Fundação de Medicina Tropical Dr. Heitor Vieira Dourado, Manaus, AM, Brasil.
Mem Inst Oswaldo Cruz. 2011 Aug;106 Suppl 1:52-63. doi: 10.1590/s0074-02762011000900007.
Despite not being a criterion for severe malaria, thrombocytopenia is one of the most common complications of both Plasmodium vivax and Plasmodium falciparum malaria. In a systematic review of the literature, platelet counts under 150,000/mm³ ranged from 24-94% in patients with acute malaria and this frequency was not different between the two major species that affected humans. Minor bleeding is mentioned in case reports of patients with P. vivax infection and may be explained by medullary compensation with the release of mega platelets in the peripheral circulation by megakaryocytes, thus maintaining a good primary haemostasis. The speculated mechanisms leading to thrombocytopenia are: coagulation disturbances, splenomegaly, bone marrow alterations, antibody-mediated platelet destruction, oxidative stress and the role of platelets as cofactors in triggering severe malaria. Data from experimental models are presented and, despite not being rare, there is no clear recommendation on the adequate management of this haematological complication. In most cases, a conservative approach is adopted and platelet counts usually revert to normal ranges a few days after efficacious antimalarial treatment. More studies are needed to specifically clarify if thrombocytopenia is the cause or consequence of the clinical disease spectrum.
虽然血小板减少症不是重症疟疾的标准之一，但它是间日疟原虫和恶性疟原虫疟疾最常见的并发症之一。在对文献的系统评价中，急性疟疾患者的血小板计数在 150,000/mm³以下的范围为 24-94%，且在两种主要影响人类的疟原虫之间并无差异。在报道的间日疟原虫感染患者的病例报告中提到了轻微出血，这可能是骨髓通过巨核细胞在外周循环中释放巨大血小板来代偿的结果，从而维持良好的初级止血。导致血小板减少症的推测机制包括：凝血紊乱、脾肿大、骨髓改变、抗体介导的血小板破坏、氧化应激以及血小板在引发重症疟疾中的辅助因子作用。本文介绍了实验模型中的数据，尽管这种情况并不罕见，但对于这种血液学并发症的适当处理方法并没有明确的建议。在大多数情况下，采用保守治疗方法，血小板计数通常在有效抗疟治疗后几天内恢复正常范围。需要进一步研究来明确血小板减少症是疾病临床谱的原因还是结果。
