喀麦隆西部高地地区艾滋病毒血清阳性患者发热发作的疟疾归因比例

T. Tchuinkam, François Fopa, Anna Maria Doro-Altan, Innocent Djikolbe-Gondje, M. Mendaza, L. Djamouko-Djonkam, F. Taafo, R. Bamou, Armand Defo-Talom, Yacouba Poumachu, E. Buonomo, M. Mpoame
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引用次数: 0

摘要

背景:发烧是疟疾和艾滋病毒/艾滋病最常见的症状,但它是非特异性的;因此,它不能有效地用于高流行区疟疾的临床诊断。在疟疾低流行地区,这种说法并不明显,因为人们缺乏自然获得的免疫力。本研究旨在确定低流行高原地区hiv阳性患者发热发作(MAFE)的疟疾归因比例。方法:在为期两年的前瞻性横断面研究中,收集HIV/AIDS门诊患者的血液样本,检查疟疾寄生虫的存在和密度。除了疟疾相关症状外,还记录了一些其他患者的数据:性别、年龄、体重指数(BMI)、t淋巴细胞CD4计数、病毒载量、血象和转氨酶测量。结果:共有729例hiv血清阳性患者入组研究。平均疟原虫感染率和寄生虫率分别为0.823%和1.050只/µl;与血清阴性对照组相比,两者都明显降低,这与我们的假设相反。转氨酶的平均值与未感染疟原虫的患者比较无显著差异。119例发热个体(16.32%)计算出的mae几乎为零(0.15%)。他们的平均CD4细胞计数、红细胞计数和血红蛋白率分别为226个细胞/µl、3.83 × 106个红细胞/µl和10.4 g/dl;均明显低于无发热组。然而,两组的疟疾寄生虫感染率和平均密度相似。同样,两组之间的性别比例、平均年龄、身体质量指数、总白细胞计数和病毒载量也没有差异。结论:在低流行的高原地区,尽管免疫缺陷导致HIV感染,但不会增加疟原虫感染的风险。即使在罕见的合并感染病例中,疟疾也很少引起发烧。这些发烧确实与较高的贫血和免疫缺陷有关,而且可能是由机会性传染病引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Malaria-attributable fraction of fever episodes among HIV-seropositive patients in the Western highland area of Cameroon
Background: Fever is the most frequent symptom for Malaria and HIV/AIDS, but it is non-specific; therefore it can’t be used efficiently in clinical diagnosis of malaria in hyperendemic zones. In hypoendemic areas of malaria, this assertion is not obvious, since people lack naturally acquired immunity. The present study aims at determining the Malaria-attributable fraction of fever episodes (MAFE) among HIV-positive patients in a hypoendemic highland area. Methods: During two-years prospective cross-sectional study, blood samples were collected from outpatients of an HIV/AIDS clinic and examined for the presence and density of malaria parasites. In addition to malaria related symptoms, some other patients’ data were recorded: sexe, age, body mass index (BMI), T-lymphocyte CD4 counts, viral loads, haemograms and transaminases measurements. Results: A total of 729 HIV-seropositive patients were enrolled into the study. Their mean Plasmodial infection rate and parasitaemia were: 0.823% and 1.050 parasites/µl of blood respectively; and were both significantly lower, compared to the control seronegative group, in contrast to our hypothesis. No significant difference was observed when the mean values of transaminases were compared between those with and without plasmodial infection. For the 119 (16.32%) febrile individuals found, the calculated MAFE was almost null (0.15%). Their mean CD4 count, red blood cells (RBC) count and haemoglobin rate were: 226 cell/µl, 3.83x10 6 RBC/µl and 10.4 g/dl respectively; and were all significantly lower than in the non-febrile group. However, malaria parasite infection rates and mean densities were similar in both groups. Likewise, there was no difference between: sex ratios, mean ages, BMI, total white blood cells counts and viral loads between the two groups. Conclusion: HIV infection in spite of the immunodeficiency induced does not enhance the risk of Plasmodium infection in hypoendemic highland settings. Even in the scarce cases of co-infection occurring here, malaria is rarely responsible for fever episodes. These fevers are indeed associated with higher anaemia and immunodeficiency, and likely due instead to opportunistic infectious diseases.
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