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Assessment of glucose-6-phosphate dehydrogenase activity using CareStart G6PD rapid diagnostic test and associated genetic variants in Plasmodium vivax malaria endemic setting in Mauritania

机译:使用Carestart G6PD快速诊断测试和毛里塔尼亚疟原虫疟疾疟疾特性疗法中的快速诊断测试和相关遗传变异评估葡萄糖-6-磷酸脱氢酶活性

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摘要

BackgroundPrimaquine is recommended by the World Health Organization (WHO) for radical treatment of Plasmodium vivax malaria. This drug is known to provoke acute hemolytic anemia in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency. Due to lack of data on G6PD deficiency, the use of primaquine has been limited in Africa. In the present study, G6PD deficiency was investigated in blood donors of various ethnic groups living in Nouakchott, a P. vivax endemic area in Mauritania.Methodology/principal findingsVenous blood samples from 443 healthy blood donors recruited at the National Transfusion Center in Nouakchott were screened for G6PD activity using the CareStart G6PD deficiency rapid diagnostic test. G6PD allelic variants were investigated using DiaPlexC G6PD genotyping kit that detects African (A-) and Mediterranean (B-) variants. Overall, 50 of 443 (11.3%) individuals (49 [11.8%] men and 1 [3.7%] woman) were phenotypically deficient. Amongst men, Black Africans had the highest prevalence of G6PD deficiency (15 of 100 [15%]) and White Moors the lowest (10 of 168, [5.9%]). The most commonly observed G6PD allelic variants among 44 tested G6PD-deficient men were the African variant A- (202A/376G) in 14 (31.8%), the Mediterranean variant B- (563T) in 13 (29.5%), and the Betica-Selma A- (376G/968C) allelic variant in 6 (13.6%). The Santamaria A- variant (376G/542T) and A variant (376G) were observed in only one and two individuals, respectively. None of the expected variants was observed in 8 (18.2%) of the tested phenotypically G6PD-deficient men.ConclusionThis is the first published data on G6PD deficiency in Mauritanians. The prevalence of phenotypic G6PD deficiency was relatively high (11.3%). It was mostly associated with either African or Mediterranean variants, in agreement with diverse Arab and Black African origins of the Mauritanian population.
机译:世界卫生组织(世卫组织)建议先天化以获得疟原虫疟疾的激进治疗。已知该药物在具有葡萄糖-6-磷酸脱氢酶(G6PD)缺乏的个体中引发急性溶血性贫血。由于G6PD缺乏数据缺乏数据,在非洲的使用情况有限。在目前的研究中,在毛里塔尼亚的P.Vivax流行区域的各种民族献血者的献血者中调查了G6PD缺乏。筛选了来自Nouakchott国家输血中心的443名健康献血者的方法/主要成因血液样本对于使用Carestart G6PD缺陷的G6PD活动快速诊断测试。使用DiaproplC G6PD基因分型试剂盒研究了G6PD等位基因变体,检测非洲(A-)和地中海(B型)变体。总体而言,50个中的50个(11.3%)个体(49 [11.8%]男性和1 [3.7%]是表型缺乏。在男性中,黑人非洲人的G6PD缺陷患病率最高(15%[15%])和白色摩尔最低(168个,[5.9%])。在14名(31.8%),13例(29.5%)和Betica中,44个测试的G6PD缺陷男性中最常见的G6PD缺乏男性中的G6PD缺乏男性中的最常见的G6PD缺陷型男性是非洲变异A-(202A / 376g),即21.8%)和Betica -Selma A-(376G / 968C)等位基因变异,6(13.6%)。仅在一个和两个个体中观察到Santamaria A-变体(376g / 542t)和变体(376g)。在8(18.2%)的测试表型G6PD缺陷男性中没有观察到预期变体没有任何预期变体。结论是第一个出版的毛里塔诺人G6PD缺乏的公开数据。表型G6PD缺乏的患病率相对较高(11.3%)。它主要与非洲或地中海变异有关,同意毛里塔尼亚人口的不同阿拉伯和黑色非洲起源。

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