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Published ahead of print on November 8, 2002, doi:10.1164/rccm.200205-446OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 4, February 2003, 512-520

A more recent version of this article appeared on February 15, 2003
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Submitted on June 13, 2002
Accepted on October 31, 2002

Immunological and hemodynamic effects of 'low-dose' hydrocortisone in septic shock

Didier Keh1*, Thomas Boehnke1, Steffen Weber-Carstens1, Cristina Schulz1, Olaf Ahlers1, Sven Bercker1, Hans D Volk2, Wolf D Doecke2, Konrad J Falke1, and Herwig Gerlach3

1 Anesthesiology, Charite-Campus Virchow Clinic, Humboldt University, Berlin, Germany, 2 Immunology, Charite-Campus Virchow Clinic, Humboldt University, Berlin, Germany, 3 Anesthesiology, Vivantes Klinikum Neukoelln, Berlin, Germany

* To whom correspondence should be addressed. E-mail: didier.keh{at}charite.de.

Within the last few years, increasing evidence of relative adrenal insufficiency in septic shock evoked a reassessment of hydrocortisone therapy. To evaluate effects of hydrocortisone on the balance between pro- and anti-inflammation, forty patients with septic shock were randomized in a double-blind crossover study to receive either first 100 mg hydrocortisone as a loading dose and 10 mg per hour until day three (n=20) or placebo (n=20), followed by the opposite medication until day six. Hydrocortisone infusion induced an increase of mean arterial pressure, systemic vascular resistance, and a decline of heart rate, cardiac index, and norepinephrine requirement. A reduction of plasma nitrite/nitrate indicated inhibition of nitric oxide formation and correlated with reduction of vasopressor support. The inflammatory response (interleukin-6 and 8), endothelial (soluble E-selectin) and neutrophil activation (expression of CD11b, CD64), and antiinflammatory response (soluble tumor necrosis factor receptors I and II and interleukin 10) were attenuated. In peripheral blood monocytes, HLA-DR expression was only slightly depressed, whereas in-vitro phagocytosis and the monocyte activating cytokine interleukin 12 increased. Hydrocortisone withdrawal induced hemodynamic and immunological rebound effects. In conclusion, hydrocortisone therapy restored hemodynamic stability and differentially modulated the immunological response to stress in a way of antiinflammation rather than immunosuppression.
Key words: Sepsis, Glucocorticoids, Immune System




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