SARS患者死因的病理机制探讨——急性肺损伤与继发感染

Study on the Pathogenesis of the Cause of Death of Severe Acute Respiratory Syndrome--Acute Lung Injury and Secondary Infection

目的分析严重急性呼吸综合征(SARS)患者的临床病理特点,探讨SARS死亡原因的病理生理机制。方法以4例SARS患者的尸检肺组织、经皮或经支纤镜肺活检标本为观察对象,组织病理切片经常规HE染色,免疫组化,并与临床表现进行联系。结果2例发病早期患者肺组织病理切片可见Ⅱ型肺泡上皮细胞增生,肺泡壁明显增宽,血管充血水肿,纤维母细胞增生,肺泡腔见纤维素及红细胞渗出,单个核细胞浸润,透明膜形成。另2例病程较长的死亡病例可见肺组织内大量曲霉菌菌丝,血管内见真菌栓,血管壁破坏。免疫组织化学染色:B细胞的CD20+在肺组织中的表达为阴性;T细胞的CD45RO+表达阳性增加;吞噬细胞的CD68+阳性表达显著增加。结论SAPS发病早期肺部主要表现为急性肺损伤,其发生机制可能与超敏反应有关,也是SARS患者早期死亡的主要原因,与免疫抑制有关的继发严重霉菌感染是晚期病人的重要死因。

Objective To investigate the pathogenesis of the cause of death of severe acute respiratory syndrome (SARS). Method Tissue specimens from 4 cases of SARS were studied by HE staining and immunohistochemical technique. Results Lung tissue samples from two cases died at early phase revealed a mixed features of type Ⅱ alveolus cell and fibroblast hyperplasia, thicken walls of alveoli, engorgement and edematous of blood vessels, intra-alveolar exudation of fibrinoid materials, erythrocytes with hyaline-membrane formation, and pulmonary interstitial infiltration of mononuclear cells. The pathological changes of the lung tissues from another two dead cases with long courses of illness showed large amount of intra-alveolar aspergillus, and pulmonary vascular walls destruction with an invasion of aspergillus into blood vessels. The result of immunohistochemical study showed that CD45RO+ positive cells were found in those lung tissues but not CD20+ positive cells. There was increased number of CD68+ positive cells. Conclusions The results indicated that the pathological changes of lungs in SARS patients were acute lung injury. Hyper reaction of the immune system may be one of the reasons responsible for main cause of death at early phase after onset,but secondary fungi infection was an important cause of death in those SARS patients with significant immunodepression at late phase.