Duration of Glucocorticoid Treatment and Outcome in Sepsis

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Duration of Glucocorticoid Treatment and Outcome in Sepsis G. Umberto Meduri, MD, FCCP, George P. Chrousos, MD CHEST Volume 114, Issue 2, Pages 355-360 (August 1998) DOI: 10.1378/chest.114.2.355-a Copyright © 1998 The American College of Chest Physicians Terms and Conditions

FIGURE 1 Cortisol inhibits monocyte/macrophage and TH1 functions by suppressing the secretion of proinflammatory cytokines. Cortisol stimulates TH2 functions by default, in the presence of elevated catecholamines as during inflammatory stress, by suppressing TH1-mediated inhibition of catecholamine-stimulated TH2 functions. Cortisol has weak IL-6/anti-inflammatory cytokine suppressing properties, if any, with the stimulant effects of catecholamines predominating. Note that IL-6 is both a proinflammatory and an anti-inflammatory cytokine. CHEST 1998 114, 355-360DOI: (10.1378/chest.114.2.355-a) Copyright © 1998 The American College of Chest Physicians Terms and Conditions

FIGURE 2 Effect of cortisol on arterial blood pressure. Cortisol potentiates the effects of vasoconstrictor systems, inhibits vasodilatory systems, and through its mineralocorticoid properties, retains salt and increases blood volume. TNF-α and IL-1, both of which are inhibited by cortisol, represent major vasodilatory stimulants during the inflammatory stress of sepsis, septic shock, and ARDS. CHEST 1998 114, 355-360DOI: (10.1378/chest.114.2.355-a) Copyright © 1998 The American College of Chest Physicians Terms and Conditions