisol and reduced CBG levels (a result of increased CBG cleavage/catabolism and inhibited synthesis) 25,26 . Inflammatory cytokines such as IL-6, glucocorticoids, insulin, hyperthyroidism, nephrotic syndrome, and cirrhosis can also reduce CBG concentrations.…”

mentioning

confidence: 99%