[A pathological report of three COVID-19 cases by minimal invasive autopsies].
[A pathological report of three COVID-19 cases by minimal invasive autopsies].
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DOI：
10.3760/cma.j.cn112151-20200312-00193
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发表时间：
2020-05-08
期刊：
影响因子：
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通讯作者：
Bian, X W
中科院分区：
文献类型：
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作者：
Yao, X H;Li, T Y;Bian, X W
目的：探讨新型冠状病毒(2019-NCoV)感染性肺炎(世界卫生组织冠状病毒病2019新冠肺炎)的病理特点及临床意义。方法：对重庆市中国3例新型冠状病毒肺炎死亡病例进行肺、心、肾、脾、骨髓、肝、胰腺、胃、肠、甲状腺和皮肤微创尸检。苏木精-伊红染色、透射电子显微镜和组织化学染色观察各脏器或组织的病理变化。免疫组织化学染色检测免疫细胞的浸润及2019-nCoV蛋白的表达。用实时荧光定量聚合酶链式反应检测2019-nCoV的RNA。结果：肺泡结构有不同程度的损害，有少量浆液性渗出和纤维蛋白渗出。部分肺泡内可见透明膜形成。肺泡内的免疫细胞主要为巨噬细胞和单核细胞。可见中度多核巨细胞、极小淋巴细胞、嗜酸性粒细胞和中性粒细胞。浸润性淋巴细胞以CD4+T细胞为主。Ⅱ肺泡上皮细胞明显增殖，肺泡局灶性脱屑。肺泡间隔血管充血、肿胀、增宽，单核细胞和淋巴细胞轻度浸润。少数微血管内可见透明血栓。肺组织局灶性出血，部分肺泡腔渗出物机化，肺间质纤维化。部分支气管上皮细胞脱落。在电子显微镜下观察了支气管粘膜上皮和Ⅱ肺泡上皮中的冠状病毒颗粒。免疫组织化学染色显示部分肺泡上皮细胞和巨噬细胞对2019-nCoV抗原呈阳性反应。实时聚合酶链式反应分析确定了2019-nCoV核酸的阳性信号。脾淋巴细胞数量减少，细胞变性、坏死。此外，在其他器官和组织中还观察到实质细胞的变性和坏死，小血管内透明血栓的形成和慢性疾病的病理改变，而这些器官中没有冠状病毒感染的证据。结论：新型冠状病毒肺炎患者的肺组织有明显的病理改变，包括肺泡渗出性炎症和间质性炎症，肺泡上皮细胞增殖和透明膜形成。虽然2019-nCoV主要分布在肺部，但感染还涉及心、血管、肝、肾等器官的损害。有必要进行进一步的研究，以探讨该病的病理变化机制。
Objective: To investigate the pathological characteristics and the clinical significance of novel coronavirus (2019-nCoV)-infected pneumonia (termed by WHO as coronavirus disease 2019, COVID-19). Methods: Minimally invasive autopsies from lung, heart, kidney, spleen, bone marrow, liver, pancreas, stomach, intestine, thyroid and skin were performed on three patients died of novel coronavirus pneumonia in Chongqing, China. Hematoxylin and eosin staining (HE), transmission electron microcopy, and histochemical staining were performed to investigate the pathological changes of indicated organs or tissues. Immunohistochemical staining was conducted to evaluate the infiltration of immune cells as well as the expression of 2019-nCoV proteins. Real time PCR was carried out to detect the RNA of 2019-nCoV. Results: Various damages were observed in the alveolar structure, with minor serous exudation and fibrin exudation. Hyaline membrane formation was observed in some alveoli. The infiltrated immune cells in alveoli were majorly macrophages and monocytes. Moderate multinucleated giant cells, minimal lymphocytes, eosinophils and neutrophils were also observed. Most of infiltrated lymphocytes were CD4-positive T cells. Significant proliferation of type Ⅱ alveolar epithelia and focal desquamation of alveolar epithelia were also indicated. The blood vessels of alveolar septum were congested, edematous and widened, with modest infiltration of monocytes and lymphocytes. Hyaline thrombi were found in a minority of microvessels. Focal hemorrhage in lung tissue, organization of exudates in some alveolar cavities, and pulmonary interstitial fibrosis were observed. Part of the bronchial epithelia were exfoliated. Coronavirus particles in bronchial mucosal epithelia and type Ⅱ alveolar epithelia were observed under electron microscope. Immunohistochemical staining showed that part of the alveolar epithelia and macrophages were positive for 2019-nCoV antigen. Real time PCR analyses identified positive signals for 2019-nCoV nucleic acid. Decreased numbers of lymphocyte, cell degeneration and necrosis were observed in spleen. Furthermore, degeneration and necrosis of parenchymal cells, formation of hyaline thrombus in small vessels, and pathological changes of chronic diseases were observed in other organs and tissues, while no evidence of coronavirus infection was observed in these organs. Conclusions: The lungs from novel coronavirus pneumonia patients manifest significant pathological lesions, including the alveolar exudative inflammation and interstitial inflammation, alveolar epithelium proliferation and hyaline membrane formation. While the 2019-nCoV is mainly distributed in lung, the infection also involves in the damages of heart, vessels, liver, kidney and other organs. Further studies are warranted to investigate the mechanism underlying pathological changes of this disease.