Bahia School of Medicine and Public Health, Salvador, Brazil.
Acta Trop. 2010 Jul-Aug;115(1-2):155-62. doi: 10.1016/j.actatropica.2010.02.016. Epub 2010 Mar 3.
The frequency of massive pulmonary hemorrhages seems to be increasing in different geographic areas; however, there is no clear explanation for this trend. Although data on the pathogenesis of such complications are scarce, recent research indicates a potential role of autoimmunity and/or multifactorial mechanisms. However, much information is already available on the disturbance of hemostasis and blood vessels in leptospirosis-related literature, even if some contradictory concepts coexist. The purpose of this review is to integrate both new and classical information from human and animal studies on severe pulmonary forms of leptospirosis and disorders of hemostasis and blood vessels. We propose that the involvement of blood vessels in leptospirosis must be understood as a sepsis-like, diffuse process of endothelial activation/damage rather than as a classical systemic vasculitis. Pulmonary hemorrhages are most likely multifactorial and there has recently been evidence against the role of autoimmunity; however, further investigation of strain variations, exposure to hydrocarbons and association with renal dysfunction is required. Thrombocytopenia is a consistent feature of leptospirosis but it is not clear whether it is attributable to sepsis-related mechanisms. In addition, further investigation is required to define whether platelet function is activated or inhibited during severe leptospirosis.
肺大出血的频率似乎在不同的地理区域都有所增加；然而，目前还没有明确的解释。尽管关于这些并发症发病机制的数据很少，但最近的研究表明，自身免疫和/或多因素机制可能发挥作用。然而，在与钩端螺旋体病相关的文献中，已经有大量关于止血和血管紊乱的信息，尽管存在一些相互矛盾的概念。本综述的目的是整合来自人类和动物研究的关于严重肺型钩端螺旋体病和止血及血管紊乱的新信息和经典信息。我们提出，必须将血管在钩端螺旋体病中的参与理解为一种类似败血症的弥漫性内皮激活/损伤过程，而不是一种经典的系统性血管炎。肺出血很可能是多因素的，最近有证据表明自身免疫作用不大；然而，需要进一步研究菌株变异、接触碳氢化合物以及与肾功能不全的关联。血小板减少是钩端螺旋体病的一个常见特征，但尚不清楚其是否归因于与败血症相关的机制。此外，还需要进一步研究以确定在严重钩端螺旋体病期间血小板功能是被激活还是被抑制。
