Evidence map›Paper›PMID 30278967›Full record

ArticleThe Journal of surgical research2018

MC1R gene polymorphisms are associated with dysfunctional immune responses and wound infection after burn injury.

Damien W Carter, Ravi F Sood, Max E Seaton, Lara A Muffley, Shari Honari, Ann M Hocking, Saman A Arbabi, Nicole S Gibran

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Article in The Journal of surgical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 9 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

8 authors at 3 institutions in 1 country.

Damien W CarterDepartment of Surgery, Maine Medical Center, Tufts University School of Medicine, Portland, Maine. Electronic address: dcarter@mmc.org.
Ravi F SoodDepartment of Surgery, University of Washington, Washington.
Max E SeatonDepartment of Surgery, University of Maryland, College Park, Maryland.
Lara A MuffleyDepartment of Surgery, University of Washington, Washington.
Shari HonariDepartment of Surgery, University of Washington, Washington.
Ann M HockingDepartment of Surgery, University of Washington, Washington.
Saman A ArbabiDepartment of Surgery, University of Washington, Washington.
Nicole S GibranDepartment of Surgery, University of Washington, Washington.
University of Washington · USTufts University · USUniversity of Maryland, College Park · US

Funding

Response to Burn Injury: Role of the Melanocortin System in Wound RepairR01GM089704 · NIGMS · UNIVERSITY OF WASHINGTON · PI GIBRAN, NICOLE SIMONE · 2010 to 2013
$1.2M
Surgical Wound Repair: fibroproliferative responses to cutaneous injuryR01GM121369 · NIGMS · UNIVERSITY OF WASHINGTON · PI GIBRAN, NICOLE SIMONE · 2017 to 2020
$1.2M
NIGMS NIH HHS R01 GM089704NIGMS NIH HHS R01 GM121369
6 · The paper itself

Abstract

backgroundSystemic inflammatory response syndrome (SIRS) is associated with organ failure and infectious complications after major burn injury. Recent evidence has linked melanocortin signaling to anti-inflammatory and wound-repair functions, with mutations in the melanocortin 1 receptor (MC1R) gene leading to increased inflammatory responses. Our group has previously demonstrated that MC1R gene polymorphisms are associated with postburn hypertrophic scarring. Thus, we hypothesized that MC1R single nucleotide polymorphisms (SNPs) would be associated with increased burn-induced SIRS and increased infectious complications.

methodsWe performed a retrospective cohort study of adults (>18 y of age) admitted to our burn center with >20% total body surface area (TBSA) partial/full thickness burns between 2006 and 2013. We screened for five MC1R SNPs (V60L, V92M, R151C, R163Q, T314T) by polymerase chain reaction from genomic DNA isolated from blood samples. We performed a detailed review of each patient chart to identify age, sex, race, ethnicity, %TBSA burned, burn wound infections (BWIs), and 72-hr intravenous fluid volume, the latter a surrogate for a dysfunctional inflammatory response to injury. Association testing was based on multivariable regression.

resultsOf 106 subjects enrolled, 82 had complete data for analysis. Of these, 64 (78%) were male, with a median age of 39 and median burn size of 30% TBSA. A total of 36 (44%) subjects developed BWIs. The median total administered IV crystalloid in first 72h was 24.6 L. In multivariate analysis, the R151C variant allele was a significant independent risk factor for BWI (adjusted prevalence ratio 2.03; 95% CI: 1.21-3.39; P = 0.007), and the V60L variant allele was independently associated with increased resuscitation fluid volume (P = 0.021).

conclusionsThis is the first study to demonstrate a significant association between genetic polymorphisms and a nonfatal burn-induced SIRS complication. Our findings suggest that MC1R polymorphisms contribute to dysfunctional responses to burn injury that may predict infectious and inflammatory complications.

Indexed as

Polymorphism, Single NucleotideAdolescentAdultAgedBurnsFemaleGenetic MarkersGenotyping TechniquesHumansLinear ModelsMaleMiddle AgedMultivariate AnalysisReceptor, Melanocortin, Type 1Retrospective StudiesSystemic Inflammatory Response SyndromeGenetic MarkersMC1R protein, humanReceptor, Melanocortin, Type 1

Identifiers

PMID30278967
PMCPMC6464811
OpenAlexW2887714328

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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.