Review of key knowledge gaps in glucose-6-phosphate dehydrogenase deficiency detection with regard to the safe clinical deployment of 8-aminoquinoline treatment regimens: a workshop report.

Review of key knowledge gaps in glucose-6-phosphate dehydrogenase deficiency detection with regard to the safe clinical deployment of 8-aminoquinoline treatment regimens: a workshop report.
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DOI:
10.1186/1475-2875-12-112
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发表时间:
2013-03-27
期刊:
影响因子:
3
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Price R
Price R
中科院分区:
医学3区
文献类型:
--
作者:
von Seidlein L;Auburn S;Espino F;Shanks D;Cheng Q;McCarthy J;Baird K;Moyes C;Howes R;Ménard D;Bancone G;Winasti-Satyahraha A;Vestergaard LS;Green J;Domingo G;Yeung S;Price R

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葡萄糖-6-磷酸脱氢酶(G6 PD)缺乏症的诊断和管理是当前疟疾控制和消除阶段的一个关键方面,这将需要更广泛地使用8-氨基喹啉,以减少恶性疟原虫传播并实现间日疟原虫的根治。8-氨基喹啉类药物,如伯氨喹,可在G6 PD缺陷个体中诱导严重的溶血,可能造成严重的发病率,并破坏对8-氨基喹啉处方的信心。另一方面,在安全性方面犯错误,并将大量未经证实的G6 PD缺乏症患者排除在8-氨基喹啉治疗之外,将削弱这些药物的影响。估计剩余的G6 PD酶活性是对表型最直接、最容易获得和最可靠的评估,并且仍然是诊断可能因伯氨喹给药而受到伤害的患者的金标准。基因分型似乎是一种明确的技术,但它的使用受到成本和公认的G6 PD基因型的大范围的限制。许多酶活性测定诊断G6 PD缺乏症,但它们需要冷链,专业设备和实验室技能。这些测定对于大多数疟疾患者生活的护理提供是不切实际的。G6 PD缺乏症的诊断需要改进,以更广泛和更安全地使用8-氨基喹啉杀死催眠虫,而较低剂量的伯氨喹可以安全地用于杀死配子体而无需测试。本文报告了2012年5月在韩国仁川举行的研讨会的讨论和结论,以审查G6 PD缺乏症的关键知识差距。
The diagnosis and management of glucose-6-phosphate dehydrogenase (G6PD) deficiency is a crucial aspect in the current phases of malaria control and elimination, which will require the wider use of 8-aminoquinolines for both reducing Plasmodium falciparum transmission and achieving the radical cure of Plasmodium vivax. 8-aminoquinolines, such as primaquine, can induce severe haemolysis in G6PD-deficient individuals, potentially creating significant morbidity and undermining confidence in 8-aminoquinoline prescription. On the other hand, erring on the side of safety and excluding large numbers of people with unconfirmed G6PD deficiency from treatment with 8-aminoquinolines will diminish the impact of these drugs. Estimating the remaining G6PD enzyme activity is the most direct, accessible, and reliable assessment of the phenotype and remains the gold standard for the diagnosis of patients who could be harmed by the administration of primaquine. Genotyping seems an unambiguous technique, but its use is limited by cost and the large range of recognized G6PD genotypes. A number of enzyme activity assays diagnose G6PD deficiency, but they require a cold chain, specialized equipment, and laboratory skills. These assays are impractical for care delivery where most patients with malaria live. Improvements to the diagnosis of G6PD deficiency are required for the broader and safer use of 8-aminoquinolines to kill hypnozoites, while lower doses of primaquine may be safely used to kill gametocytes without testing. The discussions and conclusions of a workshop conducted in Incheon, Korea in May 2012 to review key knowledge gaps in G6PD deficiency are reported here.
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