title: Oxidative stress is associated with liver damage, inflammatory status, and corticosteroid therapy in patients with systemic lupus erythematosus.
abstract: Oxidative stress exerts an important role on the pathophysiological mechanisms of systemic lupus erythematosus (SLE). This study investigated oxidative stress in patients with SLE and its correlation with disease activity, corticosteroid therapy, and liver function biomarkers. The study included 58 patients with SLE and 105 healthy volunteers. Patients showed oxidative stress increase evaluated by tert-butyl hydroperoxide-initiated chemiluminescence (CL-LOOH), advanced oxidation protein products (AOPP), and nitric oxide metabolites. C-reactive protein (CRP) was associated with CL-LOOH and with AOPP. Aspartate aminotransferase correlated significantly with CL-LOOH and with AOPP. Patients with disease activity showed an inverse significant correlation of daily prednisone doses and CL-LOOH and a direct correlation with total antioxidant capacity. In conclusion, patients with SLE have persistent lipoperoxidation and protein oxidation even with inactive disease or mild disease activity. The significant correlation between oxidative stress and CRP suggests that, despite clinical remission, the persistence of an inflammatory condition favors oxidative stress. Oxidative stress was associated with liver enzymes, and this relationship seems to support the hypothesis of drug-induced oxidative stress with consequent liver injury. In relation to non-active disease, patients with active SLE did not present oxidative stress and antioxidant capacity changes, due to the antioxidant drugs used in SLE treatment, especially prednisone.
authors.affiliation: Department of Clinical Analysis, University North of Paraná (UNOPAR), Londrina, Brazil.
authors.forename: M A B
authors.initials: MA
authors.lastname: Lozovoy
authors.forename: A N C
authors.initials: AN
authors.lastname: Simão
authors.forename: C
authors.initials: C
authors.lastname: Panis
authors.forename: M A C
authors.initials: MA
authors.lastname: Rotter
authors.forename: E M V
authors.initials: EM
authors.lastname: Reiche
authors.forename: H K
authors.initials: HK
authors.lastname: Morimoto
authors.forename: E
authors.initials: E
authors.lastname: Lavado
authors.forename: R
authors.initials: R
authors.lastname: Cecchini
authors.forename: I
authors.initials: I
authors.lastname: Dichi
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000328:Adult; D000975:Antioxidants / Q000627:therapeutic use; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D015227:Lipid Peroxidation; D008099:Liver / Q000293:injuries / Q000503:physiopathology; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress
chemical_list: D000305:Adrenal Cortex Hormones; D000975:Antioxidants; D015415:Biomarkers; D018836:Inflammation Mediators; D009569:Nitric Oxide; D002097:C-Reactive Protein