Laboratory for Human Nutrition, Swiss Federal Institute of Technology Zürich, Zurich, Switzerland.
Am J Clin Nutr. 2010 Dec;92(6):1385-92. doi: 10.3945/ajcn.2010.30051. Epub 2010 Oct 6.
Iron deficiency anemia (IDA) affects many young women in sub-Saharan Africa. Its etiology is multifactorial, but the major cause is low dietary iron bioavailability exacerbated by parasitic infections such as malaria.
We investigated whether asymptomatic Plasmodium falciparum parasitemia in Beninese women would impair absorption of dietary iron or utilization of circulating iron.
Iron absorption and utilization from an iron-fortified sorghum-based meal were estimated by using oral and intravenous isotope labels in 23 afebrile women with a positive malaria smear (asexual P. falciparum parasitemia; > 500 parasites/μL blood). The women were studied while infected, treated, and then restudied 10 d after treatment. Iron status, hepcidin, and inflammation indexes were measured before and after treatment.
Treatment reduced low-grade inflammation, as reflected by decreases in serum ferritin, C-reactive protein, interleukin-6, interleukin-8, and interleukin-10 (P < 0.05); this was accompanied by a reduction in median serum hepcidin of ≈ 50%, from 2.7 to 1.4 nmol/L (P < 0.005). Treatment decreased serum erythropoietin and growth differentiation factor 15 (P < 0.05). Clearance of parasitemia increased geometric mean dietary iron absorption (from 10.2% to 17.6%; P = 0.008) but did not affect systemic iron utilization (85.0% compared with 83.1%; NS).
Dietary iron absorption is reduced by ≈ 40% in asymptomatic P. falciparum parasitemia, likely because of low-grade inflammation and its modulation of circulating hepcidin. Because asymptomatic parasitemia has a protracted course and is very common in malarial areas, this effect may contribute to IDA and blunt the efficacy of iron supplementation and fortification programs. This trial was registered at clinicaltrials.gov as NCT01108939.
缺铁性贫血（IDA）影响撒哈拉以南非洲的许多年轻女性。其病因是多因素的，但主要原因是低膳食铁生物利用度，加剧了寄生虫感染，如疟疾。
我们研究了贝宁无症状恶性疟原虫感染是否会损害膳食铁的吸收或循环铁的利用。
在 23 名无发热、疟原虫涂片阳性（无性疟原虫寄生虫血症；>500 个寄生虫/μL 血液）的妇女中，使用口服和静脉同位素标记物估计强化高粱基膳食中铁的吸收和利用。这些妇女在感染、治疗后进行研究，并在治疗后 10 天再次进行研究。在治疗前后测量铁状态、hepcidin 和炎症指标。
治疗降低了低度炎症，反映在血清铁蛋白、C 反应蛋白、白细胞介素-6、白细胞介素-8 和白细胞介素-10 的降低（P < 0.05）；同时，血清 hepcidin 中位数降低了约 50%，从 2.7 降至 1.4 nmol/L（P < 0.005）。治疗降低了血清促红细胞生成素和生长分化因子 15（P < 0.05）。寄生虫清除增加了几何平均膳食铁吸收（从 10.2%增至 17.6%；P = 0.008），但不影响全身铁利用（85.0%比 83.1%；NS）。
无症状恶性疟原虫寄生虫血症使膳食铁吸收减少约 40%，可能是由于低度炎症及其对循环 hepcidin 的调节。由于无症状寄生虫血症持续时间长且在疟疾地区非常常见，这种影响可能导致 IDA 并削弱铁补充和强化计划的疗效。本试验在 clinicaltrials.gov 上注册为 NCT01108939。
