边缘型人格障碍（BPD）和进食障碍（ED）都是情绪失调的障碍疾病，可能存在一些相似的生物学基础，导致氧化/炎症改变。然而，到目前为止，尚无研究评估这些障碍之间的临床特征、炎症改变和童年创伤之间的关系。我们的目标是确定潜在的共同和障碍特异性炎症途径，并研究这些失调的途径与临床特征之间的可能关联。我们研究了108名女性样本（平均年龄27.17岁，标准差7.64），分为四组：23名患有限制性ED（ED-R）的患者，23名患有进食/催吐ED（ED-P）的患者和26名患有BPD的患者；对照组包括23名健康受试者。测定了几种炎症/氧化参数：肿瘤坏死因子α（TNFα）、硫代巴比妥酸反应物（TBARS）、诱导型一氧化氮合酶（iNOS）、环氧合酶-2（COX2）、p38线粒体激活蛋白激酶、ERK线粒体激活蛋白激酶和c-Jun NH2-末端激酶（JNK），以及一些抗炎抗氧化元素：谷胱甘肽过氧化物酶（GPx）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、Kelch样ECH相关蛋白（Keap1），这些参数在血浆或外周血单个核细胞中确定。此外，还进行了临床、冲动性、创伤和进食行为问卷调查。主成分分析提取了三个主要的炎症/氧化成分（解释了59.19%的生物标志物方差）。通过与特定主成分的关系（p < 0.01），揭示了BPD和ED患者炎症和氧化途径中的障碍特异功能。BPD患者表现出JNK水平升高、GPx和SOD水平降低的成分水平较高。ED-R和冲动性与ERK的活化以及Keap1的负面影响相关联。抑制过氧化氢酶和COX2的成分与ED亚型和创伤暴露都相关。无论诊断如何，创伤、冲动性和进食障碍症状等多种风险因素与一些炎症改变有跨诊断关联。这些发现表明，具有创伤暴露和情绪失调障碍的临床特征可能构成与炎症改变高度相关的特定内源表型。版权所有© 2023 Elsevier Ltd.保留所有权利。

Borderline personality disorder (BPD) and eating disorders (ED) are both disorders with emotional dysregulation that may share some similar biological underpinnings, leading to oxidative/inflammatory alterations. Unfortunately, to date, no studies have assessed the relationship between clinical features, inflammatory alterations and childhood trauma across these disorders. Our aim was to identify the potential common and disorder-specific inflammatory pathways and examine possible associations between these dysregulated pathways and the clinical features.We studied a sample of 108 women (m = 27.17 years; sd = 7.64), divided into four groups: 23 patients with a restrictive ED (ED-R), 23 patients with a bingeeating/ purging ED (ED-P) and 26 patients with BPD; whereas the control group included 23 healthy subjects. Several inflammatory/oxidative parameters: tumor necrosis factor alpha (TNFα), Thiobarbituric Acid Reactive Substances (TBARS), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), p38 mitogenactivated protein kinases, ERK mitogen-activated protein kinases and c-Jun NH2- terminal kinase (JNK), and some antiinflammatory antioxidant elements: glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), Kelch-like ECHassociated protein (Keap1) were determined in plasma or peripheral blood mononuclear cells. Furthermore, clinical, impulsivity, trauma and eating behavior questionnaires were administered.Three main inflammatory/oxidative components were extracted using principal component analysis (59.19 % of biomarker variance explained). Disorder-specific dysfunction in the inflammatory and oxidative pathways in patients with BPD and ED were revealed by means of relationships with specific principal components (p < .01). BPD patients showed higher levels of a component featured by elevated levels of JNK and lower of GPx and SOD. ED-R and impulsivity were associated with a component featured by the activation of ERK and negative influence of Keap1. The component featured by the suppression of catalase and COX2 was associated with both ED subtypes and trauma exposure.Several risk factors such as trauma, impulsivity and eating disorder symptoms were transdiagnostically associated with some inflammatory alterations regardless of diagnosis. These findings suggest that the clinical profile comprising trauma exposure and an emotional dysregulation disorder might constitute a specific endophenotype highly linked with inflammatory alterations.Copyright © 2023 Elsevier Ltd. All rights reserved.