Department of Pathogen Biology and Immunology, Kunming Medical University, Kunming, Yunnan, 650500, People's Republic of China.
Shanglin County People's Hospital, Shanglin, Guangxi, 530500, People's Republic of China.
BMC Infect Dis. 2019 Aug 9;19(1):704. doi: 10.1186/s12879-019-4357-9.
Plasmodium vivax transmission in West Africa, dominant for the Duffy-negative blood group, has been increasingly recognized from both local residents as well as international travelers who contracted P. vivax malaria there. However, the relapsing pattern and sensitivity to antimalarial treatment of P. vivax strains originated from this region are largely unknown. There is evidence that the efficacy of primaquine for radical cure of relapsing malaria depends on host factors such as the hepatic enzyme cytochrome P450 (CYP) 2D6.
A 49-year-old Chinese man was admitted to the Shanglin County Hospital in Guangxi Province, China, on December 19, 2016, 39 days after he returned from Ghana, where he stayed for one and a half years. He was diagnosed by microscopy as having uncomplicated P. vivax malaria. Treatment included 3 days of intravenous artesunate (420 mg total), and 3 days of chloroquine (1550 mg total), and 8 days of primaquine (180 mg total). Although parasites and symptoms were cleared rapidly and he was malaria-negative for almost two months, he suffered four relapses with relapse intervals ranging from 58 to 232 days. The last relapse occurred at 491 days from his first vivax attack. For the first three relapses, he was treated similarly with chloroquine and primaquine, sometimes supplemented with additional artemisinin combination therapies (ACTs). For the last relapse, he was treated with intravenous artesunate, 3 days of an ACT, and 7 days of azithromycin, and had remained healthy for 330 days. Molecular studies confirmed P. vivax infections for all the episodes. Although this patient was diagnosed to have normal glucose-6-phosphate dehydrogenase (G6PD) activity, his CYP2D6 genotype corresponded to a *2A/*36 allele variant suggesting of an impaired primaquine metabolizer phenotype.
This clinical case suggests that P. vivax malaria originating from West Africa may produce multiple relapses extending beyond one year. The failures of primaquine as an anti-relapse therapy may be attributed to the patient's impaired metabolizer phenotype of the CYP2D6. This highlights the importance of knowing the host G6PD and CYP2D6 activities for effective radical cure of relapsing malaria by primaquine.
西非人因缺乏 Duffy 阴性血型而易于感染间日疟原虫，因此西非人及前往西非地区的国际旅行者中都有间日疟原虫感染病例报告。然而，人们对源于该地区的间日疟原虫的复发模式和对抗疟药物的敏感性知之甚少。有证据表明，伯氨喹根治复发疟疾的疗效取决于宿主因素，如细胞色素 P450（CYP）2D6 酶。
一名 49 岁的中国男性于 2016 年 12 月 19 日因从加纳返回后 39 天（在加纳停留了一年半）出现发热入住广西上林县医院。他经镜检诊断为无并发症的间日疟原虫感染。治疗方案包括 3 天静脉注射青蒿琥酯（总剂量 420mg）、3 天氯喹（总剂量 1550mg）和 8 天伯氨喹（总剂量 180mg）。尽管寄生虫和症状迅速清除，且在将近两个月内疟疾检测均为阴性，但他出现了 4 次复发，复发间隔时间为 58 至 232 天。最后一次复发发生在初次间日疟发作后 491 天。前 3 次复发时，他接受了类似的氯喹和伯氨喹治疗，有时还辅以其他青蒿素类复方药物（ACT）。最后一次复发时，他接受了静脉注射青蒿琥酯、3 天的 ACT 和 7 天的阿奇霉素治疗，此后他一直健康状况良好，随访 330 天。分子研究证实了所有发作均为间日疟原虫感染。尽管该患者被诊断为葡萄糖-6-磷酸脱氢酶（G6PD）活性正常，但他的 CYP2D6 基因型对应于*2A/*36 等位基因变异，提示为伯氨喹代谢不良表型。
本临床病例表明，源于西非的间日疟原虫感染可能会导致多次复发，复发时间超过一年。伯氨喹作为抗复发治疗的失败可能归因于患者 CYP2D6 代谢不良表型。这凸显了了解宿主 G6PD 和 CYP2D6 活性对伯氨喹根治复发疟疾的重要性。
