Erdoğan O, Oner A, Aydin A, Işimer A, Demircin G, Bülbül M
Department of Paediatric Nephrology, Dr Sami Ulus Children's Hospital, Ankara, Turkey.
Acta Paediatr. 2003 May;92(5):546-50. doi: 10.1080/08035350310011461.
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.
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.
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.
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.
评估活性氧分子（ROMs）在过敏性紫癜发病机制中的作用以及维生素E对氧化损伤的影响。已有研究表明，ROMs在包括肾脏疾病和血管炎在内的多种病理状况中发挥作用。
检测了27例过敏性紫癜患儿在疾病发作期和缓解期作为抗氧化酶的超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性，以及作为脂质过氧化指标的丙二醛（MDA）水平。将本研究结果与11例作为对照组的健康儿童的结果进行比较。
在急性和缓解期，患者与对照组之间在所有氧化损伤参数如SOD、GSH-Px和MDA方面均检测到显著差异。但在有肾脏受累和无肾脏受累的患者之间未检测到此类差异。在15例接受维生素E治疗的患者中，尽管血浆维生素E水平显著升高，但氧化损伤参数和临床病程并未改善。
氧化损伤和脂质过氧化可能在过敏性紫癜的发病机制中起重要作用，但在脂质过氧化启动后给予维生素E（脂质过氧化是细胞损伤的最后阶段）对分解已经触发的氧化链反应没有作用。
