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目的 探讨严重急性呼吸综合征 (SARS)的主要脏器的病理改变特点及发病机制。方法 详细检查 7例SARS患者的肺、心、脾、肝、肾等标本的大体特点及用常规方法研究光镜下SARS累及各脏器的病变特点。结果 7例中 ,病程短 (5d)的患者肺部表现以肺水肿为主。与通常的肺水肿相比 ,其水肿液中纤维素成分多 ,可见透明膜形成。 5例病程超过 3周的患者出现肺泡内机化及肺泡间隔内的纤维母细胞增生 ,造成肺泡的实变和闭塞。 6例可见到肺小血管内的微血栓。 7例均可见到散在的肺出血、小叶性肺炎、肺泡上皮脱落、增生等病变。 2例可见真菌感染 ,1例累及左全肺及右肺部分区域 ,还累及心脏和肾脏 ,1例出现在肺门淋巴结。肺门淋巴结多表现为充血、出血及淋巴组织减少 ,窦组织细胞增多。 5例心脏有明显的肥大 ,2例有心内血栓 ,1例有灶性心肌炎 ,1例为真菌性心肌炎。 7例中有 1例为结节性肝硬化 ,另 1例出现广泛的肝细胞带状坏死。脾内均有白髓变小或消失 ,红髓明显充血和出血。 1例腹腔内淋巴结肿大 ,但其内淋巴滤泡亦减少 ,有明显充血和出血及窦组织细胞增生。结论 SARS的主要病变为肺 ,以各期弥漫性肺泡损伤的病变为基本特征。发病机制可能为病毒造成肺泡上皮及毛细血管的严重损伤导致肺水肿及肺泡及细支气管的纤维
Objective To investigate the pathological changes and pathogenesis of major organ in patients with severe acute respiratory syndrome (SARS). Methods The characteristics of lung, heart, spleen, liver and kidney in seven cases of SARS were examined in detail and the pathological changes of SARS in various organs under light microscope were studied by routine methods. Results Among the 7 cases, pulmonary edema was the most common in patients with short course of disease (5 days). Compared with the usual pulmonary edema, the edema fluid has many cellulose components, and the transparent membrane can be seen. Five patients with a course of more than 3 weeks developed alveolar endoplasma and fibroblast proliferation within the alveolar space, resulting in consolidation and occlusion of the alveoli. 6 cases of pulmonary thrombosis can be seen within the small blood vessels. 7 cases can be seen scattered pulmonary hemorrhage, lobular pneumonia, alveolar epithelial shedding, hyperplasia and other lesions. 2 cases of fungal infection, 1 case involving the left lung and right lung part of the area, but also involved the heart and kidney, 1 case of hilar lymph nodes. More hilar lymph nodes showed congestion, reduced bleeding and lymphoid tissue, sinus tissue cells increased. 5 cases of significant hypertrophy of the heart, 2 cases of intracardiac thrombosis, 1 case of focal myocarditis, 1 case of fungal myocarditis. One of seven cases had nodular cirrhosis and the other had extensive banding of hepatic necrosis. Spleen have white pulp smaller or disappear, red pulp obvious congestion and bleeding. One case of intra-abdominal lymphadenopathy, but the lymphatic follicles also reduced, there was significant congestion and bleeding and sinusoidal cell proliferation. Conclusions The main lesion of SARS is lung, and the lesions of diffuse alveolar injury are the basic features of each stage. Pathogenesis may be caused by the virus caused by severe damage to the alveolar epithelium and capillaries leading to pulmonary edema and alveolar and bronchial fibers