Marqués de Valdecilla University Hospital, Eating Disorders Unit, Department of Psychiatry, Santander, Spain; Valdecilla Biomedical Research Institute (IDIVAL), Santander, Spain.
Marqués de Valdecilla University Hospital, Eating Disorders Unit, Department of Psychiatry, Santander, Spain; Center for Biomedical Research in Mental Health (CIBERSAM), Spain; Valdecilla Biomedical Research Institute (IDIVAL), Santander, Spain.
Psychoneuroendocrinology. 2023 Dec;158:106383. doi: 10.1016/j.psyneuen.2023.106383. Epub 2023 Sep 6.
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.
边缘型人格障碍（BPD）和饮食障碍（ED）均存在情绪调节障碍，可能具有一些相似的生物学基础，导致氧化/炎症改变。遗憾的是，迄今为止，尚无研究评估这些疾病的临床特征、炎症改变和童年创伤之间的关系。我们的目的是确定潜在的共同和特定于疾病的炎症途径，并检查这些失调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（m=27.17 岁；sd=7.64），分为四组：23 名限制性 ED（ED-R）患者、23 名暴食/清除 ED（ED-P）患者和 26 名 BPD 患者；而对照组包括 23 名健康受试者。我们测定了几种炎症/氧化参数：肿瘤坏死因子-α（TNF-α）、硫代巴比妥酸反应物质（TBARS）、诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX2）、p38 丝裂原激活蛋白激酶、细胞外信号调节激酶（ERK）丝裂原激活蛋白激酶和 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）在血浆或外周血单核细胞中。此外，还进行了临床、冲动、创伤和饮食行为问卷评估。
使用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，揭示了 BPD 和 ED 患者炎症和氧化途径的特定功能障碍（p<.01）。BPD 患者表现出更高水平的 JNK 升高和更低水平的 GPx 和 SOD 为主的成分。ED-R 和冲动与 ERK 激活和 Keap1 负面影响为主的成分相关。以抑制过氧化氢酶和 COX2 为主的成分与两种 ED 亚型和创伤暴露有关。
一些风险因素，如创伤、冲动和饮食障碍症状，与一些炎症改变有关，无论诊断如何，这些改变都具有跨诊断相关性。这些发现表明，包含创伤暴露和情绪调节障碍的临床特征可能构成与炎症改变高度相关的特定内表型。
