Department of Biochemistry and Molecular Medicine, College of Medicine, Alfaisal University, Riyadh 11533, Saudi Arabia.
Department of Basic Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, King Abdul Aziz Medical City, Ministry of National Guard-Health Affairs, Riyadh 11481, Saudi Arabia.
Nutrients. 2019 Apr 30;11(5):987. doi: 10.3390/nu11050987.
This study examined the effect of permissive underfeeding compared to target feeding and intensive insulin therapy (IIT) compared to conventional insulin therapy (CIT) on the inflammatory mediators monocyte chemoattractant protein 1 (MCP-1), soluble intercellular adhesion molecule 1 (sICAM-1), and tissue factor (TF) in critically ill patients.
This was a substudy of a 2 × 2 factorial design randomized controlled trial in which intensive care unit (ICU) patients were randomized into permissive underfeeding compared to target feeding groups and into IIT compared to CIT groups (ISRCTN96294863). In this substudy, we included 91 patients with almost equal numbers across randomization groups. Blood samples were collected at baseline and at days 3, 5, and 7 of an ICU stay. Linear mixed models were used to assess the differences in MCP-1, sICAM-1, and TF across randomization groups over time.
Baseline characteristics were balanced across randomization groups. Daily caloric intake was significantly higher in the target feeding than in the permissive underfeeding groups (-value < 0.01), and the daily insulin dose was significantly higher in the IIT than in the CIT groups (-value < 0.01). MCP-1, sICAM-1, and TF did not show any significant difference between the randomization groups, while there was a time effect for MCP-1. Baseline sequential organ failure assessment (SOFA) score and platelets had a significant effect on sICAM-1 (-value < 0.01). For TF, there was a significant association with age (-value < 0.01).
Although it has been previously demonstrated that insulin inhibits MCP-1, sICAM-1 in critically ill patients, and TF in non-critically ill patients, our study demonstrated that IIT in critically ill patients did not affect these inflammatory mediators. Similarly, caloric intake had a negligible effect on the inflammatory mediators studied.
本研究旨在探讨在危重症患者中,与目标喂养相比,允许性低喂养以及与常规胰岛素治疗(CIT)相比,强化胰岛素治疗(IIT)对炎症介质单核细胞趋化蛋白 1(MCP-1)、可溶性细胞间黏附分子 1(sICAM-1)和组织因子(TF)的影响。
这是一项 2×2 析因设计的随机对照试验的子研究,其中将重症监护病房(ICU)患者随机分为允许性低喂养组与目标喂养组,以及 IIT 组与 CIT 组(ISRCTN96294863)。在这个子研究中,我们纳入了几乎在随机分组中数量相等的 91 名患者。在 ICU 住院的第 3、5 和 7 天采集血样。线性混合模型用于评估随机分组组间在不同时间点的 MCP-1、sICAM-1 和 TF 的差异。
随机分组组间的基线特征均衡。与允许性低喂养组相比,目标喂养组的每日热量摄入显著更高(P 值<0.01),与 CIT 组相比,IIT 组的每日胰岛素剂量显著更高(P 值<0.01)。MCP-1、sICAM-1 和 TF 各组间无显著差异,而 MCP-1 存在时间效应。基线序贯器官衰竭评估(SOFA)评分和血小板对 sICAM-1 有显著影响(P 值<0.01)。对于 TF,与年龄有显著相关性(P 值<0.01)。
尽管先前的研究表明胰岛素可抑制危重症患者的 MCP-1、sICAM-1 和非危重症患者的 TF,但本研究表明,IIT 对危重症患者的这些炎症介质没有影响。同样,热量摄入对所研究的炎症介质影响甚微。