Evidence map›Paper›PMID 29216383›Full record

ArticleThe Journal of infectious diseases2018

Genetic Susceptibility to Postdiarrheal Hemolytic-Uremic Syndrome After Shiga Toxin-Producing Escherichia coli Infection: A Centers for Disease Control and Prevention FoodNet Study.

Asha R Kallianpur, Yuki Bradford, Rajal K Mody, Katie N Garman, Nicole Comstock, Sarah L Lathrop, Carol Lyons, Amy Saupe, Katie Wymore, Jeffrey A Canter and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. The Virulence ofFrontiers in cellular and infection microbiology · 2020
    Article
  3. Review
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

13 authors at 10 institutions in 1 country.

Asha R KallianpurGenomic Medicine Institute, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio.
Yuki BradfordDepartment of Biomedical and Translational Informatics, Geisinger Health System, Danville, Pennsylvania.
Rajal K ModyDivision of Foodborne, Waterborne, and Environmental Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia.
Katie N GarmanTennessee Department of Health, Nashville.
Nicole ComstockColorado Department of Public Health and Environment, Denver.
Sarah L LathropDepartment of Pathology, University of New Mexico, Albuquerque.
Carol LyonsConnecticut Emerging Infections Program, Yale University School of Public Health, New Haven, Connecticut.
Amy SaupeMinnesota Department of Health, St. Paul, Oakl.
Katie WymoreCalifornia Emerging Infections Program, Oakl.
Jeffrey A CanterDepartment of Molecular Physiology and Biophysics, Nashville, Tennessee.
Lana M OlsonCenter for Quantitative Sciences, Vanderbilt University School of Medicine, Nashville, Tennessee.
Amanda PalmerMaryland Department of Health and Mental Hygiene, Baltimore.
Timothy F JonesTennessee Department of Health, Nashville.
Tennessee Department of Health · USCleveland Clinic Lerner College of Medicine · USColorado Department of Public Health and Environment · USGeisinger Health System · USMaryland Department of Health · USMinnesota Department of Health · USUniversity of New Mexico · USVanderbilt University · USWaterborne Environmental (United States) · USYale University · US

Funding

Intramural CDC HHS CC999999NCEZID CDC HHS U50 CK000315
6 · The paper itself

Abstract

Background: Postdiarrheal hemolytic-uremic syndrome (D+HUS) following Shiga toxin-producing Escherichia coli (STEC) infection is a serious condition lacking specific treatment. Host immune dysregulation and genetic susceptibility to complement hyperactivation are implicated in non-STEC-related HUS. However, genetic susceptibility to D+HUS remains largely uncharacterized. Methods: Patients with culture-confirmed STEC diarrhea, identified through the Centers for Disease Control and Prevention FoodNet surveillance system (2007-2012), were serotyped and classified by laboratory and/or clinical criteria as having suspected, probable, or confirmed D+HUS or as controls and underwent genotyping at 200 loci linked to nondiarrheal HUS or similar pathologies. Genetic associations with D+HUS were explored by multivariable regression, with adjustment for known risk factors. Results: Of 641 enrollees with STEC O157:H7, 80 had suspected D+HUS (41 with probable and 32 with confirmed D+HUS). Twelve genes related to cytokine signaling, complement pathways, platelet function, pathogen recognition, iron transport, and endothelial function were associated with D+HUS in multivariable-adjusted analyses (P ≤ .05). Of 12 significant single-nucleotide polymorphisms (SNPs), 5 were associated with all levels of D+HUS (intergenic SNP rs10874639, TFRC rs3804141, EDN1 rs5370, GP1BA rs121908064, and B2M rs16966334), and 7 SNPs (6 non-complement related) were associated with confirmed D+HUS (all P < .05). Conclusions: Polymorphisms in many non-complement-related genes may contribute to D+HUS susceptibility. These results require replication, but they suggest novel therapeutic targets in patients with D+HUS.

Indexed as

Centers for Disease Control and Prevention, U.S.Genetic Predisposition to DiseaseAdolescentChildChild, PreschoolDiarrheaEscherichia coli InfectionsFemaleHemolytic-Uremic SyndromeHumansMaleRisk FactorsShiga-Toxigenic Escherichia coliUnited States

Identifiers

PMID29216383
PMCPMC11318523
OpenAlexW2775664070

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.