Trial reportPloS one2016
Molecular Analysis of Glucose-6-Phosphate Dehydrogenase Gene Mutations in Bangladeshi Individuals.
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.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Probiotic potential of mangrove sediment-derived purple non-sulfur bacteria: effects on Artemia growth, vibrio resistance, and nutritional profile.World journal of microbiology & biotechnology · 2026Article
- Mental distress or psychiatric condition? Exploring the gray area of categorizing psychological suffering among adolescents with obesity: a mixed methods study.European child & adolescent psychiatry · 2025Article
- Parent Intention to Participate in an Online Intervention to Enhance Health Behavior Change Among Youth Treated with Psychotropic Medication Who are Overweight or Obese: An Application of the Theory of Planned Behavior.Journal of prevention (2022) · 2024Article
- Prevalence and molecular analysis of glucose-6-phosphate dehydrogenase deficiency in Chin State, Myanmar.Parasites, hosts and diseases · 2023Article
- Article
- Active Pharmacovigilance for Primaquine Radical Cure of Plasmodium vivax Malaria in Odisha, India.The American journal of tropical medicine and hygiene · 2022Article
- Glucose-6-phosphate dehydrogenase activity in individuals with and without malaria: Analysis of clinical trial, cross-sectional and case-control data from Bangladesh.PLoS medicine · 2021Article
- Wide range of G6PD activities found among ethnic groups of the Chittagong Hill Tracts, Bangladesh.PLoS neglected tropical diseases · 2020Article
- Prevalence and distribution of G6PD deficiency: implication for the use of primaquine in malaria treatment in Ethiopia.Malaria journal · 2019Article
- Prevalence and Genetic Characterization of Glucose-6-Phosphate Dehydrogenase Deficiency in Anemic Subjects from Uttar Pradesh, India.Journal of pediatric genetics · 2019Article
- High resolution melting curve analysis enables rapid and reliable detection of G6PD variants in heterozygous females.BMC genetics · 2018Article
- Use of primaquine and glucose-6-phosphate dehydrogenase deficiency testing: Divergent policies and practices in malaria endemic countries.PLoS neglected tropical diseases · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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