AIM: To evaluate the role of reactive oxygen molecules (ROMs) in the pathogenesis of Henoch-Schönlein purpura and the effect of vitamin E on oxidative damage. ROMs have been suggested to contribute in many pathological conditions including renal diseases and vasculitis. METHODS: The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as antioxidant enzymes were measured, and the level of malondialdehyde (MDA) as an indicator of lipid peroxidation in 27 children with Henoch-Schönlein purpura at the onset of the disease and during the remission period. The results of this study were compared with those of 11 healthy children studied as a control group. RESULTS: With regard to all the oxidative damage parameters such as SOD, GSH-Px and MDA, significant differences were detected between the patients and the control group in both the acute and remission periods. But no such differences were detected between patients with and those without renal involvement. In 15 patients receiving vitamin E treatment, oxidative damage parameters and clinical course showed no improvement despite significant increases in plasma vitamin E levels. CONCLUSION: Oxidative damage and lipid peroxidation may play an important part in the pathogenesis of Henoch-Schönlein purpura but vitamin E given after initiation of lipid peroxidation, which is the last phase of cellular damage, is of no use in breaking down the oxidative chain reactions that have already been triggered.
AIM: To evaluate the role of reactive oxygen molecules (ROMs) in the pathogenesis of Henoch-Schönlein purpura and the effect of vitamin E on oxidative damage. ROMs have been suggested to contribute in many pathological conditions including renal diseases and vasculitis. METHODS: The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as antioxidant enzymes were measured, and the level of malondialdehyde (MDA) as an indicator of lipid peroxidation in 27 children with Henoch-Schönlein purpura at the onset of the disease and during the remission period. The results of this study were compared with those of 11 healthy children studied as a control group. RESULTS: With regard to all the oxidative damage parameters such as SOD, GSH-Px and MDA, significant differences were detected between the patients and the control group in both the acute and remission periods. But no such differences were detected between patients with and those without renal involvement. In 15 patients receiving vitamin E treatment, oxidative damage parameters and clinical course showed no improvement despite significant increases in plasma vitamin E levels. CONCLUSION: Oxidative damage and lipid peroxidation may play an important part in the pathogenesis of Henoch-Schönlein purpura but vitamin E given after initiation of lipid peroxidation, which is the last phase of cellular damage, is of no use in breaking down the oxidative chain reactions that have already been triggered.