嗜酸性心内膜疾病患者心内膜活检的电镜和免疫组织化学研究。

Y Nakayama, T Kohriyama, S Yamamoto, H Deguchi, M Suwa, M Kino, Y Hirota, K Imamura, Y Kitaura, K Kawamura
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引用次数: 7

摘要

我们对一名68岁男性患者的嗜酸性粒细胞和左心室心肌内膜活检进行了光镜和电镜研究和免疫组织化学检查,该患者嗜酸性粒细胞为8.2 X 10(9)/l,并因嗜酸性心肌内膜疾病引起充血性心力衰竭。部分血嗜酸性粒细胞空泡化,脱颗粒,电镜下可见嗜酸性粒细胞颗粒正常染色模式逆转。活检显示心肌细胞退行性改变,间质纤维化,大量嗜酸性细胞、肥大细胞和巨噬细胞浸润。浸润心肌的嗜酸性粒细胞显示颗粒数量减少,其中许多颗粒不明显或含有溶解的晶体,偶见颗粒排出到邻近心肌细胞表面。使用单克隆抗体对活化的嗜酸性粒细胞特异,并结合分泌形式的嗜酸性粒细胞阳离子蛋白(ECP)和嗜酸性粒细胞蛋白- x (EP-X)的心内膜活检进行免疫组织化学研究,表明病变含有大量活化的嗜酸性粒细胞和分泌的ECP和EP-X。这些发现支持了嗜酸性心内膜疾病的概念,即活化的嗜酸性粒细胞浸润并在心肌中脱粒,释放嗜酸性阳离子蛋白,然后损害邻近的心肌细胞。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Electron-microscopic and immunohistochemical studies on endomyocardial biopsies from a patient with eosinophilic endomyocardial disease.

Light- and electron-microscopic studies and immunohistochemical procedures were carried out on blood eosinophils and left ventricular endomyocardial biopsies from a 68-year-old man with an eosinophilia of 8.2 X 10(9)/l and congestive cardiac failure due to eosinophilic endomyocardial disease. Some blood eosinophils were vacuolated and degranulated, and reversal of the normal staining pattern of eosinophil granules was seen by means of electron microscopy. The biopsies showed degenerative changes in the cardiac myocytes, with interstitial fibrosis and infiltration by numerous eosinophils, mast cells, and macrophages. Eosinophils infiltrating the myocardium showed a decrease in the number of granules, many of which were indistinct or contained dissolving crystalloids, which occasionally were seen to be discharged onto the surface of adjacent cardiac myocytes. Immunohistochemical studies of the endomyocardial biopsies with a monoclonal antibody, which is specific for activated eosinophils and binds to the secreted forms of eosinophil cationic protein (ECP) and eosinophil protein-X (EP-X), demonstrated that the lesions contained numerous activated eosinophils and secreted ECP and EP-X. These findings support the concept that in eosinophilic endomyocardial disease, activated eosinophils infiltrate and degranulate in the myocardium, releasing eosinophil cationic proteins which then damage adjacent myocardial cells.

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