title: Significant increase of serum high-mobility group box chromosomal protein 1 levels in patients with severe acute pancreatitis.
abstract: OBJECTIVE
  Multiple organ failure because of systemic inflammatory response in the early phase and sepsis in the late phase is the main contributor to high mortality in severe acute pancreatitis (SAP). High-mobility group box chromosomal protein 1 (HMGB1) was recently identified as a potent proinflammatory mediator and increases in various pathological conditions such as sepsis. The aim of this study was to investigate contributions of HMGB1 in SAP.
  
  
  METHODS
  We measured serum HMGB1 concentrations by an enzyme-linked immunosorbent assay in 45 patients with SAP at the time of admission. Furthermore, relationship between their serum HMGB1 levels and clinical factors was analyzed.
  
  
  RESULTS
  The mean value of serum HMGB1 levels was significantly higher in patients with SAP (5.4 +/- 1.3 ng/mL) than that in healthy volunteers (1.7 +/- 0.3 ng/mL). Serum HMGB1 levels were significantly positively correlated with the Japanese severity score and Glasgow score. Serum HMGB1 levels were significantly positively correlated with lactate dehydrogenase, C-reactive protein, and total bilirubin. The HMGB1 levels were higher in patients with organ dysfunction and infection during the clinical course. The HMGB1 levels in nonsurvivors were higher than those in survivors. Serum HMGB1 levels gradually declined after the admission.
  
  
  CONCLUSIONS
  Serum HMGB1 levels were significantly increased in patients with SAP and were correlated with disease severity. These results suggest that HMGB1 may act as a key mediator for inflammation and organ failure in SAP.
authors.affiliation: Department of Gastroenterological Surgery, Kobe University Graduate School of Medical Sciences, Japan. yasudatk@med.kobe-u.ac.jp
authors.forename: Takeo
authors.initials: T
authors.lastname: Yasuda
authors.forename: Takashi
authors.initials: T
authors.lastname: Ueda
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Takeyama
authors.forename: Makoto
authors.initials: M
authors.lastname: Shinzeki
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Sawa
authors.forename: Takahiro
authors.initials: T
authors.lastname: Nakajima
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Ajiki
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Fujino
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Kuroda
mesh_terms: D001424:Bacterial Infections / Q000097:blood / Q000150:complications; D001663:Bilirubin / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D024243:HMGB1 Protein / Q000097:blood*; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood / Q000209:etiology; D010195:Pancreatitis / Q000097:blood* / Q000150:complications; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood; D011379:Prognosis; D012720:Severity of Illness Index; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology; D013997:Time Factors
chemical_list: D015415:Biomarkers; D024243:HMGB1 Protein; D002097:C-Reactive Protein; D007770:L-Lactate Dehydrogenase; D001663:Bilirubin