Evidence map›Paper›PMID 31845023›Full record

ArticleInternational journal of colorectal disease2020

Genetic polymorphism patterns suggest a genetic driven inflammatory response as pathogenesis in appendicitis.

Jan Dimberg, Marie Rubér, Marita Skarstedt, Manne Andersson, Roland E Andersson

Open access · hybridAbstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in International journal of colorectal disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

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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 3 institutions in 1 country.

Jan DimbergDepartment of Natural Science and Biomedicine, School of Health and Welfare, Jönköping University, Jönköping, Sweden.ORCID http://orcid.org/0000-0003-2328-7334
Marie RubérDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.ORCID http://orcid.org/0000-0002-3582-4988
Marita SkarstedtDepartment of Laboratory Medicine, Division of Clinical Microbiology, Region Jönköping County, Jönköping, SE 551 85, Sweden.ORCID http://orcid.org/0000-0001-9577-8357
Manne AnderssonDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.ORCID http://orcid.org/0000-0002-2013-9574
Roland E AnderssonDepartment of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. roland.andersson@rjl.se.ORCID http://orcid.org/0000-0002-1460-0248
Linköping University · SEJönköping University · SERegion Jönköpings län · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe pathogenesis of appendicitis is not well understood. Environmental factors are regarded most important, but epidemiologic findings suggest a role of inflammatory and genetic mechanisms. This study determines the association of single nucleotide polymorphisms (SNPs) of inflammatory genes with appendicitis.

methodsAs part of a larger prospective study on the diagnostic value of inflammatory variables in appendicitis, the genotype frequency of 28 polymorphisms in 26 inflammatory response genes from the appendicitis and control patients was analyzed in blood samples from 343 patients, 100 with appendicitis, and 243 with non-specific abdominal pain, using TaqMan SNP genotyping assays.

resultsAssociations with appendicitis were found for SNPs IL-13 rs1800925 with odds ratio (OR) 6.02 (95% CI 1.52-23.78) for T/T versus C/C + T/T, for IL-17 rs2275913 with OR 2.38 (CI 1.24-4.57) for A/A vs G/G + GA, for CCL22 rs223888 with OR 0.12 (0.02-0.90), and for A/A vs G/G + GA. Signs of effect modification of age for the association with appendicitis were found for IL-13 rs1800925 and CTLA4 rs3087243. Stratified analysis showed difference in association with severity of disease for IL-17 rs2275913 and CD44 rs187115.

conclusionsThe association of gene variants on risk of appendicitis and its severity suggest an etiologic role of genetically regulated inflammatory response. This may have implications for understanding the prognosis of untreated appendicitis as a possible self-limiting disorder and for understanding the inverse association of appendicitis with ulcerative colitis.

Indexed as

Inflammation MediatorsPolymorphism, Single NucleotideAge FactorsAppendicitisCase-Control StudiesCytokinesFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHumansMalePhenotypeProspective StudiesRisk FactorsSeverity of Illness IndexCytokinesInflammation MediatorsAppendicitisGene polymorphismInflammatory bowel diseasePathophysiology

Identifiers

PMID31845023
OpenAlexW2995610307

What OpenQuestion holds

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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 OpenQuestion graph.