Evidence map›Paper›PMID 28704535›Full record

ArticlePloS one2017

Interferon-related genetic markers of necroinflammatory activity in chronic hepatitis C.

Rosario López-Rodríguez, Ángel Hernández-Bartolomé, María Jesús Borque, Yolanda Rodríguez-Muñoz, Samuel Martín-Vílchez, Luisa García-Buey, Leticia González-Moreno, Yolanda Real-Martínez, Paloma Muñoz de Rueda, Javier Salmerón and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Article
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  6. Review
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  8. 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

15 authors at 3 institutions in 1 country.

Rosario López-RodríguezLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Ángel Hernández-BartoloméLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
María Jesús BorqueMolecular Biology Unit, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Yolanda Rodríguez-MuñozLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Samuel Martín-VílchezLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Luisa García-BueyLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Leticia González-MorenoLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Yolanda Real-MartínezLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Paloma Muñoz de RuedaCIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain.
Javier SalmerónCIBERehd, Instituto de Salud Carlos III (ISCIII), Madrid, Spain.
José Ramón Vidal-CastiñeiraInmunology Service, Hospital, Universitario Central de Asturias, Oviedo, Spain.
Carlos López-LarreaInmunology Service, Hospital, Universitario Central de Asturias, Oviedo, Spain.
Luis RodrigoDigestive Service, Hospital Universitario Central de Asturias, Oviedo, Spain.
Ricardo Moreno-OteroLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
Paloma Sanz-CamenoLiver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.ORCID http://orcid.org/0000-0001-5308-2167
Hospital Universitario de La Princesa · ESInstituto de Salud Carlos III · ESHospital Universitario Central de Asturias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic hepatitis C (CHC) is a major cause of liver disease worldwide which often leads to progressive liver inflammation, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). CHC displays heterogeneous progression depending on a broad set of factors, some of them intrinsic to each individual such as the patient's genetic profile. This study aims to evaluate the contribution of certain genetic variants of crucial interferon alpha and lambda signaling pathways to the hepatic necroinflammatory activity (NIA) grade of CHC patients.

methodsNIA was evaluated in 119 CHC patients by METAVIR scale and classified as low (NIA = 0-2, n = 80) or high grade (NIA = 3, n = 39). In a candidate gene approach, 64 SNPs located in 30 different genes related to interferon pathways (IL-28B, IFNAR1-2, JAK-STAT and OAS1-3, among others) were genotyped using the Illumina GoldenGate® Genotyping Assay. Statistical association was determined by logistic regression and expressed as OR and 95% CI. Those SNPs significantly associated were further adjusted by other covariates.

resultsSeven SNPs located in IL-28B (rs12979860), JAK1 (rs11576173 and rs1497056), TYK2 (rs280519), OAS1 (rs2057778), SOCS1 (rs33932899) and RNASEL (rs3738579) genes were significantly related to severe NIA grade (p<0.05). Regarding to clinical variables, elevated NIA was notably associated with aspartate aminotransferase (AST) serum levels >40 IU/L (p<0.05) but not with other clinical factors. Multivariate logistic regression analysis of these factors reflected that AST (>40 IU/L), TYK2 rs280519 (G allele) and RNASEL rs3738579 (G allele) were factors independently associated with elevated NIA (p<0.05). AST concentration showed a moderate AUC value (AUC = 0.63), similar to TYK2 (rs280519) and RNASEL (rs3738579) SNPs (AUC = 0.61, both) in the ROC_AUC analysis. Interestingly, the model including all significant variables reached a considerable predictive value (AUC = 0.74).

conclusionThe identified genetic variants in interferon signaling pathways may constitute useful prognostic markers of CHC progression. Further validation in larger cohorts of patients is needed.

Indexed as

Polymorphism, Single Nucleotide2',5'-Oligoadenylate SynthetaseAdultAgedAspartate AminotransferasesEndoribonucleasesFemaleHepatitis C, ChronicHumansInterferon LambdaInterferonsInterleukinsJanus Kinase 1MaleMiddle AgedSuppressor of Cytokine Signaling 1 Protein2-5A-dependent ribonuclease2',5'-Oligoadenylate SynthetaseAspartate AminotransferasesEndoribonucleasesInterferon Lambdainterferon-lambda, humanInterferonsInterleukinsJAK1 protein, humanJanus Kinase 1OAS1 protein, humanSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinTYK2 KinaseTYK2 protein, human

Identifiers

PMID28704535
PMCPMC5507534
OpenAlexW2734685634

What OpenQuestion holds

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LicenceCC BY
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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.