Digestive Diseases and Sciences, Vol. 49, No. 9 (September 2004), pp. 1433–1437 ( C  2004) Decreased Total and Corrected Antioxidant Capacity in Patients with Inflammatory Bowel Disease IOANNIS E. KOUTROUBAKIS, MD,* NIKI MALLIARAKI, MD,† PHILIPPOS D. DIMOULIOS, MD,* KONSTANTINOS KARMIRIS, MD,* ELIAS CASTANAS, MD, PhD,§ and ELIAS A. KOUROUMALIS, MD, PhD* Oxidative stress and depletion of antioxidants may play a key role in the pathogenesis 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 disease (CD) in comparison to healthy controls (HC). Ninety-four patients with UC, 97 patients with CD, and 72 HC were included in this study. Serum TAC was measured in all patients and controls on an Olympus AU-600 chemistry analyzer using 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 cTAC 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 those with inactive disease. Patients with active CD had significantly lower mean TAC compared to those with inactive disease but cTAC was not different between the two phases of disease activity. Patients with proctitis had significantly higher TAC and cTAC compared to patients with left-sided colitis and total colitis. In CD patients no association between disease localization and these markers was found. TAC and cTAC are significantly reduced in IBD patients compared with controls 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. KEY WORDS: antioxidants; Crohn’s disease; oxidative stress; ulcerative colitis. Oxidative stress has been recognized as one of the key elements of tissue injury in inflammatory bowel disease (IBD) (1). It has been suggested that intestinal damage in IBD is related both to increased free radical production, mainly resulting from a respiratory burst of infiltrating phagocytic cells, and to a low concentration of endogenous antioxidant defenses (2). Neutrophils and monocytes from patients with active IBD produce higher concentrations of Manuscript received January 16, 2004; accepted June 8, 2004. From the Departments of *Gastroenterology, †Clinical Chemistry and §Experimental Endocrinology, University Hospital Heraklion, Crete, Greece. Address for reprint requests: Ioannis E. Koutroubakis, MD, Depart- ment of Gastroenterology, University Hospital Heraklion, P.O. Box 1352, Heraklion 71110, Greece; ktjohn@her.forthnet.gr. oxygen-derived free radicals than controls (3, 4). On the other hand, the levels of the most important antioxidants have been found to be seriously impaired within the in- testinal mucosa from IBD patients compared with normal mucosa (5–9). Efficacy of various therapies in IBD has been suggested to be related to antioxidant actions (10– 12). 5-Aminosalicylic acid, which is used as standard ther- apy in IBD, is a highly potent scavenger of reactive oxygen species (ROS) and was shown to reduce lipid peroxidation in Crohn’s disease (CD) and ulcerative colitis (UC) (10). Several methods have been proposed for determina- tion of total serum or plasma antioxidant capacity (TAC). They can rely on either the measurement of individual antioxidant components (e.g., vitamin E and ascorbic acid) or the estimation of the total antioxidant potency by the Digestive Diseases and Sciences, Vol. 49, No. 9 (September 2004) 1433 0163-2116/04/0900-1433/0 C  2004 Springer Science+Business Media, Inc.