Oxidative stress may be one of the important complex pathogenetic mechanisms that lead to damage in scleroderma;free radicals may provoke endothelial injury, fibroblast proliferation and fragmentation of autoantigens favouring inductionof autoantibodies. The present study investigates the oxidant status in scleroderma patients by measuring the urinaryconcentration of 8-isoprostaglandin-F2a, an F2-isoprostane, and a product of free radical-mediated peroxidation ofarachidonic acid.Methods. Forty-three scleroderma patients (42 women and 1 man, mean age 54.1 yr, mean disease duration 9.0 yr) underwentclinical evaluation and instrumental investigations in order to assess skin, vascular, lung and heart involvement. Von Willebrandfactor was evaluated as marker of vascular dysfunction in 36 out of the 43 cases. The urinary level of 8-isoprostaglandin-F2awas measured in all scleroderma patients and in the 43 age- and sex-matched healthy controls.Results. Urinary levels of 8-isoprostaglandin-F2a were higher in scleroderma patients than in the healthy control group (341.7 vs147.6 pg/mg creatinine; P_0.001). Values of 8-isoprostaglandin-F2a were strongly correlated with the nailfold videocapillaroscopypattern and lung involvement (P^0.002 and 0.003, respectively), showing increasing levels with the progression ofpulmonary severity. Correlation between 8-isoprostaglandin-F2a level and von Willebrand factor narrowly failed to reachstatistical significance (P^0.05). There was no correlation between 8-isoprostaglandin-F2a concentration and disease activity,vascular, skin and heart involvement, disease pattern or autoantibody profile.Conclusions. Our study further supports the role of oxidant stress in the pathogenesis of scleroderma, showing a strongcorrelation between a marker of free radical damage with both the severity of lung involvement and the videocapillaroscopicpatterns.

Levels of F2-isoprostanes in systemic sclerosis:correlation with clinical features

Volpe A.;Biasi D.;Mantovani W.;Bambara L. M.;Ferrari M.;Poli G.;Degan M.;Carletto A;Pieropan S.;Minuz P.
2006-01-01

Abstract

Oxidative stress may be one of the important complex pathogenetic mechanisms that lead to damage in scleroderma;free radicals may provoke endothelial injury, fibroblast proliferation and fragmentation of autoantigens favouring inductionof autoantibodies. The present study investigates the oxidant status in scleroderma patients by measuring the urinaryconcentration of 8-isoprostaglandin-F2a, an F2-isoprostane, and a product of free radical-mediated peroxidation ofarachidonic acid.Methods. Forty-three scleroderma patients (42 women and 1 man, mean age 54.1 yr, mean disease duration 9.0 yr) underwentclinical evaluation and instrumental investigations in order to assess skin, vascular, lung and heart involvement. Von Willebrandfactor was evaluated as marker of vascular dysfunction in 36 out of the 43 cases. The urinary level of 8-isoprostaglandin-F2awas measured in all scleroderma patients and in the 43 age- and sex-matched healthy controls.Results. Urinary levels of 8-isoprostaglandin-F2a were higher in scleroderma patients than in the healthy control group (341.7 vs147.6 pg/mg creatinine; P_0.001). Values of 8-isoprostaglandin-F2a were strongly correlated with the nailfold videocapillaroscopypattern and lung involvement (P^0.002 and 0.003, respectively), showing increasing levels with the progression ofpulmonary severity. Correlation between 8-isoprostaglandin-F2a level and von Willebrand factor narrowly failed to reachstatistical significance (P^0.05). There was no correlation between 8-isoprostaglandin-F2a concentration and disease activity,vascular, skin and heart involvement, disease pattern or autoantibody profile.Conclusions. Our study further supports the role of oxidant stress in the pathogenesis of scleroderma, showing a strongcorrelation between a marker of free radical damage with both the severity of lung involvement and the videocapillaroscopicpatterns.
2006
Systemic sclerosis; Oxidative stress; F2-isoprostanes.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/304747
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