无症状恶性疟原虫药物治疗后的配子母细胞血症。

Samuel Dunyo, Paul Milligan, Tansy Edwards, Colin Sutherland, Geoffrey Targett, Margaret Pinder
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引用次数: 0

摘要

目的:用磺胺乙胺嘧啶(SP)治疗恶性疟原虫疟疾后,配子细胞的流行率和密度会急剧上升。我们进行了一项随机试验,以确定用SP或SP加一剂青蒿琥酯(SP+AS)治疗无症状感染对配子体携带的影响:该研究是一项三臂开放标签随机试验。我们将无症状的恶性疟原虫携带者随机分配为接受抗疟治疗或安慰剂,并在接下来的2个月中记录配子细胞的流行率和密度:试验于旱季(疟疾传播低发季节)在冈比亚的四个农村进行:参与者:无性恶性疟原虫感染的成人和6个月以上的儿童,在2天的筛查期间确认无疟疾临床症状:干预措施:参与者随机接受单剂量 SP 或 SP+AS 或安慰剂:干预措施:参与者随机接受单剂SP或SP+AS或安慰剂。结果测量:结果测量为治疗后7天和56天内配子细胞的存在,以及2个月内配子细胞血症的持续时间和密度:共有 372 名无症状带原者接受了随机治疗。安慰剂组第7天的配子细胞率为10.5%,SP组为11.2%(与安慰剂的风险差异为0.7%,95%置信区间为-7.4%至8.7%,p=0.87),SP+AS组为7.1%(与安慰剂的风险差异为4.1%,95%置信区间为-3.3%至12%,p=0.28)。到第 56 天,安慰剂组的配子体流行率为 13%,而两组药物治疗组的配子体流行率均为 2%。与安慰剂相比,SP 组的配子细胞携带率(配子细胞密度随时间变化的曲线下面积)降低了 71%,SP+AS 组降低了 74%。配子母细胞携带量随年龄而变化,15岁以下儿童的携带量高于成人:结论:用 SP 治疗无症状的恶性疟原虫携带者不会增加配子体携带量或密度。在旱季对无性寄生虫血症进行有效治疗可在4周后将配子细胞携带量降至很低水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Gametocytaemia after drug treatment of asymptomatic Plasmodium falciparum.

Gametocytaemia after drug treatment of asymptomatic Plasmodium falciparum.

Gametocytaemia after drug treatment of asymptomatic Plasmodium falciparum.

Gametocytaemia after drug treatment of asymptomatic Plasmodium falciparum.

Objectives: Treatment of Plasmodium falciparum malaria with sulfadoxine-pyrimethamine (SP) is followed by a sharp rise in the prevalence and density of gametocytes. We did a randomized trial to determine the effect of treatment of asymptomatic infections with SP or SP plus one dose of artesunate (SP+AS) on gametocyte carriage.

Design: The study was a three-arm open-label randomized trial. We randomized asymptomatic carriers of P. falciparum to receive antimalarial treatment or placebo, and recorded the prevalence and density of gametocytes over the next 2 mo.

Setting: The trial was conducted during the dry (low malaria transmission) season in four rural villages in Gambia.

Participants: Participants were adults and children aged over 6 mo with asexual P. falciparum infection and confirmed free of clinical symptoms of malaria over a 2-d screening period.

Interventions: Participants were randomized to receive a single dose of SP or SP+AS or placebo.

Outcome measures: The outcome measures were the presence of gametocytes 7 and 56 d after treatment, and the duration and density of gametocytaemia over 2 mo.

Results: In total, 372 asymptomatic carriers were randomized. Gametocyte prevalence on day 7 was 10.5% in the placebo group, 11.2% in the SP group (risk difference to placebo 0.7%, 95% confidence interval -7.4% to 8.7%, p = 0.87), and 7.1% in the SP+AS group (risk difference to placebo 4.1%, 95% confidence interval -3.3% to 12%, p = 0.28). By day 56, gametocyte prevalence was 13% in the placebo group and 2% in both drug-treated groups. Gametocyte carriage (the area under the curve of gametocyte density versus time), was reduced by 71% in the SP group, and by 74% in the SP+AS group, compared to placebo. Gametocyte carriage varied with age and was greater among children under 15 than among adults.

Conclusions: Treatment of asymptomatic carriers of P. falciparum with SP does not increase gametocyte carriage or density. Effective treatment of asexual parasitaemia in the dry season reduces gametocyte carriage to very low levels after 4 wk.

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