Objective. Evidence from previous studies that malnourished children are protected against malaria is controversial. In individuals repeatedly exposed to malaria, immunity may develop first against severe disease, then against pyrogens, and last, against parasites. If this is true, this would suggest that reduced immune function that may exist in stunted children exacerbates the severity of malarial signs and symptoms, rather than the occurrence of parasitemia. On the other hand, several studies have suggested that malnourished children are protected to some degree against malaria. Our aim was to evaluate whether observational data support the hypothesis that nutritional inadequacies that cause stunting modify the associations between malaria and hematologic indicators such as hemoglobin concentration and serum concentrations of C-reactive protein and soluble transferrin receptor (sTfR). We showed earlier that increased serum concentrations of these receptors in asymptomatic malaria may be explained, at least in part, by increased erythropoiesis to compensate for malaria-induced hemolysis.Methodology. Community-based cluster survey among Kenyan children aged 2 to 36 months asymptomatic for malaria or anemia ( n = 318).Results. When adjusted for age and wasting, the malaria-associated decrease in mean hemoglobin concentration was 8.5 g/L and 15.8 g/L in nonstunted and stunted children, respectively. The malaria-associated increase in geometric mean serum concentrations of sTfR was 1.1-fold and 1.8-fold in nonstunted and stunted children, respectively. The malaria-associated increase in geometric mean serum concentrations of C-reactive protein was 1.4-fold and 2.3-fold in nonstunted and stunted children, respectively. Thus, children with malaria and those who were stunted suffered from more severe anemia and had higher serum concentrations of C-reactive protein and sTfR than would be expected from the combined effect of the 2 working independently.Conclusions. Our results are consistent with the notion that the nutritional inadequacies causing stunting also impair host immunity, thus increasing the degree to which malaria is associated with decreased concentrations of hemoglobin, with increased inflammation, and with increased iron demand in developing erythroblasts. Increased intake of micronutrients may not only reduce stunting and nutritional anemia, but also reduce malaria-associated anemia.
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机译：目的。先前的研究表明营养不良的儿童可以预防疟疾，这是有争议的。在反复暴露于疟疾的个体中，免疫力可能首先针对严重疾病，然后针对热原，最后针对寄生虫。如果这是真的，则表明发育不良儿童中可能存在的免疫功能降低会加剧疟疾症状和体征的严重性，而不是寄生虫血症的发生。另一方面，一些研究表明营养不良的儿童在某种程度上可以预防疟疾。我们的目的是评估观察数据是否支持以下假设，即造成发育迟缓的营养不足会改变疟疾与血液学指标（例如血红蛋白浓度和C反应蛋白和可溶性转铁蛋白受体（sTfR）的血清浓度）之间的关联。较早前我们发现，无症状疟疾中这些受体的血清浓度升高可能至少部分地通过增加红细胞生成来弥补疟疾引起的溶血而得到解释。对2至36个月大的无疟疾或贫血症状的肯尼亚儿童进行的社区聚类调查（n = 318）。调整年龄和消瘦后，未受惊吓和发育不良的儿童与疟疾相关的平均血红蛋白浓度降低分别为8.5 g / L和15.8 g / L。与非疟疾和发育不良儿童相比，与疟疾有关的sTfR几何平均血清浓度分别增加了1.1倍和1.8倍。与疟疾有关的非反应性和发育不良儿童血清C反应蛋白的几何平均浓度分别增加了1.4倍和2.3倍。因此，疟疾患儿和发育迟缓患儿患更严重的贫血，其C反应蛋白和sTfR的血清浓度高于两种独立工作的综合作用所预期的水平。我们的结果与以下观念相吻合：造成发育迟缓的营养不足也会损害宿主免疫力，从而增加疟疾与血红蛋白浓度降低，炎症增加以及发育中的成红细胞中铁需求增加相关的程度。增加微量营养素的摄入不仅可以减少发育迟缓和营养性贫血，还可以减少与疟疾有关的贫血。
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