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目的通过研究严重急性呼吸综合征(severeacuterespiratorysyndrome,SARS)患者的尸检肺部标本,总结SARS的肺部病变特点及发病机制。方法详细检查SARS患者肺脏标本的大体特点,并用常规方法研究显微光镜下SARS累及各肺叶的病变特点。结果7例SARS患者的双肺均明显膨胀,镜下表现以弥漫性肺泡损伤(DAD)不同时期的病变为主。7例均有肺水肿及透明膜形成,肺水肿尤以早期明显。病程超过3周者开始有肺泡内机化及肺间质纤维化,造成肺泡的纤维性闭塞。几乎每例都可见到小血管内的微血栓和肺出血、散在的小叶性肺炎、肺泡上皮脱落、增生等病变。2例可见曲霉菌感染,1例累及左全肺及右肺部分区域,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。结论SARS肺可能为SARS病毒造成的弥漫性肺泡损伤,表现为肺泡上皮及毛细血管的严重损伤导致肺水肿和肺泡及细支气管的纤维素性渗出性炎症,出现透明膜,继而出现肺泡内机化及肺泡间隔的成纤维细胞增生,共同使肺泡萎陷、机化,最终形成纤维化实变。肺门淋巴组织的减少可能是此病影响免疫系统的又一形态学表现。
Objective To study the characteristics and pathogenesis of pulmonary lesions in SARS by studying autopsy lung specimens from patients with severe acute respiratory syndrome (SARS). Methods The characteristics of lung specimens from SARS patients were examined in detail. The pathological features of SARS involving lung lobes under microscope were studied by routine methods. Results The lungs of 7 patients with SARS were obviously inflated. The pathological changes in different stages of diffuse alveolar damage (DAD) were mainly observed under microscope. 7 cases were pulmonary edema and transparent membrane formation, especially early pulmonary edema. Course of more than 3 weeks began with alveolar internalization and interstitial lung fibrosis, resulting in alveolar fibrous occlusion. Microvascular thrombosis and pulmonary hemorrhage can be seen in almost every case of small blood vessels, scattered lobular pneumonia, alveolar epithelial shedding, hyperplasia and other lesions. 2 cases of Aspergillus infection, 1 case involving the left lung and right lung partial area, 1 case of hilar lymph nodes. More hilar lymph nodes showed congestion, reduced bleeding and lymphoid tissue, sinus tissue cells increased. Conclusions The SARS lung may cause diffuse alveolar damage caused by SARS virus. The severe damage to the alveolar epithelium and capillaries results in pulmonary edema and cellulolytic exudative inflammation of the alveoli and bronchioles, the appearance of a transparent membrane, and the subsequent development of alveolar intima And alveolar septa of fibroblasts, alveolar collapse together, mechanization, and ultimately the formation of fibrosis. The reduction in hilar lymphoid tissue may be another morphological manifestation of the immune system affected by the disease.