摘要
Oxidative stress and depletion of antioxidants may play a key role in the path ogenesis of inflammatory bowel disease (IBD) -related intestinal damage. A new automated assay for the determination of blood total antioxidant capacity (TAC), based on the crocin bleaching method, has been used for the measurement of TAC and corrected TAC (cTAC) in patients with ulcerative colitis (UC) and Crohn’s d isease (CD) in comparison to healthy controls (HC). Ninety-four patients with U C, 97 patients with CD, and 72 HC were included in this study. Serum TAC was mea sured in all patients and controls on an Olympus AU-600 chemistry analyzer usin g a TAC kit. cTAC was calculated from TAC after subtraction of the interactions due to endogenous uric acid, bilirubin and albumin. Mean serum TAC as well as cT AC levels were significantly lower in both UC and CD patients compared with HC ( P<0.0001). Patients with active UC had no different TAC and cTAC compared to tho se with inactive disease. Patients with active CD had significantly lower mean T AC compared to those with inactive disease but cTAC was not different between th e two phases of disease activity. Patients with proctitis had significantly high er TAC and cTAC compared to patients with left-sided colitis and total colitis. In CD patients no association between disease localization and these markers wa s found. TAC and cTAC are significantly reduced in IBD patients compared with co ntrols irrespective of disease activity. The decreased antioxidant defenses may be a primary phenomenon severely compromising the mucosa and therefore increase susceptibility to oxidative tissue damage.
Oxidative stress and depletion of antioxidants may play a key role in the path ogenesis of inflammatory bowel disease (IBD) -related intestinal damage. A new automated assay for the determination of blood total antioxidant capacity (TAC), based on the crocin bleaching method, has been used for the measurement of TAC and corrected TAC (cTAC) in patients with ulcerative colitis (UC) and Crohn's d isease (CD) in comparison to healthy controls (HC). Ninety-four patients with U C, 97 patients with CD, and 72 HC were included in this study. Serum TAC was mea sured in all patients and controls on an Olympus AU-600 chemistry analyzer usin g a TAC kit. cTAC was calculated from TAC after subtraction of the interactions due to endogenous uric acid, bilirubin and albumin. Mean serum TAC as well as cT AC levels were significantly lower in both UC and CD patients compared with HC ( P<0.0001). Patients with active UC had no different TAC and cTAC compared to tho se with inactive disease. Patients with active CD had significantly lower mean T AC compared to those with inactive disease but cTAC was not different between th e two phases of disease activity. Patients with proctitis had significantly high er TAC and cTAC compared to patients with left-sided colitis and total colitis. In CD patients no association between disease localization and these markers wa s found. TAC and cTAC are significantly reduced in IBD patients compared with co ntrols irrespective of disease activity. The decreased antioxidant defenses may be a primary phenomenon severely compromising the mucosa and therefore increase susceptibility to oxidative tissue damage.
