Evidence map›Paper›PMID 27853304›Full record

ArticleScientific reports2016

Genetic Epidemiology of Glucose-6-Phosphate Dehydrogenase Deficiency in the Arab World.

C George Priya Doss, Dima R Alasmar, Reem I Bux, P Sneha, Fadheela Dad Bakhsh, Iman Al-Azwani, Rajaa El Bekay, Hatem Zayed

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 3 pooled it
16.3field-weighted citation impact, top 1% 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

26 citing papers in PubMed, 3 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  8. Molecular dynamics of G6PD variants from sub-Saharan Africa.Biochemistry and biophysics reports · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

C George Priya DossDepartment of Integrative Biology, School of Biosciences and Technology, VIT University, Vellore, India.
Dima R AlasmarCollege of Health Sciences, Biomedical Sciences Department, Qatar University, Doha, Qatar.
Reem I BuxCollege of Health Sciences, Biomedical Sciences Department, Qatar University, Doha, Qatar.
P SnehaDepartment of Integrative Biology, School of Biosciences and Technology, VIT University, Vellore, India.
Fadheela Dad BakhshCollege of Health Sciences, Biomedical Sciences Department, Qatar University, Doha, Qatar.
Iman Al-AzwaniCollege of Health Sciences, Biomedical Sciences Department, Qatar University, Doha, Qatar.
Rajaa El BekayCIBER Pathophysiology of obesity and nutrition CB06/03, Carlos III Health Institute. Unidad de Gestion Clínica Intercentros de Endocrinología y Nutrición, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga/Universidad de Málaga, 29009, Málaga, Spain.
Hatem ZayedCollege of Health Sciences, Biomedical Sciences Department, Qatar University, Doha, Qatar.
Qatar University · QAVellore Institute of Technology University · INInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A systematic search was implemented using four literature databases (PubMed, Embase, Science Direct and Web of Science) to capture all the causative mutations of Glucose-6-phosphate dehydrogenase (G6PD) deficiency (G6PDD) in the 22 Arab countries. Our search yielded 43 studies that captured 33 mutations (23 missense, one silent, two deletions, and seven intronic mutations), in 3,430 Arab patients with G6PDD. The 23 missense mutations were then subjected to phenotypic classification using in silico prediction tools, which were compared to the WHO pathogenicity scale as a reference. These in silico tools were tested for their predicting efficiency using rigorous statistical analyses. Of the 23 missense mutations, p.S188F, p.I48T, p.N126D, and p.V68M, were identified as the most common mutations among Arab populations, but were not unique to the Arab world, interestingly, our search strategy found four other mutations (p.N135T, p.S179N, p.R246L, and p.Q307P) that are unique to Arabs. These mutations were exposed to structural analysis and molecular dynamics simulation analysis (MDSA), which predicting these mutant forms as potentially affect the enzyme function. The combination of the MDSA, structural analysis, and in silico predictions and statistical tools we used will provide a platform for future prediction accuracy for the pathogenicity of genetic mutations.

Indexed as

Glucosephosphate DehydrogenaseMolecular Dynamics SimulationMutationArabsGlucosephosphate Dehydrogenase DeficiencyHumansProtein DomainsGlucosephosphate Dehydrogenase

Identifiers

PMID27853304
PMCPMC5112515
OpenAlexW2555141287

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.