Evidence map›Paper›PMID 32702756›Full record

ArticleBlood2020

Glucose-6-phosphate dehydrogenase deficiency.

Lucio Luzzatto, Mwashungi Ally, Rosario Notaro

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 7 pooled it
62.1field-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

228 citing papers in PubMed, 7 syntheses or guidelines pooled it, 361 citations in OpenAlex.

  1. Pooled it
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  3. Genetics of catatonia: a systematic review of case reports and a gene pathway analysis.European psychiatry : the journal of the Association of European Psychiatrists · 2025
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  6. Guideline
  7. Pooled it
  8. Trial
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  16. Efficacy of universal genome sequencing in infant extracorporeal membrane oxygenation.Journal of perinatology : official journal of the California Perinatal Association · 2026
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  20. Review

168 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Lucio LuzzattoDepartment of Haematology and Blood Transfusion, Muhimbili University of Health and Allied Sciences, Dar es Salaam, United Republic of Tanzania.
Mwashungi AllyDepartment of Haematology and Blood Transfusion, Muhimbili University of Health and Allied Sciences, Dar es Salaam, United Republic of Tanzania.
Rosario NotaroLaboratory of Cancer Genetics and Gene Transfer, Core Research Laboratory, Institute for Cancer Research, Prevention and Clinical Network (ISPRO), Florence, Italy.
Muhimbili University of Health and Allied Sciences · TZPiedmont Reference Center for Epidemiology and Cancer Prevention · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose 6-phosphate dehydrogenase (G6PD) deficiency is 1 of the commonest human enzymopathies, caused by inherited mutations of the X-linked gene G6PD. G6PD deficiency makes red cells highly vulnerable to oxidative damage, and therefore susceptible to hemolysis. Over 200 G6PD mutations are known: approximately one-half are polymorphic and therefore common in various populations. Some 500 million persons with any of these mutations are mostly asymptomatic throughout their lifetime; however, any of them may develop acute and sometimes very severe hemolytic anemia when triggered by ingestion of fava beans, by any of a number of drugs (for example, primaquine, rasburicase), or, more rarely, by infection. Approximately one-half of the G6PD mutations are instead sporadic: rare patients with these mutations present with chronic nonspherocytic hemolytic anemia. Almost all G6PD mutations are missense mutations, causing amino acid replacements that entail deficiency of G6PD enzyme activity: they compromise the stability of the protein, the catalytic activity is decreased, or a combination of both mechanisms occurs. Thus, genotype-phenotype correlations have been reasonably well clarified in many cases. G6PD deficiency correlates remarkably, in its geographic distribution, with past/present malaria endemicity: indeed, it is a unique example of an X-linked human polymorphism balanced through protection of heterozygotes from malaria mortality. Acute hemolytic anemia can be managed effectively provided it is promptly diagnosed. Reliable diagnostic procedures are available, with point-of-care tests becoming increasingly important where primaquine and its recently introduced analog tafenoquine are required for the elimination of malaria.

Indexed as

Glucosephosphate Dehydrogenase DeficiencyHIV InfectionsBlood DonorsBlood SafetyGlucosephosphate DehydrogenaseHumansPrimaquineGlucosephosphate DehydrogenasePrimaquine

Identifiers

PMID32702756
OpenAlexW3044899919

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.