Asymptomatic malaria in the etiology of iron deficiency anemia: a nutritionist's viewpoint  

Oleh:

Prentice, Andrew M. ; Cox, Sharon E. ; Nweneka, Chidi V.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 92 no. 06 (Dec. 2010), page 1283-1284.
Topik: MALARIA; Inflammatory Disease
Fulltext: Am J Clin Nutr-2010-Prentice-1283-4.pdf (43.78KB)

Ketersediaan

Perpustakaan FK Nomor Panggil: A07.K.2010.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

An acute episode of malaria usually precipitates anemia of a varying severity which, in extreme cases, can be fatal. This postmalarial anemia has the characteristics of iron deficiency anemia (IDA). It results largely from a redistribution of iron because there is minimal iron excretion after the lysis of infected (and uninfected) red cells caused by malaria. Instead, the potentially toxic hemoglobin released when the erythrocyte ruptures is complexed to haptoglobin and hemopexin. The haptoglobin-hemoglobin complex is recognized by specific receptors on circulating macrophages (CD163) and internalized. The iron-loaded macrophages migrate to the reticuloendothelial system where they can lodge for long periods of time. The hemopexin-heme complex undergoes receptor-mediated uptake by liver cells where again the iron can persist for a long time.

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