Gheorghiţă Valeriu, Barbu Alina Elena, Gheorghiu Monica Livia, Căruntu Florin Alexandru
MD, PhD, Dr Carol Davila Central Universitary Emergency Military Hospital, Bucharest, Romania; National Institute for Infectious Diseases "Prof. Dr. Matei Balş", Bucharest, Romania.
MD, National Institute for Infectious Diseases "Prof. Dr. Matei Balş", Bucharest, Romania.
Germs. 2015 Mar 2;5(1):17-25. doi: 10.11599/germs.2015.1067. eCollection 2015 Mar.
Sepsis is a systemic, deleterious inflammatory host response triggered by an infective agent leading to severe sepsis, septic shock and multi-organ failure. The host response to infection involves a complex, organized and coherent interaction between immune, autonomic, neuroendocrine and behavioral systems. Recent data have confirmed that disturbances of the autonomic nervous and neuroendocrine systems could contribute to sepsis-induced organ dysfunction. Through this review, we aimed to summarize the current knowledge about the endocrine dysfunction as response to sepsis, specifically addressed to vasopressin, copeptin, cortisol, insulin and leptin. We searched the following readily accessible, clinically relevant databases: PubMed, UpToDate, BioMed Central. The immune system could be regarded as a "diffuse sensory organ" that signals the presence of pathogens to the brain through different pathways, such as the vagus nerve, endothelial activation/dysfunction, cytokines and neurotoxic mediators and the circumventricular organs, especially the neurohypophysis. The hormonal profile changes substantially as a consequence of inflammatory mediators and microorganism products leading to inappropriately low levels of vasopressin, sick euthyroid syndrome, reduced adrenal responsiveness to ACTH, insulin resistance, hyperglycemia as well as hyperleptinemia. In conclusion, clinical diagnosis of this "pan-endocrine illness" is frequently challenging due to the many limiting factors. The most important benefits of endocrine markers in the management of sepsis may be reflected by their potential to be used as biomarkers in different scoring systems to estimate the severity of the disease and the risk of death.
脓毒症是由感染因子引发的全身性有害炎症宿主反应，可导致严重脓毒症、脓毒性休克和多器官功能衰竭。宿主对感染的反应涉及免疫、自主神经、神经内分泌和行为系统之间复杂、有组织且协调的相互作用。近期数据证实，自主神经系统和神经内分泌系统的紊乱可能导致脓毒症诱发的器官功能障碍。通过本综述，我们旨在总结当前关于作为脓毒症反应的内分泌功能障碍的知识，特别针对血管加压素、 copeptin、皮质醇、胰岛素和瘦素。我们检索了以下易于获取且与临床相关的数据库：PubMed、UpToDate、BioMed Central。免疫系统可被视为一个“弥散性感觉器官”，它通过不同途径向大脑发出病原体存在的信号，如迷走神经、内皮激活/功能障碍、细胞因子和神经毒性介质以及室周器官，尤其是神经垂体。由于炎症介质和微生物产物的作用，激素谱会发生显著变化，导致血管加压素水平异常降低、低甲状腺素病态综合征、肾上腺对促肾上腺皮质激素的反应性降低、胰岛素抵抗、高血糖以及高瘦素血症。总之，由于存在许多限制因素，这种“全内分泌疾病”的临床诊断常常具有挑战性。内分泌标志物在脓毒症管理中的最重要益处可能体现在它们有潜力作为生物标志物用于不同的评分系统，以评估疾病的严重程度和死亡风险。
