Evidence mapPaperPMID 38015312Full record

ReviewIntensive care medicine experimental2023

Impact of critical illness on cholesterol and fatty acids: insights into pathophysiology and therapeutic targets.

Caroline Lauwers, Lauren De Bruyn, Lies Langouche

Open access · goldAbstract readReview
In one paragraph

Review in Intensive care medicine experimental, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Determinants of diagnostic yield and scan quality of [Critical care (London, England) · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

3 authors at 1 institution in 1 country.

Caroline Lauwers *Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, O&N1 Box 503, 3000, Leuven, Belgium.
Lauren De Bruyn *Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, O&N1 Box 503, 3000, Leuven, Belgium.
Lies LangoucheClinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, O&N1 Box 503, 3000, Leuven, Belgium. lies.langouche@kuleuven.be.ORCID http://orcid.org/0000-0002-8564-6809
KU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Critical illness is characterized by a hypercatabolic response encompassing endocrine and metabolic alterations. Not only the uptake, synthesis and metabolism of glucose and amino acids is majorly affected, but also the homeostasis of lipids and cholesterol is altered during acute and prolonged critical illness. Patients who suffer from critically ill conditions such as sepsis, major trauma, surgery or burn wounds display an immediate and sustained reduction in low plasma LDL-, HDL- and total cholesterol concentrations, together with a, less pronounced, increase in plasma free fatty acids. The severity of these alterations is associated with severity of illness, but the underlying pathophysiological mechanisms are multifactorial and only partly clarified. This narrative review aims to provide an overview of the current knowledge of how lipid and cholesterol uptake, synthesis and metabolism is affected during critical illness. Reduced nutritional uptake, increased scavenging of lipoproteins as well as an increased conversion to cortisol or other cholesterol-derived metabolites might all play a role in the decrease in plasma cholesterol. The acute stress response to critical illness creates a lipolytic cocktail, which might explain the increase in plasma free fatty acids, although reduced uptake and oxidation, but also increased lipogenesis, especially in prolonged critical illness, will also affect the circulating levels. Whether a disturbed lipid homeostasis warrants intervention or should primarily be interpreted as a signal of severity of illness requires further research.

Identifiers

PMID38015312
PMCPMC10684846
OpenAlexW4389086820

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.