Interferon Gamma-1b in the Treatment of Compensatory Anti-inflammatory Response Syndrome: A New Approach: Proof of Principle

doi:10.1001/archinte.1997.00440250031004

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Vol. 157 No. 4, 24 FEBRUARY 1997

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Interferon Gamma-1b in the Treatment of Compensatory Anti-inflammatory Response Syndrome

A New Approach: Proof of Principle

Wolfgang J. Kox, MD, PhD; Roger C. Bone, MD; Dietmar Krausch, MD; Wolf-Dietrich Döcke, MD; S. Nilden Kox, PhD; Helmar Wauer, MD; Karl Egerer, MD; Susanne Querner, PhD; Khusru Asadullah, MD; Rüdiger von Baehr, MD; Hans-Dieter Volk, MD

Arch Intern Med. 1997;157(4):389-393.

Abstract

Background
Immunoparalysis is defined as a decrease in the level of HLA-DRexpression on monocytes during the course of sepsis.

Objective
To evaluate whether interferon gamma-1b has an immunoregulatoryeffect in patients with immunoparalysis during the compensatoryanti-inflammatory response syndrome.

Methods
Of the patients admitted consecutively to the intensive careunit for the management of sepsis, 10 received interferon gamma-1b,100 µg per 0.5 mL, after confirmation of HLA-DR expressionof less than 30% on 2 consecutive days. The therapy was continueduntil HLA-DR expression remained more than 50% for 3 days.

Results
Interferon gamma-1b therapy resulted in the recovery of diminishedlevels of HLA-DR expression on monocytes. Of the 10 patients,8 responded to treatment within 1 day. On the first day of interferongamma-1b therapy, HLA-DR expression increased from mean (±SEM)pretreatment levels of 27%±6% to 62%±8% (P<.01)and remained high during the 28-day study period in 8 patients.The therapy was given to 2 patients a second time when HLA-DRexpression on monocytes was less than 30%. The recovery of monocyticHLA-DR expression levels after administration of interferongamma-1b was associated with restitution of monocytic function,reflected by a significant increase of plasma interleukin-6(P<.05) and tumor necrosis factor a (P<.05) levels in9 patients.

Conclusions
This study shows that HLA-DR expression is a good marker ofcompensatory anti-inflammatory response syndrome. It also showsthat interferon gamma-1b not only restored the levels of HLA-DRexpression but also reestablished the ability of monocytes tosecrete the cytokines interleukin-6 and tumor necrosis factora.

Arch Intern Med. 1997;157:389-393

Author Affiliations

From the Department of Anaesthesiology and Intensive Therapy (Drs W. J. Kox, Krausch, S. N. Kox, Wauer, and Egerer), the Institute of Medical Immunology (Drs Döcke, Asadullah, von Baehr, and Volk), University Hospital Charité), Humboldt University, Berlin, Germany; Rush-Presbyterian-St Luke's Medical Center (Dr Bone), Chicago, Ill; and Boehringer Ingelheim GmbH (Dr Querner), Ingelheim/Rhein, Germany.

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