Evidence map›Paper›PMID 30377885›Full record

ArticleDigestive diseases and sciences2019

Bactericidal/Permeability-Increasing Fold-Containing Family B Member 4 May Be Associated with NSAID-Induced Enteropathy.

Shunji Fujimori, Koya Fukunaga, Atsushi Takahashi, Taisei Mushiroda, Michiaki Kubo, Ryuzo Hanada, Mari Hayashida, Toshiyuki Sakurai, Katsuhiko Iwakiri, Choitsu Sakamoto

Open access · hybridAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 3 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

10 authors at 6 institutions in 1 country.

Shunji FujimoriDepartment of Gastroenterology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo, 113-8603, Japan. s-fujimori@nms.ac.jp.ORCID 0000-0002-6214-2595
Koya FukunagaRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Atsushi TakahashiRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Taisei MushirodaRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Michiaki KuboRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Ryuzo HanadaSumida Hospital, SOUSEIKAI, Tokyo, Japan.
Mari HayashidaThe Third Department of Internal Medicine, Kyorin University School of Medicine, Tokyo, Japan.
Toshiyuki SakuraiDepartment of Gastroenterology and Hepatology, National Center for Global Health and Medicine, Tokyo, Japan.
Katsuhiko IwakiriDepartment of Gastroenterology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo, 113-8603, Japan.
Choitsu SakamotoDepartment of Gastroenterology, Graduate School of Medicine, Nippon Medical School, 1-1-5, Sendagi, Bunkyo-ku, Tokyo, 113-8603, Japan.
Nippon Medical School · JPRIKEN Center for Integrative Medical Sciences · JPKyorin University · JPNational Center for Global Health and Medicine · JPNational Cerebral and Cardiovascular Center · JPSOUSEIKAI Global Clinical Research Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThere is considerable individual variability in nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy.

aimTo identify the SNP that is most significantly involved with NSAID-induced enteropathy.

methodsOne hundred fifty human subjects who were known to have a certain degree of loxoprofen- or celecoxib-induced small-intestinal damage from a previous study were enrolled. The subjects were divided into groups based on treatments and also on the increased number of small intestinal mucosal breaks. The candidate SNP was selected by an initial analysis of GWAS among the groups in various combinations. After the initial analysis, the gene including the specified SNP was analyzed in detail using GWAS and genotype imputation.

resultsAfter analysis, 70 subjects receiving the loxoprofen treatment and 69 subjects receiving celecoxib treatment were determined to be eligible for the analysis. The minimum p value in GWAS was detected in the analysis of 16 cases with an increase of five or more mucosal breaks and 123 controls with zero to four mucosal breaks. In the GWAS, five SNPs in the bactericidal/permeability-increasing fold-containing family B member 4 (BPIFB4) gene showed the lowest p value (p = 2.69 × 10

conclusionThe results indicate that SNPs in BPIFB4 were associated with NSAID-induced small intestinal mucosal injury (UMIN: 000007936).

Indexed as

AdultAnti-Inflammatory Agents, Non-SteroidalCapsule EndoscopyCelecoxibFemaleGenome-Wide Association StudyHumansIntercellular Signaling Peptides and ProteinsIntestinal DiseasesIntestinal MucosaIntestine, SmallMaleMiddle AgedPhenylpropionatesPhosphoproteinsPolymorphism, Single NucleotideAnti-Inflammatory Agents, Non-SteroidalBPIFB4 protein, humanCelecoxibIntercellular Signaling Peptides and ProteinsloxoprofenPhenylpropionatesPhosphoproteinsBPICapsule endoscopyEnteropathyGWASNSAIDSmall intestinal injury

Identifiers

PMID30377885
PMCPMC6514250
OpenAlexW2898658721

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Registered trials

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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.