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恶性三日疟血小板减少症的机制

Mechanisms of thrombocytopenia in malignant tertian malaria.

作者信息

Skudowitz R B, Katz J, Lurie A, Levin J, Metz J

出版信息

Br Med J. 1973 Jun 2;2(5865):515-8. doi: 10.1136/bmj.2.5865.515.

Abstract

The mechanism of thrombocytopenia in six patients with falciparum malaria has been studied. All the patients recovered after antimalarial therapy, and cerebral malaria was not a feature. Radioactive-labelled platelets and fibrinogen were injected into the patients during the phase of thrombocytopenia. In all cases recovery of injected platelets was notably subnormal, indicating excessive splenic pooling of platelets. Platelet life span was moderately shortened in all patients, and platelet turnover increased approximately two-fold. Fibrinogen catabolism was moderately increased in all patients, but coagulation tests failed to reveal evidence of disseminated intravascular coagulation. The results suggest that in uncomplicated cases of malaria thrombocytopenia is the result of splenic pooling of platelets aggravated by a moderate decrease in platelet life span. In such cases thrombocytopenia is thus not the result of disseminated intravascular coagulation (D.I.C.), and heparin therapy is not indicated unless there is unequivocal ancillary evidence of D.I.C.

摘要

对6例恶性疟患者血小板减少的机制进行了研究。所有患者经抗疟治疗后均康复,且无脑型疟表现。在血小板减少阶段,将放射性标记的血小板和纤维蛋白原注入患者体内。在所有病例中,注入的血小板恢复明显低于正常水平,表明血小板在脾脏过度蓄积。所有患者的血小板寿命均适度缩短,血小板周转率增加约两倍。所有患者的纤维蛋白原分解代谢均适度增加,但凝血试验未发现弥散性血管内凝血的证据。结果表明,在无并发症的疟疾病例中,血小板减少是血小板在脾脏蓄积的结果,同时血小板寿命适度缩短加重了这种情况。因此,在这种情况下,血小板减少不是弥散性血管内凝血(DIC)的结果,除非有明确的DIC辅助证据,否则不建议使用肝素治疗。

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