University of Washington, Seattle, WA 98104, USA.
Lancet Infect Dis. 2012 Dec;12(12):925-32. doi: 10.1016/S1473-3099(12)70207-4. Epub 2012 Sep 10.
Co-infection with HIV and helminths is common in sub-Saharan Africa and findings from previous studies have suggested that anthelmintic treatment might delay immunosuppression in people with HIV. We aimed to assess the efficacy of empiric deworming of adults with HIV in delaying HIV disease progression.
In this non-blinded randomised trial, we enrolled adults (aged ≥18 years) with HIV who did not meet criteria for the initiation of antiretroviral treatment from three sites in Kenya. Using a computer-generated sequence, we randomly assigned (1:1) eligible participants to either empiric albendazole every 3 months plus praziquantel annually (treatment group) or to standard care (control group). Participants were followed up for 24 months. We measured CD4 cell counts every 6 months and plasma HIV RNA annually. The primary endpoints were a CD4 count of less than 350 cells per μL and a composite endpoint consisting of the first occurrence of a CD4 count of less than 350 cells per μL, first reported use of antiretroviral treatment, and non-traumatic deaths. We compared these measures by use of Cox proportional hazards regression and Kaplan-Meier survival analyses. Primary analysis was done by intention to treat. The trial was registered with ClinicalTrials.gov, number NCT0050722.
Between Feb 6, 2008, and June 21, 2011, we enrolled and followed-up 948 participants; 469 were allocated to the treatment group and 479 to the control group. All participants were provided with co-trimoxazole prophylaxis. Median baseline CD4 cell counts and HIV RNA concentrations did not differ between groups. We recorded no statistically significant difference between the treatment and control groups in the number of people reaching a CD4 count of fewer than 350 cells per μL (41·6 events per 100 person-years vs 46·2 events per 100 person-years; hazard ratio 0·89, 95% CI 0·75-1·06, p=0·2) or the composite endpoint (44·0 events per 100 person-years vs 49·8 events per 100 person-years; 0·88, 0·74-1·04, p=0·1). Serious adverse events, none of which thought to be treatment-related, occurred at a similar frequency in both groups.
Our findings do not suggest an effect of empiric deworming in the delaying of HIV disease progression in adults with HIV in an area where helminth infection is common. Alternative approaches are needed to delay HIV disease progression in areas where co-infections are common.
在撒哈拉以南非洲地区，艾滋病毒和寄生虫共同感染很常见，先前的研究结果表明驱虫治疗可能会延缓艾滋病毒感染者的免疫抑制。我们旨在评估对艾滋病毒感染者进行经验性驱虫治疗以延缓艾滋病毒疾病进展的效果。
在这项非盲随机试验中，我们招募了来自肯尼亚三个地点的未符合开始抗逆转录病毒治疗标准的成年艾滋病毒感染者（年龄≥18 岁）。使用计算机生成的序列，我们将符合条件的参与者随机分配（1:1）至经验性阿苯达唑每 3 个月一次加吡喹酮每年一次（治疗组）或标准护理（对照组）。参与者随访 24 个月。我们每 6 个月测量一次 CD4 细胞计数，每年测量一次血浆 HIV RNA。主要终点是 CD4 计数小于 350 个细胞/μL 和包括 CD4 计数小于 350 个细胞/μL、首次报告使用抗逆转录病毒治疗和非创伤性死亡的复合终点。我们使用 Cox 比例风险回归和 Kaplan-Meier 生存分析比较了这些措施。主要分析采用意向治疗。该试验在 ClinicalTrials.gov 上注册，编号为 NCT0050722。
在 2008 年 2 月 6 日至 2011 年 6 月 21 日期间，我们招募并随访了 948 名参与者；其中 469 名分配到治疗组，479 名分配到对照组。所有参与者均接受了复方磺胺甲噁唑预防。基线时，两组的 CD4 细胞计数和 HIV RNA 浓度中位数无差异。我们没有记录到治疗组和对照组在达到 CD4 计数小于 350 个细胞/μL 的人数（每 100 人年发生 41.6 例 vs 每 100 人年发生 46.2 例；风险比 0.89，95%CI 0.75-1.06，p=0.2）或复合终点（每 100 人年发生 44.0 例 vs 每 100 人年发生 49.8 例；0.88，0.74-1.04，p=0.1）方面有统计学显著差异。两组发生的严重不良事件频率相似，均无任何被认为与治疗相关的事件。
我们的研究结果表明，在寄生虫感染普遍的地区，经验性驱虫治疗对艾滋病毒感染者的艾滋病毒疾病进展没有延缓作用。在寄生虫共同感染普遍的地区，需要采取替代方法来延缓艾滋病毒疾病的进展。
