Evidence map›Paper›PMID 25177689›Full record

ArticleBioMed research international2014

The association of toll-like receptor 4 polymorphism with hepatitis C virus infection in Saudi Arabian patients.

Ahmed A Al-Qahtani, Mashael R Al-Anazi, Fahad Al-Zoghaibi, Ayman A Abdo, Faisal M Sanai, Mohammed Q Khan, Ali Albenmousa, Hamad I Al-Ashgar, Mohammed N Al-Ahdal

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 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

9 authors at 4 institutions in 1 country.

Ahmed A Al-QahtaniDepartment of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh 11211, Saudi Arabia ; Department of Microbiology and Immunology, Alfaisal University School of Medicine, Riyadh, Saudi Arabia ; Liver Disease Research Center, King Saud University, Riyadh, Saudi Arabia.
Mashael R Al-AnaziDepartment of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh 11211, Saudi Arabia.
Fahad Al-ZoghaibiMolecular BioMedicine Program, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
Ayman A AbdoLiver Disease Research Center, King Saud University, Riyadh, Saudi Arabia ; Department of Medicine, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Faisal M SanaiLiver Disease Research Center, King Saud University, Riyadh, Saudi Arabia ; Division of Gastroenterology, Department of Medicine, King Abdulaziz Medical City, Jeddah, Saudi Arabia.
Mohammed Q KhanDepartment of Medicine, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
Ali AlbenmousaDepartment of Gastroenterology & Hepatology, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.ORCID 0000-0003-0195-380X
Hamad I Al-AshgarDepartment of Medicine, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
Mohammed N Al-AhdalDepartment of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh 11211, Saudi Arabia ; Department of Microbiology and Immunology, Alfaisal University School of Medicine, Riyadh, Saudi Arabia ; Department of Pathology and Laboratory Medicine, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
King Faisal Specialist Hospital & Research Centre · SAAlfaisal University · SAKing Saud University · SARiyadh Armed Forces Hospital · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a single stranded RNA virus. It affects millions of people worldwide and is considered as a leading cause of liver diseases including cirrhosis and hepatocellular carcinoma. A recent study reported that TLR4 gene polymorphisms are good prognostic predictors and are associated with protection from liver fibrosis among Caucasians. This study aims to investigate the implication of genetic polymorphisms of TLR4 gene on the HCV infection in Saudi Arabian patients. Two SNPs in the TLR4 gene, rs4986790 (A/G) and rs4986791 (C/T), were genotyped in 450 HCV patients and 600 uninfected controls. The association analysis confirmed that both SNPs showed a significant difference in their distribution between HCV-infected patients and uninfected control subjects (P < 0.0001; OR = 0.404, 95% CI = 0.281-0.581) and (P < 0.0001; OR = 0.298, 95% CI = 0.201-0.443), respectively. More importantly, haplotype analysis revealed that four haplotypes, AC, GT, GC, and AT (rs4986790, rs4986791), were significantly associated with HCV infection when compared with control subjects. One haplotype AC was more prominently found when chronic HCV-infected patients were compared with cirrhosis/HCC patients (frequency = 94.7% and P = 0.04). Both TLR4 SNPs under investigation were found to be significantly implicated with HCV-infection among Saudi Arabian population.

Indexed as

AdultAgedAged, 80 and overComorbidityFemaleGenetic Association StudiesGenetic MarkersGenetic Predisposition to DiseaseHepatitis CHumansLiver CirrhosisMaleMiddle AgedPolymorphism, Single NucleotidePrevalenceRisk FactorsGenetic MarkersTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID25177689
PMCPMC4142570
OpenAlexW2067980128

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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.