Biological and oxidative stress markers in the evolution of patients with rheumatoid arthritis
Keywords:
rheumatoid arthritis, differential leukocytes count, oxidative stressAbstract
Introduction: rheumatoid arthritis is an autoimmune and inflammatory disease of unknown cause. In the Rheumatology services, the evolution of the patients is valued by means of erythrocyte sedimentation rate and C-reactive protein. It has been suggested that the oxidative stress contributes to the joint tissue damage.
Objective: to analyze differential leukocyte count and oxidative damage in patients with Rheumatoid Arthritis in crisis and remission periods.
Methods: prospective study in which global and differential leukocytes count, thiobarbituric acid reactive substances as a marker of lipid peroxidation, the superoxide dismutase, as well as the catalase activities were measured in 23 patients during their crisis and remission periods. C-reactive protein, erythrocyte sedimentation rate and rheumatoid factor were measured, too.
Results: rheumatoid factor was over 15 U/ml in the 82.61 % of the patients. A minor neutrophils count was observed in the remission period in relation to the active period of the disease (5.03±1.51 vs. 4.21±1.24 ×10-9/L, p=0.003), as well as the global leukocytes count, the erythrocyte sedimentation rate and the C-reactive protein. It was verified that the catalase activity decreased in remission state in relation to the crisis period (445.31±281.87 vs. 1046.08±659.77 U×L-1min-1).
Conclusions: in the evolution of the rheumatoid arthritis, the neutrophils count is in correspondence with the inflammatory state of the patients. Catalase activity is consistent with the regulation of this enzyme to protect against oxidative stress.
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References
Sarly B, Baktir A, Cebicci M, Dogan Y, Demirbas M, Kurtul S, et al. Predictors of endothelial dysfunction in patients with rheumatoid arthritis. Angiology. 2014;65(9):778-82.
Ibn Yacoub Y, Amine B, Laatiris A, Hajjaj-Hassouni N. Rheumatoid factor and antibodies against citrullinated peptides in moroccan patients with rheumatoid arthritis: association with disease parameters and quality of life. Clin Rheumatol. 2012;31(2):329-34.
Charles J, Britt H, Pan Y. Rheumatoid arthritis. Aust Fam Physician. 2013;42(11):765.
Ogawa M, Matsuda T, Ogata A, Hamasaki T, Kumanogoh A, Toyofuku T, et al. DNA damage in rheumatoid arthritis: an age-dependent increase in the lipid peroxidation-derived DNA adduct, heptanone-etheno-2′-deoxycytidine. Autoimmune Dis. 2013; 2013:183487. Published online 2013 October 7. doi: 10.1155/2013/183487.
McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365:2205-19.
Frisell T, Holmqvist M, Källberg H, Klareskog L, Alfredsson L, Askling J. Familial risks and heritability of rheumatoid arthritis. Role of rheumatoid factor/anti–citrullinated protein antibody status, number and type of affected relatives, sex, and age. Arthritis Rheumatism. 2013;65(11):2773-82.
Desai PB, Manjunath S, Kadi S, Chetana K, Vanishree J. Oxidative stress and enzymatic antioxidant status in rheumatoid arthritis: a case control study. Eur Review Med Pharmacol Sci. 2010;14:959-67.
Stamp LK, Khalilova I, Tarr JM, Senthilmohan R, Turner R, Haigh RC, et al. Myeloperoxidase and oxidative stress in rheumatoid arthritis. Rheumatology 2012;51:1796-803.
Jan Wruck C, Fragoulis A, Gurzynski A, Brandenburg L, Wai Kan Y, Chan K. Role of oxidative stress in rheumatoid arthritis: insights from the Nrf2-knockout mice. Ann Rheum Dis. 2011;70:844-50.
Avery SV. Oxidative stress and cell function. En: Laher I (ed). System Biology of free radicals and antioxidants. Vol I Part I. Cap. 4. Ed. Springer-Verlag Berlin Heidelberg; 2014. p.89-112. doi 10.1007/978-3-642-30018-9_10.
González-Álvaro I, Ortiz AM, Seoane IV, García-Vicuña R, Martínez C, Gomariz RP. Biomarkers predicting a need for intensive treatment in patients with early arthritis. Curr Pharm Design. 2015;21:170-81.
Smith HS, Smith AR, Seidner P. Painful rheumatoid arthritis. Pain Physician. 2011;14:E427-58.
Seven A, Güzel S, Aslan M, Hamuryudan V. Lipid, protein, DNA oxidation and antioxidant status in rheumatoid arthritis. Clin Biochem. 2008;41(7-8):538-43.
Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries FJ, Cooper NS, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31(3):315-24.
Yagi K. Lipid peroxides and human diseases. Chem Phys Lipids. 1987;45:337-51
Marklund S, Marklund G. Involvement of the superoxide anion radical in autoxidation of pyrogallol as a convenient assay for superoxide dismutase. Eur J Biochem. 1974;47:469-74.
Aebi H. Catalase in vitro. Methods Enzymol. 1984;105:121-6.
Roca R. Temas de Medicina Interna. 4ta ed. La Habana: Ed. Pueblo y Educación;. 2002. p. 83-94.
Balbir-Gurman A, Fuhrman B, Braun-Moscovici Y, Markovits D, Aviram M. Consumption of pomegranate decreases serum oxidative stress and reduces disease activity in patients with active rheumatoid arthritis: A pilot study. Isr Med Ass J. 2011;13:474-9.
Yousuf M, Akhter J, Al-Khairy K, Al-Saadan MA, Bin-Salih S. Extremely elevated erythrocyte sedimentation rate. Etiology at a tertiary care center in Saudi Arabia. Saudi Med J. 2010;31(11):1227-31.
Li W, Li H, Song W, Hu Y, Liu Y, Da R. Differential diagnosis of systemic lupus erythematosus and rheumatoid arthritis with complements C3 and C4 and C-reactive protein. 2013;6(5):1271-6.
Nakamura T, Yamamoto T. Potential of a 70 kDa IL-10-like factor in synovial fluid from rheumatoid arthritis patients to augment superoxide generation by human neutrophils. International Journal of Rheumatic Diseases. 30 Sep 2013. DOI: 10.1111/1756-185X.12166
Ayala A, Muñoz MF, Argüelles S. Lipid Peroxidation: Production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal. Oxid Med Cell Longev. Oxid Med Cell Longev. [Internet] 2014 May 8. [citado 10 enero 2015]; Disponible en: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066722/pdf/OMCL2014-360438.pdf
Melguizo E, Navarro N, Hernández B, Santos K, Arrobas T, Domínguez C, et al. Diagnostic utility of oxidative damage markers for early rheumatoid arthritis in non-smokers and negative anti-CCP patients. An Sist Sanit Navar. 2014;37(1):109-15.
Staron A, Mąkosa G, Koter-Michalak M. Oxidative stress in erythrocytes from patients with rheumatoid arthritis. Rheumatol Int. 2012;32(2):331-4.
Baskol G, Demir H, Baskol M, Kilic E, Ates F, Karakukcu C, Ustdal M. Investigation of protein oxidation and lipid peroxidation in patients with rheumatoid arthritis. Cell Biochem Funct. 2006;24(4):307-11.
Ozkan Y, Yardým-Akaydýn S, Sepici A, Keskin E, Sepici V, Simsek B. Oxidative status in rheumatoid arthritis. Clin Rheumatol. 2007;26:64-8.
Hassan SZ, Gheita TA, Kenawy SA, Fahim AT, El-Sorougy IM, Abdou MS. Oxidative stress in systemic lupus erythematosus and rheumatoid arthritis patients: relationship to disease manifestations and activity. Internat J Rheumat Dis. 2011;14:325-31.
Vasanthi P, Nalini G, Rajasekhar G. Status of oxidative stress in rheumatoid arthritis. Internat J Rheumatic Dis. 2009;12:29-33
Veal E, Day A. Hydrogen peroxide as a signaling molecule. Antioxid Redox Signal. 2011;15(1):147-51.
Mansour RB, Lassoued S, Gargouri B, El Gaïd A, Attia H, Fakhfakh F. Increased levels of autoantibodies against catalase and superoxide dismutase associated with oxidative stress in patients with rheumatoid arthritis and systemic lupus erythematosus. Scand J Rheumatol. 2008;37:103-8.
Igari T, Kaneda H, Houriuchi S, Ono S. A remarkable increase of superoxide dismutase activity in synovial fluid of patient with rheumatoid arthritis. Clin Orthop Relat Res. 1982;162:282-7.
Cimen MYB, Cimen OB, Kaçmaz M, Ozturk HS, Yorgancioglu R, Durak I. Oxidant/antioxidant status of the erythrocytes from patients with rheumatoid arthritis. Clin Rheumatol. 2000;19:275-7.
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