Evidence map›Paper›PMID 29208960›Full record

SynthesisScientific reports2017

MIF -173 G > C (rs755622) Gene Polymorphism Modulates Tuberculosis Risk: Evidence from a Meta-analysis and Trial Sequential Analysis.

Mohammed Y Areeshi, Raju K Mandal, Sajad A Dar, Arshad Jawed, Mohd Wahid, Mohtashim Lohani, Aditya K Panda, B N Mishra, Naseem Akhter, Shafiul Haque

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Genetic Variants of thePharmacogenomics and personalized medicine · 2021
    Article
  7. Observational
  8. Article
  9. 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

10 authors at 4 institutions in 2 countries.

Mohammed Y AreeshiResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.
Raju K MandalResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.
Sajad A DarResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.
Arshad JawedResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.ORCID 0000-0002-3161-9864
Mohd WahidResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.
Mohtashim LohaniResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia.
Aditya K PandaCentre for Life Sciences, Central University of Jharkhand, Ranchi, 835205, Jharkhand, India.
B N MishraDepartment of Biotechnology, Institute of Engineering & Technology, Lucknow, 226021, Uttar Pradesh, India.
Naseem AkhterDepartment of Laboratory Medicine, Faculty of Applied Medical Sciences, Albaha University, Albaha, 65431, Saudi Arabia.
Shafiul HaqueResearch and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan, 45142, Saudi Arabia. shafiul.haque@hotmail.com.
Jazan University · SAAl Baha University · SACentral University of Jharkhand · INUniversity College of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The macrophage migration inhibitory factor (MIF) is a cytokine that plays an important role in inhibiting the growth of pathogenic Mycobacterium tuberculosis (M.tb) and regulates immune responses against M.tb pathogen. MIF -173 G > C gene polymorphism may affect immunity in an individual and leads to susceptibility to tuberculosis (TB). A large number of studies have investigated the relevance of this polymorphism with TB risk, but their results were inconclusive. To obtain a precise conclusion, a meta-analysis was performed by retrieving six eligible studies from Google Scholar, PubMed (Medline), and EMBASE online databases. Overall combined analysis suggested increased TB risk between MIF -173 G > C polymorphism and overall risk in four genetic models, i.e., allelic (C vs. G: p = 0.001; OR = 1.517, 95% CI = 1.312 to 1.753), homozygous (CC vs. GG: p = 0.026; OR = 1.874, 95% CI = 1.079 to 3.257), heterozygous (GC vs. GG: p = 0.001; OR = 1.542, 95% CI = 1.273 to 1.868) and dominant model (CC + GC vs. GG: p = 0.001; OR = 1.631, 95% CI = 1.362 to 1.955). Similarly, increased TB risk was observed in subgroup analysis of Asian ethnicity. No publication bias was observed. These results suggested that MIF -173 G > C variant is a significant risk factor for TB in overall and in Asian populations, and can be used as prognostic marker for TB susceptibility.

Indexed as

Polymorphism, Single NucleotideCase-Control StudiesGenetic Predisposition to DiseaseHumansIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMycobacterium tuberculosisPrognosisRisk FactorsTuberculosisIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMIF protein, human

Identifiers

PMID29208960
PMCPMC5717251
OpenAlexW2770196091

What OpenQuestion holds

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LicenceCC BY
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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.