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Antioxidant enzyme activities, lipid peroxidation, and total antioxidant status in children with Henoch–Schönlein purpura

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Abstract

The aim of this study was to assess the role of oxidative stress in the pathogenesis of Henoch–Schönlein purpura (HSP) vasculitis. The activities of catalase (CAT), arylesterase (ARYL), and paraoxonase (PON) as antioxidant enzymes and serum malondialdehyde (MDA) level as an indicator of lipid peroxidation, together with total antioxidant status (TAS), were measured in 29 children with HSP (mean age 9.3 ± 2.7 years), both at the onset of the disease and at the remission period and in matched controls. Active-stage HSP had significantly higher MDA level (15.5 ± 7.3 vs 7.8 ± 3.9 nmol/l, respectively, P < 0.001) and lower TAS (524 ± 122 vs 699 ± 122 μmol Trolox Equiv/l, P < 0.001), PON (97 ± 47 vs 136 ± 95 U/l, P = 0.042), ARYL (158 ± 39 vs 212 ± 52 U/l, P < 0.001), and CAT (50 ± 27 vs 69 ± 20 U/l, P = 0.002) activities compared with the control subjects. Although CAT (P > 0.05) and PON (P > 0.05) activities were found to be similar between active and remission stages of HSP, the active stage of the disease had significantly lower ARYL (P = 0.011) and TAS (P = 0.006) and higher MDA (P < 0.001) values compared with remission period. Significant positive correlations were found between CAT and MDA (r = 0.433, P = 0.019) and between CAT and C-reactive protein (r = 0.386, P = 0.035) in the active stage of HSP. No significant differences were detected in oxidant/antioxidant parameters between patients with or without renal, gastrointestinal, or joint involvement (P > 0.05). Increased oxidative stress and lipid peroxidation may play important roles in the pathogenesis of HSP vasculitis. Antioxidant therapeutic interventions in long-lasting vasculitis and risk of atherosclerosis secondary to increased oxidant stress remain to be investigated.

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Ece, A., Kelekçi, S., Kocamaz, H. et al. Antioxidant enzyme activities, lipid peroxidation, and total antioxidant status in children with Henoch–Schönlein purpura. Clin Rheumatol 27, 163–169 (2008). https://doi.org/10.1007/s10067-007-0671-5

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  • DOI: https://doi.org/10.1007/s10067-007-0671-5

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