Tomasi Cristiane Damiani, Vuolo Francieli, Generoso Jaqueline, Soares Márcio, Barichello Tatiana, Quevedo João, Ritter Cristiane, Dal-Pizzol Felipe
Laboratório de Fisiopatologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
D'Or Institute for Research and Education, Rio de Janeiro, Brazil.
Mol Neurobiol. 2017 Jan;54(1):722-726. doi: 10.1007/s12035-016-9708-6. Epub 2016 Jan 14.
There are different theories about the pathophysiology of sepsis-associated encephalopathy (SAE), and the majority of our knowledge was derived from critically ill patients. 7In less severe sepsis, it is probable that neuroinflammation can be a major aspect of SAE development. We hypothesized that in non-severe septic patients, blood biomarkers of inflammation, endothelial activation, coagulation, and brain function would be different when compared to patients with and without brain dysfunction. A total of 30 patients presenting with community-acquired pneumonia (CAP)-induced sepsis were included of which 10 (33 %) developed SAE. Eight medical patients admitted to the general ward, except due to sepsis or infection, which developed delirium were included as delirium, non-sepsis group. From all measured biomarkers, only brain-derived neurotrophic factor (BDNF), regulated upon activation normal T cell expressed, and presumably secreted (RANTES), and interleukin (IL)-10 where significantly different when compared to SAE and sepsis groups. In addition, SAE patients presented higher levels of BDNF, vascular cellular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), platelet-derived growth factor (PDGF)-AB/BB and RANTES when compared to delirium patients. In conclusion, the profile of biomarkers differs between SAE, sepsis, and delirium patients, suggesting that pathways related to SAE are different from delirium and from sepsis itself.
关于脓毒症相关性脑病（SAE）的病理生理学有不同的理论，而我们的大部分认知都来源于危重症患者。在不太严重的脓毒症中，神经炎症很可能是SAE发生发展的一个主要方面。我们推测，在非严重脓毒症患者中，与有或没有脑功能障碍的患者相比，炎症、内皮激活、凝血和脑功能的血液生物标志物会有所不同。总共纳入了30例因社区获得性肺炎（CAP）导致脓毒症的患者，其中10例（33%）发生了SAE。8例因非脓毒症或感染以外原因入住普通病房且发生谵妄的内科患者被纳入作为谵妄、非脓毒症组。在所有检测的生物标志物中，与SAE组和脓毒症组相比，只有脑源性神经营养因子（BDNF）、正常T细胞激活后表达并可能分泌的调节趋化因子（RANTES）和白细胞介素（IL）-10有显著差异。此外，与谵妄患者相比，SAE患者的BDNF、血管细胞黏附分子-1（VCAM-1）、细胞间黏附分子-1（ICAM-1）、血小板衍生生长因子（PDGF）-AB/BB和RANTES水平更高。总之，SAE、脓毒症和谵妄患者的生物标志物谱不同，这表明与SAE相关的途径不同于谵妄以及脓毒症本身。
