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Effect of Permissive Underfeeding with Intensive Insulin Therapy on MCP-1, sICAM-1, and TF in Critically Ill Patients
Ahmad Aljada1, Ghada Fahad AlGwaiz2, Demah AlAyadhi3
1Department of Biochemistry and Molecular Medicine, College of Medicine, Alfaisal University, Riyadh 11533, Saudi Arabia. aaljada@alfaisal.edu.
Purpose:
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.
Methodology:
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.
Results:
Baseline characteristics were balanced across randomization groups. Daily caloric intake was significantly higher in the target feeding than in the permissive underfeeding groups (P-value < 0.01), and the daily insulin dose was significantly higher in the IIT than in the CIT groups (P-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 (P-value < 0.01). For TF, there was a significant association with age (P-value < 0.01).
Conclusions:
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.
Insights
Intensive insulin therapy (IIT) and target feeding did not significantly alter inflammatory mediators like MCP-1, sICAM-1, and TF in critically ill patients. Caloric intake also showed a negligible effect on these inflammatory markers.
Area of Science:
- Critical care medicine
- Immunology
- Metabolic disorders
Background:
- Critically ill patients often exhibit dysregulated inflammatory responses.
- Understanding the impact of nutritional and glycemic management on inflammatory mediators is crucial for improving patient outcomes.
- Monocyte chemoattractant protein 1 (MCP-1), soluble intercellular adhesion molecule 1 (sICAM-1), and tissue factor (TF) are key inflammatory mediators.
Purpose of the Study:
- To investigate the effects of permissive underfeeding versus target feeding on inflammatory mediators.
- To determine the impact of intensive insulin therapy (IIT) versus conventional insulin therapy (CIT) on inflammatory mediators.
- To analyze the influence of these interventions on MCP-1, sICAM-1, and TF in critically ill patients.
Main Methods:
- A substudy of a 2x2 factorial randomized controlled trial involving 91 critically ill patients.
- Patients were randomized to either permissive underfeeding vs. target feeding and IIT vs. CIT.
- Blood samples analyzed for MCP-1, sICAM-1, and TF at baseline and days 3, 5, and 7 using linear mixed models.
Main Results:
- No significant differences in MCP-1, sICAM-1, or TF were observed between feeding or insulin therapy groups.
- A time effect was noted for MCP-1 levels.
- Sequential Organ Failure Assessment (SOFA) score and platelet count influenced sICAM-1, while age affected TF.
Conclusions:
- Intensive insulin therapy (IIT) did not alter MCP-1, sICAM-1, or TF in critically ill patients, contrary to previous findings in non-critically ill populations.
- Permissive underfeeding and target feeding strategies had a negligible impact on the studied inflammatory mediators.
- These findings suggest that current nutritional and glycemic management strategies may not modulate these specific inflammatory pathways in critically ill patients.
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