Volume 16, Issue 9 pp. 1467-1475
Original Article

Impaired erythrocyte antioxidant defense in active inflammatory bowel disease: Impact of anemia and treatment

Malgorzata Krzystek-Korpacka PhD

Corresponding Author

Malgorzata Krzystek-Korpacka PhD

Department of Medical Biochemistry, Wroclaw Medical University, Wroclaw, Poland

Dept. of Medical Biochemistry, Wroclaw Medical University, ul. Chalubinskiego 10, 50-368 Wroclaw, PolandSearch for more papers by this author
Katarzyna Neubauer MD, PhD

Katarzyna Neubauer MD, PhD

Department of Gastroenterology and Hepatology, Wroclaw Medical University, Wroclaw, Poland

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Izabela Berdowska PhD

Izabela Berdowska PhD

Department of Medical Biochemistry, Wroclaw Medical University, Wroclaw, Poland

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Bogdan Zielinski PhD

Bogdan Zielinski PhD

Department of Medical Biochemistry, Wroclaw Medical University, Wroclaw, Poland

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Leszek Paradowski MD, PhD

Leszek Paradowski MD, PhD

Department of Gastroenterology and Hepatology, Wroclaw Medical University, Wroclaw, Poland

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Andrzej Gamian PhD

Andrzej Gamian PhD

Department of Medical Biochemistry, Wroclaw Medical University, Wroclaw, Poland

Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland

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First published: 20 August 2010
Citations: 5

Abstract

Background:

Oxidative stress contributes to the propagation and exacerbation of inflammatory bowel disease (IBD) but the status of erythrocyte antioxidant defense remains unknown.

Methods:

Erythrocyte activities of superoxide dismutase-1 (SOD1), catalase, and glutathione peroxidase-1 (GPx1) were determined in 174 IBD patients and 105 controls and referred to IBD activity, inflammation severity, nutritional status, systemic oxidative stress, anemia, and treatment.

Results:

Catalase and GPx1 activities were decreased in active IBD, whereas SOD1 became upregulated by IBD-related oxidative stress. In Crohn's disease (CD) corticosteroids decreased SOD1 activity. SOD1 correlated indirectly with CD activity and erythrocyte sedimentation rate (ESR) and directly with transferrin. In ulcerative colitis (UC) anemia downregulated SOD1. Decreases in GPx activity corresponded with IBD activity, anemia, inflammation, and malnutrition. Oxidative stress in UC and corticosteroids in CD also downregulated GPx. Catalase activity was decreased by CD-related anemia, correlating directly with hemoglobin, and indirectly with CD activity, inflammatory and protein oxidative stress markers. When co-analyzed, anemia but not CD activity significantly contributed to catalase downregulation. In UC, catalase activity corresponded indirectly with UC endoscopic activity and inflammation and directly with hemoglobin. UC activity, anemia, and treatment with azathioprine negatively affected catalase. As indicators of active IBD, GPx1 showed a diagnostic accuracy of 73%, whereas catalase showed 63% as compared to 74% of C-reactive protein and ESR.

Conclusions:

Erythrocyte antioxidant defense is impaired in active IBD. SOD1, GPx1, and CAT activities are differently affected by the disease type, activity, anemia, inflammation, oxidative stress, and treatment. As an active IBD indicator, GPx1 was comparable to C-reactive protein and ESR. Inflamm Bowel Dis 2010

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