Abstract
Background. Biliary obstruction changes the spectrum of lipoproteins, which are now known to
bind and neutralize endotoxin. Postoperative septic complications related to an increased
susceptibility to endotoxin occur frequently in patients with obstructive jaundice.
The effect of preoperative biliary drainage on changes in the lipoprotein spectrum
and its relation to endotoxin sensitivity was studied. Methods. Abnormalities in the lipoprotein spectrum were assessed in 15 patients with malignant
obstructive jaundice before and 3 weeks after endoscopic biliary drainage. Changes
in endotoxin responsiveness were assessed by using endotoxin-neutralizing reagents
(anti-CD14 monoclonal antibody, polymyxin B, and recombinant bactericidal permeability
increasing protein) to block cytokine production in whole blood cell cultures that
were stimulated by cholestatic plasma taken before and after drainage. Results. Drainage normalized very-low-density, low-density, and high-density lipoprotein cholesterol
fractions from, respectively, 43% to 19%, 50% to 65%, and 6% to 16% (P <.01). Ex vivo
stimulation of whole blood with predrainage cholestatic plasma was 20-fold higher
(P <.001) than with postdrainage plasma. Blocking the endotoxin response during the
stimulation with predrainage cholestatic plasma with anti-CD14 monoclonal antibody,
polymyxin B or recombinant bactericidal permeability increasing protein resulted in
attenuation of the inflammatory response, reducing tumor necrosis factor-α levels
at least 5-fold. Conclusions. Preoperative biliary drainage normalizes the changed lipid profile and the endotoxin-stimulating
capacity of cholestatic plasma, and this signifies a change in sensitivity to endotoxin.
(Surgery 2001;129:282-91.)
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Article info
Publication history
Accepted:
August 12,
2000
Footnotes
☆Reprint requests: D. J. Gouma, Department of Surgery/G4-144, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
☆☆Surgery 2001;129:282-91
Identification
Copyright
© 2001 Mosby, Inc. Published by Elsevier Inc. All rights reserved.