Glucose-6-phosphate dehydrogenase deficiency

Cappellini, Maria Domenica; Fiorelli, G.

doi:10.1016/s0140-6736(08)60073-2

Cited by 1,294 publications

(1,369 citation statements)

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“…[45]. The highest prevalence is reported in Africa, southern Europe, the Middle East, Southeast Asia, and the central and southern Pacific islands; however, because of fairly recent migration, deficient alleles are nowadays quite prevalent in North and South America and in parts of northern Europe [19]. In most areas of high prevalence of G6PD deficiency, several polymorphic alleles are found but tropical regions of Africa are one exception, where the variant G6PD A − accounts for about 90% of G6PD deficiency with frequencies of 5-25% [16,17].…”

Section: Discussionmentioning

confidence: 99%

“…However, considering the history of Cabo Verde settlement and the reported high European contribution, [18] we also searched for the G6PD Mediterranean (Med) variant, the most common in countries surrounding the Mediterranean Sea [19]. This variant is associated with 3% of normal enzyme activity and usually ranges in frequency from 2% to 20% in Europe [20].…”

Section: Introductionmentioning

confidence: 99%

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Analysis of malaria associated genetic traits in Cabo Verde, a melting pot of European and sub Saharan settlers

Alves¹,

Machado²,

Silva³

et al. 2010

Blood Cells, Molecules, and Diseases

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Analysis of malaria associated genetic traits in Cabo Verde, a melting pot of European and sub Saharan settlers

Alves¹,

Machado²,

Silva³

et al. 2010

Blood Cells, Molecules, and Diseases

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“…The most prevalent genetically based resistance mechanisms are hemoglobinopathies such as thalassemia, sickle cell trait, and hemoglobin C, erythrocyte polymorphisms such as Duffy antigen and ovalocytosis, immunogenic variants such as in HLA alleles, nitric oxide synthase 1, and tumor necrosis factor a (reviewed in ref. 10), and enzymopathies including glucose-6-phosphate dehydrogenase (G6PD) deficiency (11). Another enzymopathy suggested to protect humans from malaria is the less common pyruvate kinase deficiency (12).…”

Section: Introductionmentioning

confidence: 99%

Glucose‐6‐phosphate metabolism in Plasmodium falciparum

2012

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Malaria is still one of the most threatening diseases worldwide. The high drug resistance rates of malarial parasites make its eradication difficult and furthermore necessitate the development of new antimalarial drugs. Plasmodium falciparum is responsible for severe malaria and therefore of special interest with regard to drug development. Plasmodium parasites are highly dependent on glucose and very sensitive to oxidative stress; two observations that drew interest to the pentose phosphate pathway (PPP) with its key enzyme glucose‐6‐phosphate dehydrogenase (G6PD). A central position of the PPP for malaria parasites is supported by the fact that human G6PD deficiency protects to a certain degree from malaria infections. Plasmodium parasites and the human host possess a complete PPP, both of which seem to be important for the parasites. Interestingly, there are major differences between parasite and human G6PD, making the enzyme of Plasmodium a promising target for antimalarial drug design. This review gives an overview of the current state of research on glucose‐6‐phosphate metabolism in P. falciparum and its impact on malaria infections. Moreover, the unique characteristics of the enzyme G6PD in P. falciparum are discussed, upon which its current status as promising target for drug development is based. © 2012 IUBMB IUBMB Life, 64(7): 603–611, 2012

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“…Dear Editor, Glucose-6-phosphate dehydrogenase (G6PD) deficiency was discovered while investigating the development of haemolysis in patients who had received primaquine, and subsequently, several drugs have been linked to acute haemolysis in G6PD-deficient individuals [1]. Whether a specific drug directly causes haemolytic crisis in G6PD-deficient patients is often difficult to establish.…”

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confidence: 99%

“…Although acute haemolytic episodes in G6PD deficiency usually occur in male patients because of X-linked inheritance [1], haemolysis can also occur especially in elderly female heterozygous patients because of lyonization and oligoclonality of the bone marrow in old age [14].…”

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confidence: 99%