Heidecker Jay, Kaplan Allen, Sahn Steven A
Division of Pulmonary and Critical Care Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Am J Med Sci. 2006 Sep;332(3):148-52. doi: 10.1097/00000441-200609000-00011.
Blood and air in the pleural space are the most common conditions associated with an eosinophilic pleural effusion. The recruitment of eosinophils is dependent upon stimulation by cytokines, specifically interleukin (IL)-3, IL-5, granulocyte-monocyte cell stimulating factor (GM-CSF), and RANTES (regulated upon activation, normal t-cell expressed and secreted), that cause eosinophil proliferation in the bone marrow, movement into the circulation, and adhesion and migration across endothelial barriers into tissues. There are several possible mechanisms that can explain eosinophilic pleural effusions. We report a case of an eosinophilic pleural effusion after spontaneous hemothorax that illustrates the course of pleural fluid and blood eosinophilia in following hemothorax and describe the different pathophysiology of eosinophil trafficking in the pleural space and serum following hemothorax and pneumothorax.
胸腔内出现血液和空气是与嗜酸性胸腔积液相关的最常见情况。嗜酸性粒细胞的募集依赖于细胞因子的刺激，特别是白细胞介素（IL）-3、IL-5、粒细胞-单核细胞集落刺激因子（GM-CSF）和调节激活正常T细胞表达和分泌因子（RANTES），这些细胞因子可导致嗜酸性粒细胞在骨髓中增殖、进入循环，并黏附及穿过内皮屏障迁移至组织中。有几种可能的机制可以解释嗜酸性胸腔积液。我们报告了一例自发性血胸后出现嗜酸性胸腔积液的病例，该病例说明了血胸后胸腔积液和血液嗜酸性粒细胞增多的过程，并描述了血胸和气胸后嗜酸性粒细胞在胸腔和血清中游走的不同病理生理学机制。
