Perlmutter Jonah, Akouris Polycronis P, Fremont Sierra, Yang Brian, Toth Evan, Eze Michael, Wiseman Marni
Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada,
Temerty Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
Skin Pharmacol Physiol. 2025;38(1-2):59-67. doi: 10.1159/000543373. Epub 2025 Jan 2.
Alopecia areata (AA) is a T-cell-mediated autoimmune disease that significantly impacts patient quality of life. The breakdown of hair follicle immune privilege underlies AA pathogenesis. However, the precise mechanism of this breakdown remains unclear. This study investigates the potential role of reactive oxygen species in AA pathogenesis.
A systematic review and meta-analysis were conducted on observational studies and randomized controlled trials from 2000 to 2024. Studies included AA patients and measured oxidative stress index (OSI), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), or paraoxonase-1 (PON1). Extracted data were analyzed using the Cochrane risk-of-bias tool and random-effects models. The review included 21 studies with 743 AA patients. OSI was elevated in AA patients (effect size = 1.58, 95% CI: 0.31-2.68, p = 0.00068). MDA levels were also elevated (effect size = 1.60, 95% CI: 0.43-2.6, p = 0.00023), while SOD (effect size = -0.97, 95% CI: -1.65 to -0.30, p = 0.00066) and GSH-Px (effect size = -1.41, 95% CI: -2.28 to -0.53, p = 0.00068) activities were reduced. PON1 levels showed no significant difference (effect size = -3.56, 95% CI: -8.63 to 1.51, p = 0.051).
The elevated OSI and MDA, and decreased antioxidant activity in AA patients suggest a substantial role for reactive oxygen species and oxidative stress in AA pathogenesis, highlighting oxidative stress as a potential target for therapeutic intervention. These results underscore the importance of oxidative stress in AA and support further research into antioxidant-based therapies.
斑秃（AA）是一种由T细胞介导的自身免疫性疾病，严重影响患者的生活质量。毛囊免疫豁免的破坏是AA发病机制的基础。然而，这种破坏的确切机制仍不清楚。本研究调查了活性氧在AA发病机制中的潜在作用。
对2000年至2024年的观察性研究和随机对照试验进行了系统综述和荟萃分析。研究对象包括AA患者，并测量了氧化应激指数（OSI）、丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）或对氧磷酶-1（PON1）。使用Cochrane偏倚风险工具和随机效应模型对提取的数据进行分析。该综述纳入了21项研究，共743例AA患者。AA患者的OSI升高（效应量=1.58，95%CI：0.31-2.68，p=0.00068）。MDA水平也升高（效应量=1.60，95%CI：0.43-2.6，p=0.00023），而SOD（效应量=-0.97，95%CI：-1.65至-0.30，p=0.00066）和GSH-Px（效应量=-1.41，95%CI：-2.28至-0.53，p=0.00068）的活性降低。PON1水平无显著差异（效应量=-3.56，95%CI：-8.63至1.51，p=0.051）。
AA患者OSI和MDA升高，抗氧化活性降低，表明活性氧和氧化应激在AA发病机制中起重要作用，突出氧化应激作为治疗干预的潜在靶点。这些结果强调了氧化应激在AA中的重要性，并支持进一步研究基于抗氧化剂的疗法。
