Selected article for: "alveolar space and inflammatory response"

Author: 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
Title: Pulmonary stromal expansion and intra-alveolar coagulation are primary causes of COVID-19 death
  • Cord-id: h7llhiom
  • Document date: 2021_5_24
  • ID: h7llhiom
    Snippet: Most COVID-19 victims are old and die from unrelated causes. Here we present twelve 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 accumulat
    Document: Most COVID-19 victims are old and die from unrelated causes. Here we present twelve 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.

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