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Updated: Aug 19, 2025

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Measuring Glucose Uptake in Drosophila Models of TDP-43 Proteinopathy
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Acquired Glucose-6-Phosphate Dehydrogenase Deficiency
Giovanni Mario Pes1,2, Maria Pina Dore1,3
1Dipartimento di Medicina, Chirurgia e Farmacia, University of Sassari, Clinica Medica, Viale San Pietro 8, 07100 Sassari, Italy.
Journal of Clinical Medicine
|November 26, 2022
Summary
Acquired Glucose-6-phosphate dehydrogenase (G6PD) deficiency can mimic the inherited form due to enzyme inhibition, not gene defects. Identifying and removing the cause can potentially cure this condition.
Area of Science:
- Biochemistry
- Genetics
- Endocrinology
Background:
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is typically an inherited X-linked condition.
- Enzyme activity impairment can occur through biochemical inhibition, independent of genetic defects.
- Acquired G6PD deficiency presents phenotypically similar to the inherited form.
Purpose of the Study:
- To review clinical settings associated with acquired G6PD deficiency.
- To examine the biochemical mechanisms underlying acquired G6PD deficiency.
- To highlight the potential curability and clinical implications of acquired G6PD deficiency.
Main Methods:
- Narrative review of existing literature.
- Examination of clinical conditions causing acquired G6PD deficiency.
- Analysis of biochemical mechanisms of enzyme inhibition.
Main Results:
- Hyperaldosteronism and diabetes are common causes of acquired G6PD deficiency.
- Other endocrine and metabolic conditions can also lead to acquired G6PD deficiency.
- Acquired deficiency is potentially reversible upon removal of the causative factor.
Conclusions:
- Acquired G6PD deficiency is a distinct clinical entity from the inherited form.
- Physician awareness can improve recognition and management of acquired G6PD deficiency.
- Treatment focuses on addressing the underlying cause of enzyme inhibition.
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