Evidence map›Paper›PMID 29288273›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2018

Pro-inflammatory cytokines after an episode of acute pancreatitis: associations with fasting gut hormone profile.

Sayali A Pendharkar, Ruma G Singh, Shayal K Chand, Aya Cervantes, Maxim S Petrov

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

15 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Global epidemiology and holistic prevention of pancreatitis.Nature reviews. Gastroenterology & hepatology · 2019
    Review
  14. Article
  15. 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

5 authors at 1 institution in 1 country.

Sayali A PendharkarSchool of Medicine, University of Auckland, Auckland, New Zealand.
Ruma G SinghSchool of Medicine, University of Auckland, Auckland, New Zealand.
Shayal K ChandSchool of Medicine, University of Auckland, Auckland, New Zealand.
Aya CervantesSchool of Medicine, University of Auckland, Auckland, New Zealand.
Maxim S PetrovSchool of Medicine, University of Auckland, Auckland, New Zealand. max.petrov@gmail.com.
University of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPro-inflammatory cytokines, such as interleukin (IL)-6, tumour necrosis factor (TNF)α, and monocyte chemoattractant protein (MCP)-1, are often elevated in individuals after acute pancreatitis but what determines their levels is poorly understood. Gut hormones have emerged as possible modulators of inflammatory response. The aim was to investigate the associations between pro-inflammatory cytokines and a comprehensive panel of gut hormones after an episode of acute pancreatitis. MATERIALS AND

methodsFasting blood samples were collected to measure cytokines (IL-6, TNFα, and MCP-1) and gut hormones (cholecystokinin, gastric inhibitory peptide (GIP), ghrelin, glicentin, glucagon-like peptide-1, oxyntomodulin, peptide YY, secretin, and vasoactive intestinal peptide). A series of linear regression analyses was conducted and four statistical models were used to adjust for patient- and pancreatitis-related covariates.

resultsA total of 83 individuals were recruited. GIP and peptide YY were significantly (p < 0.001) associated with IL-6, TNFα, MCP-1, consistently in all the four models. Every 1 ng/mL change in GIP resulted in a 16.2, 3.2, and 50.8% increase in IL-6, TNFα, and MCP-1, respectively, in the most adjusted model. Every 1 ng/mL change in peptide YY resulted in a 7.0, 2.4, and 32.1% increase in IL-6, TNFα, and MCP-1, respectively, in the most adjusted model. GIP independently contributed 29.0-36.5% and peptide YY - 17.4-48.9% to circulating levels of the studied pro-inflammatory cytokines. The other seven studied gut hormones did not show consistently significant associations with pro-inflammatory cytokines.

conclusionsGIP and peptide YY appear to be involved in perpetuation of subclinical inflammation following an episode of acute pancreatitis, which is known to play an important role in the pathogenesis of blood glucose derangements. These findings advance the understanding of mechanisms underlying diabetes of the exocrine pancreas and have translational implications.

Indexed as

Acute DiseaseAdultAgedChemokine CCL2Cross-Sectional StudiesFastingFemaleGastric Inhibitory PolypeptideGastrointestinal HormonesHumansHyperglycemiaInterleukin-6MaleMiddle AgedPancreatitisPeptide YYChemokine CCL2Gastric Inhibitory PolypeptideGastrointestinal HormonesInterleukin-6Peptide YYTumor Necrosis Factor-alphaAcute pancreatitisChronic hyperglycaemiaGastric inhibitory peptideInterleukin-6Monocyte chemoattractant protein-1Peptide YY

Identifiers

PMID29288273
OpenAlexW2781269064

What Socratic holds

Textmetadata
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.