Szekely Laszlo, Bozoky Bela, Bendek Matyas, Ostad Masih, Lavignasse Pablo, Haag Lars, Wu Jieyu, Jing Xu, Gupta Soham, Saccon Elisa, Sönnerborg Anders, Cao Yihai, Björnstedt Mikael, Szakos Attila
Department of Pathology/Cytology, Karolinska University Laboratory, 141 86 Stockholm, Sweden.
Microbiology and Tumor Biology Center, Karolinska Institutet, 171 77 Stockholm, Sweden.
Heliyon. 2021 May;7(5):e07134. doi: 10.1016/j.heliyon.2021.e07134. Epub 2021 May 24.
Most COVID-19 victims are old and die from unrelated causes. Here we present welve complete autopsies, including two rapid autopsies of young patients where the cause of death was COVID-19 ARDS. The main virus induced pathology was in the lung parenchyma and not in the airways. Most coagulation events occurred in the intra-alveolar and not in the intra-vascular space and the few thrombi were mainly composed of aggregated thrombocytes. The dominant inflammatory response was the massive accumulation of CD163 + macrophages and the disappearance of T killer, NK and B-cells. The virus was replicating in the pneumocytes and macrophages but not in bronchial epithelium, endothelium, pericytes or stromal cells. The lung consolidations were produced by a massive regenerative response, stromal and epithelial proliferation and neovascularization. We suggest that thrombocyte aggregation inhibition, angiogenesis inhibition and general proliferation inhibition may have a roll in the treatment of advanced COVID-19 ARDS.
大多数新冠病毒疾病受害者年事已高，死于其他无关病因。在此，我们展示了12例完整的尸检病例，其中包括2例年轻患者的快速尸检，其死因是新冠病毒疾病急性呼吸窘迫综合征（COVID-19 ARDS）。病毒引发的主要病理变化发生在肺实质而非气道。大多数凝血事件发生在肺泡内而非血管内，少数血栓主要由聚集的血小板组成。主要的炎症反应是CD163 +巨噬细胞的大量积聚以及杀伤性T细胞、自然杀伤细胞和B细胞的消失。病毒在肺细胞和巨噬细胞中复制，但不在支气管上皮、内皮、周细胞或基质细胞中复制。肺实变是由大量再生反应、基质和上皮增殖以及新血管形成所致。我们认为，抑制血小板聚集、抑制血管生成和一般增殖抑制可能在晚期新冠病毒疾病急性呼吸窘迫综合征的治疗中发挥作用。
