Ghosh Kanjaksha, Ghosh Kinjalka
Institute of Immunohaematology (ICMR), 13th Floor, KEM Hospital Campus, Parel, Mumbai 400 012, India.
Parasitol Res. 2007 Nov;101(6):1463-9. doi: 10.1007/s00436-007-0742-1. Epub 2007 Sep 16.
Anemia is a common complication in malarial infection, although the consequences are more pronounced with Plasmodium falciparum malaria (Ghosh, Indian J Hematol Blood Tranfus 21(53):128-130, 2003). Anemia in this infection is caused by a variety of pathophysiologic mechanisms, and in areas where malaria infection is endemic, co-morbidities like other parasitic infestations, iron, folate and Vitamin B12 deficiency, deficiency of other nutrients, and anemia, which is aggravated by anti-malarial drugs both through immune and non-immune mechanisms, are important considerations. In different endemic areas, beta-thalassemia, alpha-thalassemia, Hb S, Hb E, G6PD deficiency, or ovalocytosis in different proportions interact with this infection. Finally, aberrant immune response to repeated or chronic falciparum malarial infection may produce tropical splenomegaly syndrome, a proportion of which show clonal proliferation of B lymphocytes. Cooperation between chronic malarial infection and infection with E-B virus infection in producing Burkitt's lymphoma is well known. In this review, the fascinating and multifaceted pathophysiolgoy of malarial anemia has been discussed.
贫血是疟疾感染中的常见并发症,尽管恶性疟原虫疟疾的后果更为明显(戈什,《印度血液学与输血杂志》21(53):128 - 130,2003年)。这种感染中的贫血由多种病理生理机制引起,在疟疾感染流行地区,其他寄生虫感染、铁、叶酸和维生素B12缺乏、其他营养素缺乏以及抗疟药物通过免疫和非免疫机制加重的贫血等合并症是重要的考虑因素。在不同的流行地区,不同比例的β地中海贫血、α地中海贫血、血红蛋白S、血红蛋白E、葡萄糖-6-磷酸脱氢酶缺乏症或椭圆形红细胞增多症与这种感染相互作用。最后,对反复或慢性恶性疟原虫感染的异常免疫反应可能产生热带脾肿大综合征,其中一部分表现为B淋巴细胞的克隆增殖。慢性疟疾感染与EB病毒感染在引发伯基特淋巴瘤方面的协同作用是众所周知的。在这篇综述中,已经讨论了疟疾贫血引人入胜且多方面的病理生理学。