Evaluation of Oxidative Stress Biomarkers in Patients with Henoch-Schönlein Purpura

Abstract

Introduction: Henoch-Schönlein Purpura (HSP) is a systemic vasculitic syndrome characterized by non-thrombocytopenic purpura, arthritis/arthralgia, abdominal pain, and glomerulonephritis. The pathogenesis of HSP has not been clearly identified. Oxidative damage has a role in the pathogenesis of most cases. Aim: This study aimed to evaluate changes of oxidative stress by studying parameters like superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) in an attempt to identify the role of oxidative stress in HSP from another perspective. Materials and methods: This study enrolled 23 pediatric patients (ten girls and thirteen boys) diagnosed with HSP who were under follow-up at Sutcu Imam University School of Medicine Department of Pediatrics between 2014 and 2016 and twenty healthy children as the control group. The parents of all subjects gave informed consent to participate in the study. In the HSP group, the beginning season of the illness and the systemic involvement during follow-up were determined. Blood specimens were obtained at presentation before any treatment was started. SOD, CAT activities, and MDA values in erythrocyte and plasma samples were compared between the patient group and the healthy children. Results: Twenty-three patients with HSP (13 males, 10 females) and 20 healthy children participated in this study. The mean age of the HSP cases was 8.21±3.78 years (range 2-16 years) and of the controls was 8.6±4.2 (range 3-14 years). The mean MDA value was 2.95±0.71 nmol/ml in the patient group and 2.67±0.66 nmol/ml in the control group (p=0.787). The mean level of the CAT enzyme was 1.32±0.35 U/g Hb in the patient group and 7.8±1.74 U/g Hb in the control group (p=0.001). The mean levels of the SOD enzyme were 3.06±0.85 U/g Hb in the patient group and 0.97±0.36 U/g Hb in the control group (p=0.001). Conclusions: Although high MDA levels support the role of lipid peroxidation in the pathogenesis of HSP, statistical significance was not reached owing to a limited number of our patients. The reduced CAT enzyme activity is consistent with the findings of previous reports. This finding supports the notion that oxidative stress can play a role in the pathogenesis of HSP. Keypoints: Our findings support the notion that oxidative stress can play a role in the pathogenesis of HSP.

Protection of Proanthocyanidins Against HSP Serum-Induced Inflammation and Oxidative Stress on Human Umbilical Vein Endothelial Cells

“…Several documents have reported that the inflammatory response and OS are crucial contributors to HSP pathogenesis, 9,[54][55][56] in which the abnormal activation of TLR4 signal get closely involved. 8,19,57 When microorganisms (bacteria, viruses, etc.)…”

“…Although the pathogenesis of HSP have not been fully elucidated, it is currently considered that immune inflammation and oxidative stress (OS) get deeply involved in it, especially the activation of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear transcription factor-kappa B (NF-κB) signaling way. [7][8][9][10] TLR4 is a key transmembrane protein mediating the inflammatory and OS reaction. It binds to the cytoplasmic adapter molecule MyD88 to activate the NF-κB signal, [11][12][13] which triggers the release of pro-inflammatory factors and chemokines, and the appearance of abnormal oxidative/antioxidant indicators, eg, increased reactive oxygen species (ROS), malondialdehyde (MDA) and nitric oxide (NO), as well as decreased catalase (CAT), glutathione (GSH) and superoxide dismutase (SOD).…”