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American Journal of Clinical Nutrition, Vol. 82, No. 2, 406-412, August 2005
© 2005 American Society for Clinical Nutrition


ORIGINAL RESEARCH COMMUNICATIONS

Short-term effects of vitamin A and antimalarial treatment on erythropoiesis in severely anemic Zanzibari preschool children1,2,3

Sarah E Cusick, James M Tielsch, Mahdi Ramsan, Jape K Jape, Sunil Sazawal, Robert E Black and Rebecca J Stoltzfus

1 From the Center for Human Nutrition, Department of International Health, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (SEC, JMT, SS, REB, and RJS); the Public Health Laboratory Ivo de Carneri, Wawi, Chake Chake, Pemba Island, Zanzibar, United Republic of Tanzania (MR and JKJ); and the Division of Nutritional Sciences, Cornell University, Ithaca, NY (RJS)

Background: 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.

Objective: We investigated the 72-h effects of vitamin A and the antimalarial drug sulfadoxine pyramethamine (SP) on erythropoietin production in severely anemic (hemoglobin ≤ 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.

Design: 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.

Results: After 72 h, SP reduced the malaria parasite density (by 5029 parasites/µL; 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 µg/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).

Conclusions: 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.

Key Words: Anemia • vitamin A • malaria • erythropoiesis • erythropoietin • children • inflammation




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M. B Zimmermann, R. Biebinger, F. Rohner, A. Dib, C. Zeder, R. F Hurrell, and N. Chaouki
Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron.
Am. J. Clinical Nutrition, September 1, 2006; 84(3): 580 - 586.
[Abstract] [Full Text] [PDF]




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