BACKGROUND: Lipopolysaccharide-binding protein (LBP) is a class 1 acute-phase protein that binds and transfers bacterial lipopolysaccharide (LPS). This study investigated the clinical value of measuring LBP for stratifying biochemical severity in acute pancreatitis by using a recently developed fully automated assay technique. PATIENTS AND METHODS: We studied 71 patients with acute pancreatitis of whom 41 presented with a necrotizing course. Necrotizing pancreatitis was associated with pancreatic infections in 21 patients and with multiorgan dysfunction syndrome (MODS) in 18 patients. Serum LBP was measured for 14 days by a fully automated immunoassay and CRP was assessed on a daily routine basis. RESULTS: The relative quantitative systemic release of LBP was lower than that observed for CRP; however, the two parameters revealed similar dynamics, with a maximum increase in acute pancreatitis around the fourth day after onset of symptoms. As observed for CRP, LBP was significantly higher in patients who developed complications such as necrosis, pancreatic infections, single or combined MODS than in those who did not. Multiple regression analysis revealed that pulmonary failure and MODS were independent variables associated with enhanced LBP release, while the development of necrosis, pancreatic infections and MODS were the corresponding variables for increased CRP levels. CONCLUSIONS: Systemic LBP concentrations are significantly elevated in acute pancreatitis and closely correlate with overall disease severity. However, compared with CRP, LBP does not contribute to an improved severity stratification in acute pancreatitis.
BACKGROUND:Lipopolysaccharide-binding protein (LBP) is a class 1 acute-phase protein that binds and transfers bacterial lipopolysaccharide (LPS). This study investigated the clinical value of measuring LBP for stratifying biochemical severity in acute pancreatitis by using a recently developed fully automated assay technique. PATIENTS AND METHODS: We studied 71 patients with acute pancreatitis of whom 41 presented with a necrotizing course. Necrotizing pancreatitis was associated with pancreatic infections in 21 patients and with multiorgan dysfunction syndrome (MODS) in 18 patients. Serum LBP was measured for 14 days by a fully automated immunoassay and CRP was assessed on a daily routine basis. RESULTS: The relative quantitative systemic release of LBP was lower than that observed for CRP; however, the two parameters revealed similar dynamics, with a maximum increase in acute pancreatitis around the fourth day after onset of symptoms. As observed for CRP, LBP was significantly higher in patients who developed complications such as necrosis, pancreatic infections, single or combined MODS than in those who did not. Multiple regression analysis revealed that pulmonary failure and MODS were independent variables associated with enhanced LBP release, while the development of necrosis, pancreatic infections and MODS were the corresponding variables for increased CRP levels. CONCLUSIONS: Systemic LBP concentrations are significantly elevated in acute pancreatitis and closely correlate with overall disease severity. However, compared with CRP, LBP does not contribute to an improved severity stratification in acute pancreatitis.