Evidence map›Paper›PMID 27861181›Full record

ArticleInflammatory bowel diseases2016

Genetic Risk for Inflammatory Bowel Disease Is a Determinant of Crohn's Disease Development in Chronic Granulomatous Disease.

Chengrui Huang, Suk See De Ravin, Adam R Paul, Theo Heller, Nancy Ho, Lisa Wu Datta, Christa S Zerbe, Beatriz E Marciano, Douglas B Kuhns, Howard A Kader and 4 more

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in Inflammatory bowel diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Preventing Colitis-Associated Colon Cancer With Antioxidants: A Systematic Review.Cellular and molecular gastroenterology and hepatology · 2021
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Host-pathobiont interactions in Crohn's disease.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Chitosan functionalized MnCommunications biology · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Oxidants in Physiological Processes.Handbook of experimental pharmacology · 2021
    Review
  20. 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

14 authors at 6 institutions in 1 country.

Chengrui Huang*Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland; †Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, Maryland; ‡Department of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland; §Department of Medicine, Meyerhoff Inflammatory Bowel Disease Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; ‖National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, Maryland; ¶Laboratory of Clinical Infectious Diseases (LCID), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, Maryland; and **Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland.
Suk See De Ravin
Adam R Paul
Theo Heller
Nancy Ho
Lisa Wu Datta
Christa S Zerbe
Beatriz E Marciano
Douglas B Kuhns
Howard A Kader
Steven M Holland
Harry L Malech
Steven R Brant
NIDDK IBD Genetics Consortium,
National Institutes of Health · USJohns Hopkins Medicine · USJohns Hopkins University · USFrederick National Laboratory for Cancer Research · USNational Institute of Allergy and Infectious Diseases · USUniversity of Maryland, Baltimore · US

Funding

Gene Therapy Basic Research to Treat Inherited Primary Immune DeficienciesZIAAI000644 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MALECH, HARRY L · 2009 to 2025
$12.1M
Translational Research Enhancement CoreP30DK089502 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI ZACHOS, NICHOLAS CONSTANTINE · 2011 to 2020
$12.0M
IBD Gene Mapping by Clinical and Population SubsetsU01DK062431 · NIDDK · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Steven R Brant · 2002 to 2026
$10.7M
Development and Clinical Application of Gene and Cell therapies for Patients with Immune DeficienciesZIAAI000645 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DE RAVIN, SUK SEE · 2009 to 2025
$10.1M
Impact of Genetic Variability on Cellular Pathways and Host-Microbiome InteractioU01DK062423 · NIDDK · SINAI HEALTH SYSTEM · PI MARK S. SILVERBERG · 2002 to 2026
$7.5M
NIDDK NIH HHS P30 DK089502NIDDK NIH HHS U01 DK062423NIDDK NIH HHS U01 DK062431
6 · The paper itself

Abstract

backgroundApproximately, one-third to one-half of children with chronic granulomatous disease (CGD) develop gastrointestinal inflammation characteristic of idiopathic inflammatory bowel disease (IBD), usually Crohn's disease. We hypothesized that the overall IBD genetic risk, determined by IBD genetic risk score (GRS), might in part determine IBD development in CGD.

methodsWe reviewed medical records to establish IBD diagnoses in CGD subjects seen at NIAID. IBD risk single nucleotide polymorphism genotypes were determined using the Immunochip, and GRS were estimated by Mangrove.

resultsAmong 157 white patients with CGD, 55 were confirmed, 78 excluded, and 24 were uncertain for IBD. Two hundred one established, independent European IBD risk single nucleotide polymorphisms passed quality control. After sample quality control and removing non-IBD CGD patients with perianal disease, mean GRS for 40 unrelated patients with CGD-IBD was higher than 53 CGD non-IBD patients (in log2-scale 0.08 ± 1.62 versus -0.67 ± 1.64, P = 0.026) but lower than 239 IBD Genetics Consortium (IBDGC) young-onset Crohn's disease cases (0.76 ± 1.60, P = 0.025). GRS for non-IBD CGD was similar to 609 IBDGC controls (-0.69 ± 1.60, P = 0.95). Seven established IBD single nucleotide polymorphisms were nominally significant among CGD-IBD versus CGD non-IBD, including those near LACC1 (P = 0.005), CXCL14 (P = 0.007), and TNFSF15 (P = 0.016).

conclusionsThe weight of the common IBD risk alleles are significant determinants of IBD in CGD. However, IBD risk gene burden among CGD children with IBD is significantly lower than that in nonsyndromic pediatric Crohn's disease, congruent with the concept that defective superoxide production in CGD is also a major IBD risk factor. Individual IBD genes might interact with the CGD defect to cause IBD in CGD.

Indexed as

AdolescentAllelesChildChild, PreschoolCrohn DiseaseFemaleGenetic Predisposition to DiseaseGranulomatous Disease, ChronicHumansInflammatory Bowel DiseasesIntracellular Signaling Peptides and ProteinsMalePolymorphism, Single NucleotideProteinsRisk FactorsTumor Necrosis Factor Ligand Superfamily Member 15Intracellular Signaling Peptides and ProteinsLACC1 protein, humanProteinsTNFSF15 protein, humanTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID27861181
PMCPMC5303573
OpenAlexW2551299957

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.