BACKGROUND Acute Plasmodium vivax malaria is associated with haemolysis, bone marrow suppression, reticulocytopenia, and post-treatment reticulocytosis leading to haemoglobin recovery. Little is known how malaria affects glucose-6-phosphate dehydrogenase (G6PD) activity and whether changes in activity when patients present may lead qualitative tests, like the fluorescent spot test (FST), to misdiagnose G6PD deficient (G6PDd) patients as G6PD normal (G6PDn). Giving primaquine or tafenoquine to such patients could result in severe haemolysis. METHODS We investigated the G6PD genotype, G6PD enzyme activity over time and the baseline FST phenotype in Cambodians with acute P. vivax malaria treated with 3-day dihydroartemisinin piperaquine and weekly primaquine, 0·75 mg/kg x8 doses. RESULTS Of 75 recruited patients (males 63), aged 5-63 years (median 24), 15 were G6PDd males (14 Viangchan, 1 Canton), 3 were G6PD Viangchan heterozygous females, and 57 were G6PDn; 6 patients had α/β-thalassaemia and 26 had HbE. Median (range) Day0 G6PD activities were 0·85 U/g Hb (0·10-1·36) and 11·4 U/g Hb (6·67-16·78) in G6PDd and G6PDn patients, respectively, rising significantly to 1·45 (0·36-5·54, p<0.01) and 12·0 (8·1-17·4, p = 0.04) U/g Hb on Day7, then falling to ~Day0 values by Day56. Day0 G6PD activity did not correlate (p = 0.28) with the Day0 reticulocyte counts but both correlated over time. The FST diagnosed correctly 17/18 G6PDd patients, misclassifying one heterozygous female as G6PDn. CONCLUSIONS In Cambodia, acute P. vivax malaria did not elevate G6PD activities in our small sample of G6PDd patients to levels that would result in a false normal qualitative test. Low G6PDd enzyme activity at disease presentation increases upon parasite clearance, parallel to reticulocytosis. More work is needed in G6PDd heterozygous females to ascertain the effect of P. vivax on their G6PD activities. TRIAL REGISTRATION The trial was registered (ACTRN12613000003774) with the Australia New Zealand Clinical trials (https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363399&isReview=true).

中文翻译：

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每周接受伯氨喹治疗间日疟原虫疟疾患者的 G6PD 活性动态。

背景技术急性间日疟原虫疟疾与溶血、骨髓抑制、网状红细胞减少症和导致血红蛋白恢复的治疗后网状红细胞增多症有关。很少有人知道疟疾如何影响葡萄糖-6-磷酸脱氢酶 (G6PD) 活性，以及​​患者在场时活性的变化是否可能导致定性测试，如荧光点测试 (FST)，将 G6PD 缺乏 (G6PDd) 患者误诊为 G6PD 正常。 G6PDn)。给此类患者服用伯氨喹或他非诺喹可能会导致严重的溶血。方法 我们研究了用 3 天双氢青蒿素哌喹和每周伯氨喹（0·75 mg/kg x8 剂量）治疗的柬埔寨急性间日疟原虫的 G6PD 基因型、G6PD 酶活性和基线 FST 表型。结果 在招募的 75 名患者中（男性 63 名），年龄5-63岁（中位数24岁），G6PDd男性15人（14 Viangchan，1 Canton），G6PD Viangchan杂合子女性3人，G6PDn 57人；6 名患者患有 α/β-地中海贫血，26 名患者患有 HbE。G6PDd 和 G6PDn 患者的第 0 天 G6PD 活动中位数（范围）分别为 0·85 U/g Hb (0·10-1·36) 和 11·4 U/g Hb (6·67-16·78)，上升第 7 天显着至 1·45 (0·36-5·54, p<0.01) 和 12·0 (8·1-17·4, p = 0.04) U/g Hb，然后在第 56 天降至 ~ 第 0 天值. 第 0 天 G6PD 活性与第 0 天网织红细胞计数不相关（p = 0.28），但两者都随着时间的推移而相关。FST 正确诊断了 17/18 名 G6PDd 患者，将一名杂合女性错误分类为 G6PDn。结论 在柬埔寨，急性间日疟原虫并未将我们的 G6PDd 患者小样本中的 G6PD 活性提升到会导致错误的正常定性测试的水平。寄生虫清除后，疾病出现时的低 G6PDd 酶活性增加，与网状红细胞增多症平行。G6PDd 杂合雌性需要更多的工作来确定 P. vivax 对其 G6PD 活性的影响。试验注册 该试验已在澳大利亚新西兰临床试验 (https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363399&isReview=true) 中注册 (ACTRN12613000003774)。