Socola Hospital Iasi, Bucium 36, Iași, Romania 700282.
Department of Biology, Faculty of Biology, Alexandru Ioan Cuza University, B dul Carol I No. 11 Iasi, Romania.
Oxid Med Cell Longev. 2021 Dec 20;2021:5599265. doi: 10.1155/2021/5599265. eCollection 2021.
Posttraumatic stress disorder (PTSD) represents a pressing and generally invalidating syndrome that is triggered by a terrifying or stressful experience, relying on recurrently reliving the traumatic event feelings associated to it, which is subsequently linked to ongoing activations of stress-related neurobiological pathways and is often associated with neurodegeneration. In this paper, we examine what lies beneath this disorder, reviewing evidence that connects PTSD with a wide array of mechanisms and its intertwined pathways that can lead to the decompensation of different pathologies, such as cardiovascular disease, gastrointestinal ailments, autoimmune disorders, and endocrine diseases. Also, the significance of the oxidative stress in this frame of reference is debated. Thus, knowing and identifying the main features of the distressing experience, the circumstances around it, as well as the neuropsychological and emotional characteristics of people prone to develop PTSD after going through disturbing incidents can offer an opportunity to anticipate the development of potential destructive consequences in several psychological dimensions: cognitive, affective, relational, behavioral, and somatic. We can also observe more closely the intricate connections of the disorder to other pathologies and their underlying mechanisms such as inflammation, oxidative stress, bacterial overgrowth syndrome, irritable bowel syndrome, metabolic disorders, oxytocin, and cortisol in order to understand it better and to optimize the course of treatment and its management. The complex foundation PTSD possesses is supported by the existing clinical, preclinical, and experimental data encompassed in the current review. Different biological systems and processes such as the hypothalamic-pituitary-adrenal axis, sympathetic nervous system, oxidative stress, inflammation, and microbiome suffer modifications and changes when it comes to PTSD; that is why targeted therapies exert tremendous alleviations of symptoms in patients diagnosed with this disorder. Therefore, this implies that PTSD is not restricted to the psychiatric domain and should be viewed as a systemic condition.
创伤后应激障碍（PTSD）是一种紧迫且普遍无效的综合征，由可怕或压力性经历引发，其特征是反复体验与之相关的创伤事件感受，进而导致与应激相关的神经生物学途径持续激活，并常与神经退行性变有关。在本文中，我们探讨了这种疾病的潜在机制，综述了将 PTSD 与广泛的机制及其相互交织的途径联系起来的证据，这些途径可能导致不同病理状况的恶化，如心血管疾病、胃肠道疾病、自身免疫性疾病和内分泌疾病。此外，还讨论了在这一背景下氧化应激的重要性。因此，了解和识别痛苦经历的主要特征、其周围环境以及易患 PTSD 的人在经历困扰事件后的神经心理和情绪特征，可以提供机会预测在几个心理维度上潜在的破坏性后果的发展：认知、情感、关系、行为和躯体。我们还可以更仔细地观察这种疾病与其他病理及其潜在机制（如炎症、氧化应激、细菌过度生长综合征、肠易激综合征、代谢紊乱、催产素和皮质醇）的复杂联系，以便更好地理解它，并优化治疗过程及其管理。当前综述中包含的临床、临床前和实验数据支持 PTSD 复杂的基础。当涉及到 PTSD 时，不同的生物系统和过程（如下丘脑-垂体-肾上腺轴、交感神经系统、氧化应激、炎症和微生物组）会发生改变和变化；这就是为什么针对这些途径的靶向治疗可以极大地缓解患者的症状。因此，这意味着 PTSD 不仅限于精神领域，而应被视为一种系统性疾病。
