■糖尿病与免疫功能失调和细胞因子释放受损有关,而短暂性急性高血糖在临床前研究中已显示可增强炎性细胞因子的释放。尽管糖尿病和急性高血糖在社区获得性肺炎(CAP)患者中很常见,慢性的影响,急性,和急性对慢性高血糖对宿主的反应在这一人群中仍然知之甚少。这项研究调查了是否慢性,急性,和急性-慢性高血糖与不同的炎症介质有关,内皮,CAP患者的血管生成宿主反应途径。
■在对555名CAP患者的横断面研究中,HbA1c,入院血浆(p)-葡萄糖,和血糖差距(入院p-葡萄糖减去HbA1c-衍生的平均p-葡萄糖)被用作慢性,急性,和慢性急性高血糖症,分别。线性回归用于建立高血糖测量值与参与炎症的47种蛋白质之间的关联模型。内皮激活,和入院时测量的血管生成。模型根据年龄进行了调整,性别,CAP严重性,病原体,免疫抑制,合并症,和体重指数。以小于0.05的错误发现率阈值进行多次测试的调整。
■分析结果显示HbA1c水平与IL-8、IL-15、IL-17A/F呈正相关,IL-1RA,sFlt-1和VEGF-C。入院血浆葡萄糖也与这些蛋白质和GM-CSF呈正相关。血糖差距与IL-8、IL-15、IL-17A/F、IL-2和VEGF-C。
■总而言之,慢性,急性,急性和慢性高血糖与相似的宿主反应介质呈正相关。此外,急性和急性-慢性高血糖分别与涉及GM-CSF和IL-2的炎症途径有独特的关联.
UNASSIGNED: Diabetes is associated with dysregulated immune function and impaired cytokine release, while transient acute hyperglycaemia has been shown to enhance inflammatory cytokine release in preclinical studies. Although diabetes and acute hyperglycaemia are common among patients with community-acquired pneumonia (CAP), the impact of chronic, acute, and acute-on-chronic hyperglycaemia on the host response within this population remains poorly understood. This study investigated whether chronic, acute, and acute-on- chronic hyperglycaemia are associated with distinct mediators of inflammatory, endothelial, and angiogenic host response pathways in patients with CAP.
UNASSIGNED: In a cross-sectional study of 555 patients with CAP, HbA1c, admission plasma (p)-glucose, and the glycaemic gap (admission p-glucose minus HbA1c- derived average p-glucose) were employed as measures of chronic, acute, and acute-on-chronic hyperglycaemia, respectively. Linear regression was used to model the associations between the hyperglycaemia measures and 47 proteins involved in inflammation, endothelial activation, and angiogenesis measured at admission. The models were adjusted for age, sex, CAP severity, pathogen, immunosuppression, comorbidity, and body mass index. Adjustments for multiple testing were performed with a false discovery rate threshold of less than 0.05.
UNASSIGNED: The analyses showed that HbA1c levels were positively associated with IL-8, IL-15, IL-17A/F, IL-1RA, sFlt-1, and VEGF-C. Admission plasma glucose was also positively associated with these proteins and GM-CSF. The glycaemic gap was positively associated with IL-8, IL-15, IL-17A/F, IL-2, and VEGF-C.
UNASSIGNED: In conclusion, chronic, acute, and acute-on-chronic hyperglycaemia were positively associated with similar host response mediators. Furthermore, acute and acute-on-chronic hyperglycaemia had unique associations with the inflammatory pathways involving GM-CSF and IL-2, respectively.