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目的研究严重急性呼吸综合征(SARS)患者尸解肺标本的病理改变和致病机制。方法观察了2003年4—7月期间死于SARS的6例患者的肺标本,并采用光镜、电镜、Masson三色染色和免疫组织化学染色方法(EnVision法)进行研究。结果肺标本的病理形态改变:(1)6例的双肺均可见到弥漫性实变病灶,肺重量明显增加;(2)6例均可见到弥漫性肺泡损伤,包括透明膜形成、肺泡腔内水肿/出血、纤维素沉积和肺泡上皮细胞脱屑,AE1/AE3免疫组织化学染色显示肺泡上皮细胞的完整性明显破坏;(3)Ⅱ型肺泡上皮细胞轻度增生,有一定异型性,细胞体积增大,胞质呈双染性和颗粒状,胞质内可见小脂肪空泡聚集(5/6);(4)6例中有5例可见巨细胞在肺泡内浸润,巨细胞大多AE1/AE3阳性(5/6),少数CD68阳性(2/6);(5)组织学形态和免疫组织化学染色证实肺泡腔内和肺泡间隔内有多量巨噬细胞浸润(6/6);(6)6例中有5例可见巨噬细胞噬红细胞象;(7)6例中有5例可见肺纤维化,包括肺泡间隔和肺间质增宽(5/6)、肺泡腔内渗出物机化(6/6)和胸膜增厚(4/6)。Masson三色染色证实胶原纤维明显增生,免疫组织化学染色显示大多数为Ⅲ型胶原。光镜和免疫组织化学染色显示5例有明显的成纤维细胞/肌纤维母细胞增生灶;(8)5例可见支气管黏膜鳞状上皮化生;(9)6例患者均可见血栓;(10)2例同时合并其他感染,1例合并细菌感染,另1例合并真菌感染。此外,电镜发现在肺泡上皮细胞和肺血管内皮细胞的胞质内有冠状病毒样颗粒。结论SARS冠状病毒直接损伤肺泡上皮细胞、巨噬细胞明显浸润和成纤维细胞/肌纤维母细胞显著增生在SARS的致病机制中起重要作用。
Objective To study the pathological changes and pathogenesis of autopsy lung specimens from patients with severe acute respiratory syndrome (SARS). Methods Lung samples from 6 patients who died of SARS during April to July 2003 were observed and examined by light microscopy, electron microscopy, Masson trichrome staining and immunohistochemical staining (EnVision method). Results The pathological changes of the lung specimens were as follows: (1) diffuse consolidation lesion was found in both of the 6 cases and the lung weight was significantly increased. (2) Diffuse alveolar injury was observed in 6 cases, including the formation of the transparent membrane, AE1 / AE3 immunohistochemical staining showed that the integrity of alveolar epithelial cells was obviously destroyed; (3) Type II alveolar epithelial cells were mild hyperplasia with some atypia, Volume increased, cytoplasm showed double staining and granular, cytoplasm showed small fat vacuoles (5/6); (4) 5 cases of 6 cases of visible giant cells infiltrating in the alveolar, most of the giant cells AE1 (5/6) and a few positive for CD68 (2/6). (5) Histological and immunohistochemical staining showed that a large amount of macrophage infiltrated (6/6) in alveolar space and alveolar septum. 6) In 5 of 6 cases, macrophage erythropocytosis was observed in 5 cases. (7) Pulmonary fibrosis was observed in 5 of 6 cases, including alveolar septum and pulmonary interstitial widening (5/6) Materialized (6/6) and pleural thickening (4/6). Masson trichrome staining confirmed the proliferation of collagen fibers, immunohistochemical staining showed that the majority of type Ⅲ collagen. Light microscopy and immunohistochemical staining showed that 5 cases had obvious proliferation of fibroblasts / myofibroblasts; (5) 5 cases of bronchial mucosal squamous metaplasia; (9) 6 cases of thrombosis were seen; (10) 2 cases combined with other infections at the same time, 1 case of bacterial infection, another case of fungal infection. In addition, electron microscopy revealed coronavirus-like particles in the cytoplasm of alveolar epithelial cells and pulmonary vascular endothelial cells. Conclusions The direct invasion of alveolar epithelial cells, macrophages and significant proliferation of fibroblasts / myofibroblasts by SARS-CoV may play an important role in the pathogenesis of SARS.