Evidence map›Paper›PMID 27272151›Full record

ArticlePloS one2016

Genome-Wide Association Study in Immunocompetent Patients with Delayed Hypersensitivity to Sulfonamide Antimicrobials.

Jennifer M Reinhart, Alison Motsinger-Reif, Allison Dickey, Steven Yale, Lauren A Trepanier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Sulfonamide Hypersensitivity.Clinical reviews in allergy & immunology · 2022
    Review
  4. Review
  5. Review
  6. Sulfonamide Drug Allergy.Current allergy and asthma reports · 2018
    Review
  7. 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 3 institutions in 1 country.

Jennifer M ReinhartDepartment of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.ORCID http://orcid.org/0000-0002-3021-5075
Alison Motsinger-ReifBioinformatics Research Center, Department of Statistics, North Carolina State University, Raleigh, North Carolina, United States of America.
Allison DickeyBioinformatics Research Center, Department of Statistics, North Carolina State University, Raleigh, North Carolina, United States of America.
Steven YaleMarshfield Clinic Research Foundation, Marshfield, Wisconsin, United States of America.
Lauren A TrepanierDepartment of Medical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
North Carolina State University · USUniversity of Wisconsin–Madison · USMarshfield Clinic · US

Funding

Comparative Biomedical Sciences Training ProgramT32OD010423 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI Marulasiddappa Suresh · 2012 to 2026
$5.0M
Mechanisms of risk for sulfoniamide hypersensitivityR01GM100784 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI TREPANIER, LAUREN A · 2012 to 2015
$1.2M
NIGMS NIH HHS R01 GM100784NIH HHS T32 OD010423
6 · The paper itself

Abstract

backgroundHypersensitivity (HS) reactions to sulfonamide antibiotics occur uncommonly, but with potentially severe clinical manifestations. A familial predisposition to sulfonamide HS is suspected, but robust predictive genetic risk factors have yet to be identified. Strongly linked genetic polymorphisms have been used clinically as screening tests for other HS reactions prior to administration of high-risk drugs.

objectiveThe purpose of this study was to evaluate for genetic risk of sulfonamide HS in the immunocompetent population using genome-wide association.

methodsNinety-one patients with symptoms after trimethoprim-sulfamethoxazole (TMP-SMX) attributable to "probable" drug HS based on medical record review and the Naranjo Adverse Drug Reaction Probability Scale, and 184 age- and sex-matched patients who tolerated a therapeutic course of TMP-SMX, were included in a genome-wide association study using both common and rare variant techniques. Additionally, two subgroups of HS patients with a more refined clinical phenotype (fever and rash; or fever, rash and eosinophilia) were evaluated separately.

resultsFor the full dataset, no single nucleotide polymorphisms were suggestive of or reached genome-wide significance in the common variant analysis, nor was any genetic locus significant in the rare variant analysis. A single, possible gene locus association (COL12A1) was identified in the rare variant analysis for patients with both fever and rash, but the sample size was very small in this subgroup (n = 16), and this may be a false positive finding. No other significant associations were found for the subgroups.

conclusionsNo convincing genetic risk factors for sulfonamide HS were identified in this population. These negative findings may be due to challenges in accurately confirming the phenotype in exanthematous drug eruptions, or to unidentified gene-environment interactions influencing sulfonamide HS.

Indexed as

Polymorphism, Single NucleotideAnti-Infective AgentsDrug EruptionsFemaleGenome-Wide Association StudyHumansHypersensitivity, DelayedMaleTrimethoprim, Sulfamethoxazole Drug CombinationAnti-Infective AgentsTrimethoprim, Sulfamethoxazole Drug Combination

Identifiers

PMID27272151
PMCPMC4896425
OpenAlexW2416296981

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.