ReviewJournal of clinical medicine2022
Acquired Glucose-6-Phosphate Dehydrogenase Deficiency.
Review in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled prevalence of Glucose-6-phosphate dehydrogenase deficiency among malaria patients in Ethiopia: a systematic review and meta-analysis.Malaria journal · 2026Pooled it
- Association between G6PD gene variants and adverse pregnancy outcomes.BMC pregnancy and childbirth · 2026Article
- The association analysis between Glucose-6-Phosphate dehydrogenase deficiency and susceptibility to common diseases in children.Pediatric research · 2026Article
- Co-occurrence of acute hemolytic anemia and methemoglobinemia in a 74-year-old female with G6PD deficiency: A case report.Medicine · 2025Article
- A Case of Methemoglobinemia and Hemolysis from Sodium Chlorite Ingestion.Clinical medicine & research · 2025Article
- Revealing the secrets of Blue Zones.Frontiers in pharmacology · 2024Review
- Article
- Editorial: The culprit behind some diseases: overexpression/hyperactivity of G6PD.Frontiers in pharmacology · 2024Article
- Screening and the analysis of genotypic and phenotypic characterization of glucose-6-phosphate dehydrogenase (G6PD) deficiency in Fujian province, China.Frontiers in genetics · 2024Article
- Relationship between Glucose-6-Phosphate Dehydrogenase Deficiency, X-Chromosome Inactivation and Inflammatory Markers.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a hereditary condition caused by mutations on chromosome X and is transmitted by a sex-linked inheritance. However, impairment of G6PD activity may result from biochemical mechanisms that are able to inhibit the enzyme in specific clinical conditions in the absence of a structural gene-level defect. In this narrative review, a number of clinical settings associated with an "acquired" G6PD deficiency, phenotypically undistinguishable from the primary deficiency, as well as the mechanisms involved, were examined. Hyperaldosteronism and diabetes are the most common culprits of acquired G6PD deficiency. Additional endocrine and metabolic conditions may cause G6PD deficiency in both hospitalized and outpatients. Contrary to the inherited defect, acquired G6PD deficiency is a condition that is potentially curable by removing the factor responsible for enzyme inhibition. Awareness regarding acquired G6PD deficiency by physicians might result in improved recognition and treatment.
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What OpenQuestion holds
Registered trials
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.