Evidence map›Paper›PMID 27880809›Full record

Trial reportPloS one2016

Molecular Analysis of Glucose-6-Phosphate Dehydrogenase Gene Mutations in Bangladeshi Individuals.

Suprovath Kumar Sarker, Md Tarikul Islam, Grace Eckhoff, Mohammad Amir Hossain, Syeda Kashfi Qadri, A K M Muraduzzaman, Golam Sarower Bhuyan, Mohammod Shahidullah, Mohammad Abdul Mannan, Sarabon Tahura and 6 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 22 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

16 authors at 6 institutions in 2 countries.

Suprovath Kumar SarkerLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Md Tarikul IslamLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Grace EckhoffLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Mohammad Amir HossainLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Syeda Kashfi QadriDepartment of Paediatric Medicine, KK Women's and Children's Hospital, 100 Bukit Timah Road, Singapore, Singapore.
A K M MuraduzzamanDepartment of Virology, Institute of Epidemiology, Disease Control and Research, Mohakhali, Dhaka, Bangladesh.
Golam Sarower BhuyanLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Mohammod ShahidullahDepartment of Neonatology, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka, Bangladesh.
Mohammad Abdul MannanDepartment of Neonatology, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka, Bangladesh.
Sarabon TahuraDepartment of Paediatric Medicine, Dhaka Shishu Hospital, Dhaka, Bangladesh.
Manzoor HussainDepartment of Paediatric Medicine, Dhaka Shishu Hospital, Dhaka, Bangladesh.
Shahida AkhterDepartment of Paediatrics, Bangladesh Institute of Research & Rehabilitation in Diabetes, Endocrine and Metabolic Disorders, Shahbag, Dhaka, Bangladesh.
Nazmun NaharDepartment of Paediatrics, Bangladesh Institute of Research & Rehabilitation in Diabetes, Endocrine and Metabolic Disorders, Shahbag, Dhaka, Bangladesh.
Tahmina ShirinDepartment of Virology, Institute of Epidemiology, Disease Control and Research, Mohakhali, Dhaka, Bangladesh.
Firdausi QadriLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Kaiissar MannoorLaboratory of Genetics and Genomics, Institute for Developing Science and Health Initiatives, Mohakhali, Dhaka, Bangladesh.
Bangladesh Institute of Development Studies · BDBangabandhu Sheikh Mujib Medical University · BDBangladesh Institute of Research and Rehabilitation for Diabetes Endocrine and Metabolic Disorders · BDDhaka Shishu Hospital · BDInstitute of Epidemiology, Disease Control and Research · BDKK Women's and Children's Hospital · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common X-linked human enzyme defect of red blood cells (RBCs). Individuals with this gene defect appear normal until exposed to oxidative stress which induces hemolysis. Consumption of certain foods such as fava beans, legumes; infection with bacteria or virus; and use of certain drugs such as primaquine, sulfa drugs etc. may result in lysis of RBCs in G6PD deficient individuals. The genetic defect that causes G6PD deficiency has been identified mostly as single base missense mutations. One hundred and sixty G6PD gene mutations, which lead to amino acid substitutions, have been described worldwide. The purpose of this study was to detect G6PD gene mutations in hospital-based settings in the local population of Dhaka city, Bangladesh. Qualitative fluorescent spot test and quantitative enzyme activity measurement using RANDOX G6PDH kit were performed for analysis of blood specimens and detection of G6PD-deficient participants. For G6PD-deficient samples, PCR was done with six sets of primers specific for G6PD gene. Automated Sanger sequencing of the PCR products was performed to identify the mutations in the gene. Based on fluorescence spot test and quantitative enzyme assay followed by G6PD gene sequencing, 12 specimens (11 males and one female) among 121 clinically suspected patient-specimens were found to be deficient, suggesting a frequency of 9.9% G6PD deficiency. Sequencing of the G6PD-deficient samples revealed c.C131G substitution (exon-3: Ala44Gly) in six samples, c.G487A substitution (exon-6:Gly163Ser) in five samples and c.G949A substitution (exon-9: Glu317Lys) of coding sequence in one sample. These mutations either affect NADP binding or disrupt protein structure. From the study it appears that Ala44Gly and Gly163Ser are the most common G6PD mutations in Dhaka, Bangladesh. This is the first study of G6PD mutations in Bangladesh.

Indexed as

ExonsMutation, MissenseAdolescentAmino Acid SubstitutionBangladeshChildChild, PreschoolDNA Mutational AnalysisFemaleGlucosephosphate DehydrogenaseGlucosephosphate Dehydrogenase DeficiencyHumansInfantInfant, NewbornMaleGlucosephosphate Dehydrogenase

Identifiers

PMID27880809
PMCPMC5120827
OpenAlexW2555651359

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.