title: Anti-inflammatory response in patients with obstructive jaundice caused by biliary malignancy.
abstract: BACKGROUND
  Obstructive jaundice potentially modulates the host defense mechanism resulting in perioperative infection. It has been reported that a systemic inflammatory response occurs in patients with obstructive jaundice. An anti-inflammatory response was studied in 29 jaundiced patients undergoing biliary drainage.
  
  
  RESULTS
  Plasma concentrations of interleukin (IL)-10, soluble tumor necrosis factor receptor (STNFR) p55, STNFR p75, IL-1 receptor antagonist (IL-1ra), IL-6 and soluble CD14 (sCD14) were measured by using immunoassay. Plasma concentrations of IL-10, STNFR p55, STNFR p75, IL-1ra, IL-6 and sCD14 were significantly higher in jaundiced patients than in the controls (P < 0.01). After biliary drainage, the concentrations of IL-10, the three cytokine antagonists, and IL-6 decreased significantly (P < 0.05). The sCD14 concentration did not decrease. At the time of drainage, the concentrations of STNFR p55 and STNFR p75 were significantly higher in 10 patients with positive bile cultures than in 19 patients with negative bile cultures (P < 0.05). Bile cultures became positive 14 days after drainage in 10 patients, and remained negative in nine. The concentration of STNFR p55 before drainage was significantly higher in the former group (P = 0.05). The plasma concentrations of IL-10 and STNFRs were significantly correlated with the IL-6 concentration, body temperature and the white blood cell count (P < 0.05). Serum total bilirubin levels did not affect plasma levels of anti-inflammatory mediators, and sCD14.
  
  
  CONCLUSIONS
  Jaundiced patients exhibited an anti-inflammatory immune response that potentially modulates the host defense mechanism and results in anergy and increased susceptibility to infection. Biliary infection may be one of the major stimuli of the immune response.
authors.affiliation: Department of Surgery, Omiya Red Cross Hospital, Yono, Japan. lionkim@pop01.odn.ne.jp
authors.forename: F
authors.initials: F
authors.lastname: Kimura
authors.forename: M
authors.initials: M
authors.lastname: Miyazaki
authors.forename: T
authors.initials: T
authors.lastname: Suwa
authors.forename: T
authors.initials: T
authors.lastname: Sugiura
authors.forename: T
authors.initials: T
authors.lastname: Shinoda
authors.forename: H
authors.initials: H
authors.lastname: Itoh
authors.forename: K
authors.initials: K
authors.lastname: Nagakawa
authors.forename: S
authors.initials: S
authors.lastname: Ambiru
authors.forename: H
authors.initials: H
authors.lastname: Shimizu
authors.forename: H
authors.initials: H
authors.lastname: Yoshitome
mesh_terms: D000368:Aged; D000906:Antibodies / Q000097:blood; D000917:Antibody Formation; D001650:Bile Duct Neoplasms / Q000150:complications*; D001652:Bile Ducts / Q000382:microbiology; D002779:Cholestasis / Q000209:etiology* / Q000276:immunology* / Q000601:surgery; D004322:Drainage; D005260:Female; D006801:Humans; D007239:Infections; D007249:Inflammation / Q000276:immunology*; D018836:Inflammation Mediators / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D008111:Liver Function Tests; D008297:Male; D008875:Middle Aged
chemical_list: D000906:Antibodies; D018836:Inflammation Mediators; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors