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汉坦病毒感染的发病机制:肾综合征出血热的病理生理学

Mechanisms of disease in Hantavirus infection: pathophysiology of hemorrhagic fever with renal syndrome.

作者信息

Cosgriff T M

机构信息

Medical Division, United States Army Medical Research, Institute of Infectious Diseases, Frederick, Maryland.

出版信息

Rev Infect Dis. 1991 Jan-Feb;13(1):97-107. doi: 10.1093/clinids/13.1.97.

DOI:10.1093/clinids/13.1.97
PMID:1673261
Abstract

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease that occurs over wide areas of Europe and Asia. Hantaviruses are the cause of this syndrome. The hallmark of HFRS is the triad of fever, hemorrhage, and renal failure. In its severe form it is associated with significant mortality. The syndrome evolves through five phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The central physiologic derangement in HFRS is vascular dysfunction, manifested by impaired vascular tone and increased vascular permeability. The systemic effects of this dysfunction account for the occurrence of hypotension and shock, while local effects are probably important in the development of renal failure. Shock in HFRS has distributive and oligemic features, while renal failure has features of acute tubular necrosis. Hemorrhage is a consequence of vascular injury and a deficit of functional platelets. Vascular and platelet dysfunction are both compounded by uremia. Disseminated intravascular coagulation contributes to hemorrhage in some patients. Although hantaviruses are infectious for endothelial cells and may cause direct injury, a large body of evidence suggests that immune mechanisms play an important role in the pathogenesis of HFRS.

摘要

肾综合征出血热(HFRS)是一种在欧洲和亚洲广大地区发生的急性病毒性疾病。汉坦病毒是该综合征的病因。HFRS的标志是发热、出血和肾衰竭三联征。在其严重形式中,它与显著的死亡率相关。该综合征通过五个阶段演变:发热期、低血压期、少尿期、多尿期和恢复期。HFRS的核心生理紊乱是血管功能障碍,表现为血管张力受损和血管通透性增加。这种功能障碍的全身影响导致低血压和休克的发生,而局部影响可能在肾衰竭的发展中起重要作用。HFRS中的休克具有分布性和低血容量性特征,而肾衰竭具有急性肾小管坏死的特征。出血是血管损伤和功能性血小板缺乏的结果。血管和血小板功能障碍都因尿毒症而加重。在一些患者中,弥散性血管内凝血导致出血。虽然汉坦病毒可感染内皮细胞并可能造成直接损伤,但大量证据表明免疫机制在HFRS的发病机制中起重要作用。

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