BACKGROUND:Bilirubin oxidative metabolites (BOMs) are generated from bilirubin as a result of its scavenging action against free radicals. During sepsis, excess amounts of free radicals are produced, and they play an important role in the pathophysiological process. We studied whether urinary excretion of BOMs would increase under septic conditions in humans and compared BOM levels with other well-established clinical parameters of inflammation. METHODS: In 19 septic patients and 28 nonseptic control patients, the BOM concentrations in urine were measured by enzyme-linked immunosorbent assay with an anti-bilirubin antibody. RESULTS:Urinary BOM levels in septic patients were much higher than those in control patients (21.6 +/- 2.5 vs 1.4 +/- 0.4 micromol/g creatinine, P < 0.001). Although there was a linear correlation between urinary BOM and serum total bilirubin levels (r = 0.392, P = 0.008), serum bilirubin levels were not significantly higher in the septic group than in the control group (P = 0.072). BOM levels correlated with body temperature (r = 0.801, P < 0.001), white blood cell counts in the peripheral blood (r = 0.590, P < 0.001), serum C-reactive protein (r = 0.653, P < 0.001), and the acute physiological and chronic health evaluation (APACHE II) score (r = 0.467, P = 0.003). CONCLUSIONS: These results demonstrated a urinary increase in BOMs in septic patients. This increase indicates that urinary BOM level is a possible marker for continuous monitoring of sepsis severity in clinical practice. Copyright 2001 Academic Press.
RCT Entities:
BACKGROUND:Bilirubin oxidative metabolites (BOMs) are generated from bilirubin as a result of its scavenging action against free radicals. During sepsis, excess amounts of free radicals are produced, and they play an important role in the pathophysiological process. We studied whether urinary excretion of BOMs would increase under septic conditions in humans and compared BOM levels with other well-established clinical parameters of inflammation. METHODS: In 19 septic patients and 28 nonseptic control patients, the BOM concentrations in urine were measured by enzyme-linked immunosorbent assay with an anti-bilirubin antibody. RESULTS: Urinary BOM levels in septic patients were much higher than those in control patients (21.6 +/- 2.5 vs 1.4 +/- 0.4 micromol/g creatinine, P < 0.001). Although there was a linear correlation between urinary BOM and serum total bilirubin levels (r = 0.392, P = 0.008), serum bilirubin levels were not significantly higher in the septic group than in the control group (P = 0.072). BOM levels correlated with body temperature (r = 0.801, P < 0.001), white blood cell counts in the peripheral blood (r = 0.590, P < 0.001), serum C-reactive protein (r = 0.653, P < 0.001), and the acute physiological and chronic health evaluation (APACHE II) score (r = 0.467, P = 0.003). CONCLUSIONS: These results demonstrated a urinary increase in BOMs in septic patients. This increase indicates that urinary BOM level is a possible marker for continuous monitoring of sepsis severity in clinical practice. Copyright 2001 Academic Press.