Significant increase of serum high-mobility group box chromosomal protein 1 levels in patients with severe acute pancreatitis

被引:137
作者
Yasuda, Takeo
Ueda, Takashi
Takeyama, Yoshifumi
Shinzeki, Makoto
Sawa, Hidehiro
Nakajima, Takahiro
Ajiki, Tetsuo
Fujino, Yasuhiro
Suzuki, Yasuyuki
Kuroda, Yoshikazu
机构
[1] Kobe Univ, Grad Sch Med Sci, Dept Surg Gastroenterol, Chuo Ku, Kobe, Hyogo 6500017, Japan
[2] Kinki Univ, Sch Med, Dept Surg, Osakasayama, Japan
关键词
severe acute pancreatitis; HMGB1; mediator; inflammation; organ failure;
D O I
10.1097/01.mpa.0000236741.15477.8b
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
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收藏
页码:359 / 363
页数:5
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