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约翰内斯堡蛋白质 - 能量营养不良性贫血的机制。

Mechanisms of anemia in protein-energy malnutrition in Johannesburg.

作者信息

Macdougall L G, Moodley G, Eyberg C, Quirk M

出版信息

Am J Clin Nutr. 1982 Feb;35(2):229-35. doi: 10.1093/ajcn/35.2.229.

DOI:10.1093/ajcn/35.2.229
PMID:6461244
Abstract

Studies of red cell metabolism, erythropoeitin concentration, iron and folate status were made in 48 children with protein-energy malnutrition in Johannesburg (altitude 1800 m). Biochemical evidence of iron deficiency was presented in 26% cases on admission and developed in 90% during recovery. Biochemical evidence of folate deficiency was present in 14% of cases on admission and resolved on dietary therapy alone. Serum erythropoeitin was increased on admission and remained elevated during recovery. There was no relationship between serum erythropoeitin and Hb concentrations. Key enzymes in the red cell glycolytic and hexose monophosphate pathways and red cell membrane showed increased activity. Red cell adenosine triphosphate concentration was increased and unstable. Red cell potassium was decreased and, in the fatal cases, red cell sodium was increased. The possible significance and practical implications of these findings are discussed.

摘要

对约翰内斯堡(海拔1800米)的48名蛋白质 - 能量营养不良儿童进行了红细胞代谢、促红细胞生成素浓度、铁和叶酸状况的研究。入院时26%的病例有缺铁的生化证据,恢复过程中有90%出现缺铁。入院时14%的病例有叶酸缺乏的生化证据,仅通过饮食治疗即可缓解。入院时血清促红细胞生成素升高,恢复过程中持续升高。血清促红细胞生成素与血红蛋白浓度之间无相关性。红细胞糖酵解和磷酸戊糖途径中的关键酶以及红细胞膜的活性增加。红细胞三磷酸腺苷浓度升高且不稳定。红细胞钾含量降低,在致命病例中,红细胞钠含量升高。讨论了这些发现的可能意义和实际影响。

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Mechanisms of anemia in protein-energy malnutrition in Johannesburg.约翰内斯堡蛋白质 - 能量营养不良性贫血的机制。
Am J Clin Nutr. 1982 Feb;35(2):229-35. doi: 10.1093/ajcn/35.2.229.
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Serum folate and folic acid binding proteins in iron deficiency anaemia.缺铁性贫血中的血清叶酸和叶酸结合蛋白
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