Evidence map›Paper›PMID 24615128›Full record

ArticleThe American journal of tropical medicine and hygiene2014

G6PD A- deficiency and severe malaria in The Gambia: heterozygote advantage and possible homozygote disadvantage.

Giorgio Sirugo, Irene M Predazzi, Jacquelaine Bartlett, Alessandra Tacconelli, Michael Walther, Scott M Williams

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of tropical medicine and hygiene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Potentially pathogenic and pathogenic G6PD variants.American journal of human genetics · 2023
    Article
  3. Article
  4. Article
  5. Global perspectives onFrontiers in pharmacology · 2022
    Review
  6. Past and current biological factors affecting malaria in the low transmission setting of Botswana: A review.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Assessing risk for Mendelian disorders in a Bronx population.Molecular genetics & genomic medicine · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 5 institutions in 3 countries.

Giorgio SirugoCentro di Ricerca, Ospedale San Pietro Fatebenefratelli, Rome, Italy; Center for Human Genetics Research, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Genetics, Geisel School of Medicine, Dartmouth College, Hanover, New Hampshire; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland; Medical Research Council Laboratories, Fajara, Banjul, The Gambia.
Irene M Predazzi
Jacquelaine Bartlett
Alessandra Tacconelli
Michael Walther
Scott M Williams
Vanderbilt University Medical Center · USDartmouth College · USMRC Unit the Gambia · GMNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Quantitative Biology Research InstituteP20GM103534 · NIGMS · DARTMOUTH COLLEGE · PI AMOS, CHRISTOPHER I. · 2012 to 2016
$8.6M
NIGMS NIH HHS GM103534NIGMS NIH HHS P20 GM103534
6 · The paper itself

Abstract

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is frequent in Africa, because it confers resistance to Plasmodium falciparum malaria; however, the nature of the protection and the genotypes associated with it have been controversial. In 1972, Bienzle and others described protection from malaria in West African females heterozygous for G6PD A-. They determined that G6PD A- heterozygotes had lower parasite counts than A- homozygotes, hemizygous males, and normal individuals. However, other studies have reached different conclusions about the protective genotypes. DNA samples from 135 children with severe malaria and 146 children with mild malaria from The Gambia were genotyped for the G6PD A- mutation that is most frequent among Gambians (G6PD 968 T->C); there was a marked deficiency of heterozygotes and an excess of homozygotes with severe malaria, producing a strong deviation from Hardy-Weinberg equilibrium. Our results support the protective effect in G6PD A- heterozygous females and suggest that homozygotes might be more susceptible to severe malaria attacks.

Indexed as

HeterozygoteHomozygoteAdolescentChildChild, PreschoolDNA PrimersFemaleGambiaGlucosephosphate DehydrogenaseGlucosephosphate Dehydrogenase DeficiencyHost-Parasite InteractionsHumansInfantLogistic ModelsMalaria, FalciparumMaleDNA Primersglucose-6-phosphate dehydrogenase A-Glucosephosphate Dehydrogenase

Identifiers

PMID24615128
PMCPMC4015578
OpenAlexW2115947198

What OpenQuestion holds

Textmetadata
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.