Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation.

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Bibliographic Details
Title:	Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation.
Authors:	Singer, Mervyn, De Santis, Vincenzo, Vitale, Domenico, Jeffcoate, William
Source:	Lancet. 8/7/2004, Vol. 364 Issue 9433, p545-548. 4p.
Subjects:	Sepsis, Multiple organ failure, Cell metabolism, Mitochondria, Inflammatory mediators, Metabolic regulation, Clinical biochemistry, Critical care medicine
Abstract:	Sepsis and other critical illnesses produce a biphasic inflammatory, immune, hormonal, and metabolic response. The acute phase is marked by an abrupt rise in the secretion of so-called stress hormones with an associated increase in mitochondrial and metabolic activity. The combination of severe inflammation and secondary changes in endocrine profile diminish energy production, metabolic rate, and normal cellular processes, leading to multiple organ dysfunction. This perceived failure of organs might instead be a potentially protective mechanism, because reduced cellular metabolism could increase the chances of survival of cells, and thus organs, in the face of an overwhelming insult. We propose that, fist, multiple organ failure induced by critical illness is primarily a functional, rather than structural, abnormality. Indeed, it may not be failure as such, but a potentially protective, reactive mechanism. Second, the decline in organ function is triggered by a decrease in mitochondrial activity and oxidative phosphorylation, leading to reduced cellular metabolism. Third, this effect on mitochondria might be the consequence of acute-phase changes in hormones and inflammatory mediators. [ABSTRACT FROM AUTHOR]
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Database:	Psychology and Behavioral Sciences Collection

Description
Abstract:	Sepsis and other critical illnesses produce a biphasic inflammatory, immune, hormonal, and metabolic response. The acute phase is marked by an abrupt rise in the secretion of so-called stress hormones with an associated increase in mitochondrial and metabolic activity. The combination of severe inflammation and secondary changes in endocrine profile diminish energy production, metabolic rate, and normal cellular processes, leading to multiple organ dysfunction. This perceived failure of organs might instead be a potentially protective mechanism, because reduced cellular metabolism could increase the chances of survival of cells, and thus organs, in the face of an overwhelming insult. We propose that, fist, multiple organ failure induced by critical illness is primarily a functional, rather than structural, abnormality. Indeed, it may not be failure as such, but a potentially protective, reactive mechanism. Second, the decline in organ function is triggered by a decrease in mitochondrial activity and oxidative phosphorylation, leading to reduced cellular metabolism. Third, this effect on mitochondria might be the consequence of acute-phase changes in hormones and inflammatory mediators. [ABSTRACT FROM AUTHOR]
ISSN:	01406736
DOI:	10.1016/S0140-6736(04)16815-3