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10.1056/NEJMoa2015432

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32437596!7412750!32437596
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  • Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19 #MMPMID32437596
  • Ackermann M; Verleden SE; Kuehnel M; Haverich A; Welte T; Laenger F; Vanstapel A; Werlein C; Stark H; Tzankov A; Li WW; Li VW; Mentzer SJ; Jonigk D
  • N Engl J Med 2020[Jul]; 383 (2): 120-128 PMID32437596show ga
  • BACKGROUND: Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19. METHODS: We examined 7 lungs obtained during autopsy from patients who died from Covid-19 and compared them with 7 lungs obtained during autopsy from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 age-matched, uninfected control lungs. The lungs were studied with the use of seven-color immunohistochemical analysis, micro-computed tomographic imaging, scanning electron microscopy, corrosion casting, and direct multiplexed measurement of gene expression. RESULTS: In patients who died from Covid-19-associated or influenza-associated respiratory failure, the histologic pattern in the peripheral lung was diffuse alveolar damage with perivascular T-cell infiltration. The lungs from patients with Covid-19 also showed distinctive vascular features, consisting of severe endothelial injury associated with the presence of intracellular virus and disrupted cell membranes. Histologic analysis of pulmonary vessels in patients with Covid-19 showed widespread thrombosis with microangiopathy. Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (P<0.001). In lungs from patients with Covid-19, the amount of new vessel growth - predominantly through a mechanism of intussusceptive angiogenesis - was 2.7 times as high as that in the lungs from patients with influenza (P<0.001). CONCLUSIONS: In our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection. The universality and clinical implications of our observations require further research to define. (Funded by the National Institutes of Health and others.).
  • |*Neovascularization, Pathologic[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Autopsy[MESH]
  • |Betacoronavirus[MESH]
  • |Coronavirus Infections/mortality/*pathology[MESH]
  • |Endothelium, Vascular/*pathology/virology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Influenza A Virus, H1N1 Subtype[MESH]
  • |Influenza, Human/mortality/pathology[MESH]
  • |Lung/pathology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/mortality/*pathology[MESH]
  • |Respiratory Distress Syndrome, Adult/pathology/virology[MESH]
  • |Respiratory Insufficiency[MESH]
  • |Thrombosis/*virology[MESH]


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  • suck abstract from ncbi

    120 2.383 2020