Cusick Sarah E, Tielsch James M, Ramsan Mahdi, Jape Jape K, Sazawal Sunil, Black Robert E, Stoltzfus Rebecca J
Center for Human Nutrition, Department of International Health, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Am J Clin Nutr. 2005 Aug;82(2):406-12. doi: 10.1093/ajcn.82.2.406.
The pathophysiology of anemia in coastal East Africa is complex. Impaired erythropoietin production is one possible mechanism. Plasmodium falciparum malaria has been found to blunt erythropoietin production, whereas vitamin A stimulates erythropoietin production in vitro.
We investigated the 72-h effects of vitamin A and the antimalarial drug sulfadoxine pyramethamine (SP) on erythropoietin production in severely anemic (hemoglobin < or = 70 g/L) preschool children in Zanzibar, a region of known vitamin A deficiency. We hypothesized that both treatments would stimulate erythropoietin production directly, within 72 h, before a change in hemoglobin would occur.
One hundred forty-one severely anemic children were identified during the baseline assessment of a morbidity substudy of a community-based micronutrient supplementation trial. All severely anemic children were randomly assigned to receive either vitamin A (100,000 or 200,000 IU depending on age) or SP at baseline; 72 h later they received the opposite treatment plus daily hematinic syrup for 90 d. Erythropoietic and parasitic indicators were assessed at baseline and again after 72 h.
After 72 h, SP reduced the malaria parasite density (by 5029 parasites/microL; P < 0.001), CRP concentrations (by 10.6 mg/L; P = 0.001), and the proportion of children infected with malaria (by 32.4%; P < 0.001). Vitamin A reduced CRP (by 9.6 mg/L; P = 0.011), serum ferritin (by 18.1 microg/L; P = 0.042), and erythropoietin (by 194.7 mIU/mL; P = 0.011) concentrations and increased the reticulocyte production index (by 0.40; P = 0.041).
Contrary to our hypothesis, vitamin A significantly decreased erythropoietin concentration. The most important effect of both vitamin A and SP was the rapid reduction of inflammation. Vitamin A also mobilized iron from stores and stimulated the production of new erythrocytes.
东非沿海地区贫血的病理生理学很复杂。促红细胞生成素生成受损是一种可能的机制。已发现恶性疟原虫会抑制促红细胞生成素的生成，而维生素A在体外可刺激促红细胞生成素的生成。
我们研究了维生素A和抗疟药物周效磺胺-乙胺嘧啶（SP）对桑给巴尔严重贫血（血红蛋白≤70g/L）学龄前儿童促红细胞生成素生成的72小时效应。桑给巴尔是一个已知存在维生素A缺乏的地区。我们假设两种治疗方法都能在72小时内直接刺激促红细胞生成素的生成，且在血红蛋白发生变化之前。
在一项基于社区的微量营养素补充试验的发病情况子研究的基线评估期间，确定了141名严重贫血儿童。所有严重贫血儿童在基线时被随机分配接受维生素A（根据年龄给予100,000或200,000国际单位）或SP；72小时后，他们接受相反的治疗并加服每日补血糖浆，持续90天。在基线时和72小时后再次评估促红细胞生成和寄生虫指标。
72小时后，SP降低了疟原虫密度（降低5029个寄生虫/微升；P<0.001）、CRP浓度（降低10.6mg/L；P = 0.001）以及感染疟疾儿童的比例（降低32.4%；P<0.001）。维生素A降低了CRP（降低9.6mg/L；P = 0.011）、血清铁蛋白（降低18.1μg/L；P = 0.042）和促红细胞生成素（降低194.7mIU/mL；P = 0.011）浓度，并提高了网织红细胞生成指数（提高0.40；P = 0.041）。
与我们的假设相反，维生素A显著降低了促红细胞生成素浓度。维生素A和SP的最重要作用是迅速减轻炎症。维生素A还从储存中动员铁并刺激新红细胞的生成。
