Nutrition Programme, MRC Keneba, P.O. Box 273, Banjul, The Gambia.
Trans R Soc Trop Med Hyg. 2010 Mar;104(3):175-84. doi: 10.1016/j.trstmh.2009.08.007. Epub 2009 Sep 23.
There is consensus that the pathophysiology of malaria-associated anaemia is multifactorial, but the precise mechanisms behind many of the haematological changes during malaria remain unclear. In this review, we attempt to build a composite picture of the pathophysiology of malarial anaemia using evidence from experimental, human and animal studies. We propose that cytokine- and hepcidin-mediated iron delocalisation, a principal mechanism in the anaemia of inflammation, plays an important role in the aetiology of malarial anaemia, and can explain some of the clinical and laboratory findings. These mechanisms interact with other aetiological determinants, such as dietary iron and micronutrient supply, helminth load, other infections and genetic variation, in determining the severity and associated features of anaemia. We suggest that iron delocalisation as a mechanism for malarial anaemia could be exploited for the development of alternative therapeutic strategies for post-malaria anaemia.
人们普遍认为疟疾相关贫血的病理生理学是多因素的，但疟疾期间许多血液学变化背后的确切机制仍不清楚。在这篇综述中，我们试图利用来自实验、人类和动物研究的证据，构建疟疾性贫血病理生理学的综合图景。我们提出，细胞因子和铁调素介导的铁再分布——炎症性贫血的主要机制，在疟疾性贫血的发病机制中起着重要作用，并可以解释一些临床和实验室发现。这些机制与其他病因决定因素相互作用，如膳食铁和微量营养素供应、蠕虫负荷、其他感染和遗传变异，决定了贫血的严重程度和相关特征。我们建议，铁再分布作为疟疾性贫血的一种机制，可以被开发用于治疗疟疾后贫血的替代治疗策略。
