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Clinical and Developmental Immunology
Volume 2012, Article ID 354594, 6 pages
Clinical Study

Carbonic Anhydrases III and IV Autoantibodies in Rheumatoid Arthritis, Systemic Lupus Erythematosus, Diabetes, Hypertensive Renal Disease, and Heart Failure

1Department of Clinical Laboratory, Xuanwu Hospital, Capital Medical University, 45 Changchun Road, Beijing 100053, China
2Department of Oncology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing 100078, China
3Department of Clinical Immune, Xiangya School of Medicine, Central South University, Changsha 410078, Hunan, China

Received 8 July 2012; Accepted 14 August 2012

Academic Editor: Dimitrios Bogdanos

Copyright © 2012 Chengeng Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In the present study, the CA III and IV autoantibodies, CA activity, antioxidant enzymes and cytokines in rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), diabetes, hypertensive renal disease, and heart failure were investigated. The anti-CA III antibody titers in patients with RA, SLE, and type 1 diabetes (T1D) were significantly higher than that in control groups (P<0.05). The anti-CA IV antibody titers in patients with RA, SLE, type 1 diabetic nephropathy (T1DN), and heart failure were significantly higher than that in control groups (P<0.05) while anti-CA IV antibody could suppress the total CA activity. The SOD and GPx levels in patients with RA, SLE, and T1DN were significantly lower than that in control groups (P<0.05). IL-6, IL-17, IFN-γ, and TNF-α levels were significantly higher in SLE group compared with the control group (P<0.05). Weak but significant correlations were found between anti-CA III antibodies and ESR in RA (r=0.403, P=0.013) and SLE patients (r=0.397, P=0.007). These results suggested that the generation of CA III and IV autoantibodies, antioxidant enzymes, and cytokines might influence each other and CA autoantibodies might affect the normal physiology function of CA.