Evidence map›Paper›PMID 31052277›Full record

Trial reportNutrients2019

Effect of Permissive Underfeeding with Intensive Insulin Therapy on MCP-1, sICAM-1, and TF in Critically Ill Patients.

Ahmad Aljada, Ghada Fahad AlGwaiz, Demah AlAyadhi, Emad Masuadi, Mahmoud Zahra, Shahad H Al-Matar, Ahmad Al-Bawab, Waleed Tamimi, Dunia Jawdat, Abdulaziz Al-Dawood and 3 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Nutrients, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 51% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Ahmad AljadaDepartment of Biochemistry and Molecular Medicine, College of Medicine, Alfaisal University, Riyadh 11533, Saudi Arabia. aaljada@alfaisal.edu.
Ghada Fahad AlGwaizDepartment 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. Ghada_fahad@live.com.
Demah AlAyadhiDepartment 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. iyadhi515@ksau-hs.edu.sa.
Emad MasuadiResearch Unit, Department of Medical Education, College of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdul Aziz Medical City, Ministry of National Guard-Health Affairs, Riyadh 11481, Saudi Arabia. Masuadie@ksau-hs.edu.sa.
Mahmoud ZahraDepartment 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. mahmoud.mzhra@gmail.com.ORCID 0000-0001-5067-4984
Shahad H Al-MatarDepartment 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. Matar028@ksau-hs.edu.sa.
Ahmad Al-BawabDepartment 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. bawaba@ksau-hs.edu.sa.
Waleed TamimiDepartment of Clinical Laboratory, King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, King Abdulaziz Medical City, Riyadh 11481, Saudi Arabia. TamimiW@NGHA.MED.SA.
Dunia JawdatCord Blood Bank, King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, King Abdulaziz Medical City, Riyadh 11481, Saudi Arabia. JawdatD@NGHA.MED.SA.
Abdulaziz Al-DawoodCollege of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, Intensive Care Department, King Abdulaziz Medical City, Riyadh 11481, Saudi Arabia. dawooda@ngha.med.sa.
Maram H SakkijhaCollege of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, Intensive Care Department, King Abdulaziz Medical City, Riyadh 11481, Saudi Arabia. SakkijhaM@NGHA.MED.SA.
Musharaf SadatCollege of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, Intensive Care Department, King Abdulaziz Medical City, Riyadh 11481, Saudi Arabia. sadatmu@ngha.med.sa.
Yaseen M ArabiCollege of Medicine, King Saud bin Abdulaziz University for Health Sciences, King Abdullah International Medical Research Center, Intensive Care Department, King Abdulaziz Medical City, Riyadh 11481, Saudi Arabia. yaseenarabi@yahoo.com.ORCID 0000-0001-5735-6241
King Saud bin Abdulaziz University for Health Sciences · SAAlfaisal University · SA

Funding

King Abdulaziz City for Science and Technology LG 10-30
6 · The paper itself

Abstract

purposeThis 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.

resultsBaseline characteristics were balanced across randomization groups. Daily caloric intake was significantly higher in the target feeding than in the permissive underfeeding groups (

conclusionsAlthough 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.

Indexed as

Caloric RestrictionAdultAgedChemokine CCL2Critical CareCritical IllnessFemaleHospital MortalityHumansInsulinIntercellular Adhesion Molecule-1MaleMiddle AgedNutritional RequirementsThromboplastinCCL2 protein, humanChemokine CCL2InsulinIntercellular Adhesion Molecule-1Thromboplastincaloric intakeinflammationinsulin infusionMCP-1permissive underfeedingsICAM-1 and tissue factor

Identifiers

PMID31052277
PMCPMC6566807
OpenAlexW2942996473

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.