5 - Glucose-6-phosphate dehydrogenase deficiency
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Cited by (35)
Structure activity relationship in β-carboline derived anti-malarial agents
2021, European Journal of Medicinal ChemistryCitation Excerpt :These cells can resuscitate unpredictably and crop up the symptoms de novo, thus posing a grave challenge to the efforts of rendering viable malaria-alleviating drugs. A drug known as primaquine provides a radical cure [6], but it necessitates repeated dosing and is harmful to individuals with glucose-6-phosphate dehydrogenase [7] deficiency which is a widespread infirmity in regions endemic to malaria. Similarly, Tafenoquine, a recently approved drug, engender a single-dose radical treatment of P. vivax malaria [3], however, this drug was also not effective in patients with glucose-6-phosphate dehydrogenase deficiency and caused hemolysis in these patients [8].
A trade off between catalytic activity and protein stability determines the clinical manifestations of glucose-6-phosphate dehydrogenase (G6PD) deficiency
2017, International Journal of Biological MacromoleculesCitation Excerpt :G6PD deficiency is a hereditary genetic defect that is the most prevalent polymorphism and enzymopathy in humans, affecting more than 400 million people worldwide [3]. A wide spectrum of clinical manifestations of G6PD deficiency is observed, which includes favism, hemolytic anemia, chronic non-spherocytic hemolytic anemia (CNSHA), spontaneous abortion, and neonatal hyperbilirubinemia resulting in neonatal kernicterus, which can be fatal [4–6]. G6PD variants have been classified into five different classes according to their residual enzyme activity, ranging from Class I G6PD variants, which show less than 5% residual activity and the most severe clinical phenotypes, to Class V G6PD variants, which show increased enzyme activity but no clinical manifestations [7].
Detailed functional analysis of two clinical glucose-6-phosphate dehydrogenase (G6PD) variants, G6PD<inf>Viangchan</inf> and G6PD<inf>Viangchan + Mahidol</inf>: Decreased stability and catalytic efficiency contribute to the clinical phenotype
2016, Molecular Genetics and MetabolismCitation Excerpt :G6PD deficiency is common and responsible for a variety of clinical conditions, affecting around 400 million people worldwide [5]. Clinical manifestations of G6PD deficiency include favism, hemolytic anemia, chronic non-spherocytic hemolytic anemia (CNSHA), spontaneous abortions and neonatal hyperbilirubinemia resulting in neonatal kernicterus that can lead to death [6–8]. WHO working groups have classified G6PD variants based on enzyme activity into five classes with thresholds of 10–60% as a defined level of G6PD activity [4].
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
2013, Brenner's Encyclopedia of Genetics: Second Edition