Serum depletion of corticosteroid binding activities, an early marker of human septic shock

Savu, Lia; Zouaghi, H.; Carli, A; Nunez, Emmanuel A.

doi:10.1016/0006-291x(81)91536-9

Cited by 61 publications

(32 citation statements)

References 7 publications

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“…These data are in keeping with previous studies showing decreased CBG levels following inflammation or septic shock [43,44]. CBG is thought to be a 'negative acute-phase protein' since levels of CBG and liver mRNA for transcortin are reduced during an acute phase or inflammatory reaction in rats [45,46].…”

Section: Discussionsupporting

confidence: 80%

Neuroendocrine and Immune Responses to Acute Endotoxemia in Suckling and Weaned Piglets

Kanitz

Tuchscherer

et al. 2002

Neonatology

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The objective of this study was to characterize effects of weaning stress on behavioural, endocrine and immune responses to acute peripheral lipopolysaccharide (LPS) challenge in neonatal pigs. Weaning in 28-day-old piglets was accompanied by a significant increase in ACTH concentrations (p = 0.0378) and an increase in basal cortisol level (p = 0.0135). There was also a significant suppressive effect on lymphocyte proliferation in response to concanavalin A (p = 0.0048) in newly weaned piglets. Peripheral administration of LPS induced vomiting, diarrhoea and somnolence in both suckling and weaned piglets. The frequency of these signs of sickness was significantly higher in weaned piglets compared with suckling piglets (p = 0.0049). Additionally, LPS significantly increased plasma concentrations of TNF-α, cortisol and ACTH. While weaned piglets reacted to LPS with a higher release of ACTH (p = 0.0239) and cortisol (p = 0.0015) than suckling piglets there was no significant effect of weaning on the magnitude of TNF-α. The present data indicate that weaning suppresses the lymphocyte function, causes changes in endocrine regulation and has a substantial effect on the behavioural and endocrine response to an acute peripheral LPS challenge; consequently it could increase disease susceptibility.

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Section: Discussionsupporting

confidence: 80%

Neuroendocrine and Immune Responses to Acute Endotoxemia in Suckling and Weaned Piglets

Kanitz

Tuchscherer

et al. 2002

Neonatology

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“…Social stress (Spencer et al 1996, Alexander & Irvine 1998, septic shock (Savu et al 1981), immobilization (Tinnikov 1993, Marti et al 1997, inescapable tail shock (Fleshner et al 1995, Deak et al 1999, food deprivation (Tinnikov 1993, Lynn et al submitted), and surgery (Tinnikov et al 1996, Vogeser et al 1999 all decrease CBG capacity, although the effect is usually not apparent for at least a few hours. Given that stress tends to decrease CBG capacity, whereas CORT manipulations have no generalizable effect, the decrease in CBG capacity during stress may be due to another stress hormone (such as epinephrine or ACTH), or as a result of metabolic changes at the liver in response to one of the hormones released during stress.…”

Section: Androgen Binding Globulin?mentioning

confidence: 99%

Plasma binding proteins as mediators of corticosteroid action in vertebrates

Breuner

Orchinik

2002

Journal of Endocrinology

418

247

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Stressors elicit a complex but variable suite of endocrine events. Comparative studies of the stress response have focused primarily on the adrenocortical response to stress, in particular the measurement of plasma levels of glucocorticoids. However, a number of other factors contribute to and modify cellular and organismal responses to glucocorticoids. Notably, plasma corticosteroid binding globulins (CBGs) can regulate the general availability of steroid to tissues, and/or direct the delivery of hormones to specific sites. In this paper, we discuss possible functions of CBG and mechanisms of CBG action, review CBG characteristics among vertebrates, and discuss our recent studies indicating that CBG may indeed modulate responses to stressors. For example, in house sparrows, we found that basal and stress-induced concentrations of total corticosteroid (cortisol or corticosterone) (CORT) vary seasonally, but CBG concentrations change proportionally, so that free CORT concentrations appear static yearround. In contrast, in white-crowned sparrows and tree lizards, CBG concentrations change under conditions when total CORT levels do not, resulting in significant changes in circulating free CORT. These differences in free CORT are masked if CBG is not accounted for. We have also found that the binding properties of CBG vary considerably between species and need to be determined empirically. Such studies led to the observation that CBG in several species may also serve as a functional androgen binding protein; this is especially important for birds, because previous studies had concluded that birds lack androgen binding globulins. We propose that consideration of CBG is paramount to understanding the role of glucocorticoids in mediating behavioral and physiological responses to stress.

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“…Furthermore, the degree of cortisolaemia frequently correlates with severity of illness and mortality rate [193,194] and is associated with an altered response of the HPA axis to suppression by dexamethasone and stimulation by corticotrophin-releasing hormone (CRH) and ACTH [194]. Cortisol elevation is achieved by several mechanisms including: 1) activation of the HPA axis; 2) GC resistance resulting from alterations in GCR binding; 3) failure of pituitary and hypothalamus glucocorticoid negative feedback; 4) decreased binding to CBG [195][196][197]; and 5) decreased cortisol extraction from the blood [192,193].…”

Section: Relationship Between Exaggerated Host Defence Response and Ementioning

confidence: 99%

“…Syndromes of glucocorticoid resistance respond to treatment with exogenous glucocorticoids [44]. Additional factors contributing to hypercortisolaemia include decreased binding to CBG [195][196][197] and decreased cortisol extraction from the blood [192,193]. Septic patients have a rapid depletion in CBG with increased free (nonbound) cortisol [195][196][197].…”

Section: Relationship Between Exaggerated Host Defence Response and Ementioning

confidence: 99%

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

Gu¹

1996

Eur Respir J

114

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T Th he e r ro ol le e o of f t th he e h ho os st t d de ef fe en nc ce e r re es sp po on ns se e i in n t th he e p pr ro og gr re es ss si io on n a an nd d o ou ut tc co om me e o of f A AR RD DS S: : p pa at th ho op ph hy ys si io ol lo og gi ic ca al l c co or rr re el la at ti io on ns s a an nd d r re es sp po on ns se e t to o g gl lu uc co oc co or rt ti ic co oi id d t tr re ea at tm me en nt t

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Serum depletion of corticosteroid binding activities, an early marker of human septic shock

Cited by 61 publications

References 7 publications

Neuroendocrine and Immune Responses to Acute Endotoxemia in Suckling and Weaned Piglets

Neuroendocrine and Immune Responses to Acute Endotoxemia in Suckling and Weaned Piglets

Plasma binding proteins as mediators of corticosteroid action in vertebrates

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

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