Autopsies Turn Up Strange Feature of COVID-19 Lungs
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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.

Researchers 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 IHC analysis, micro–CT imaging, SEM, 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 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 showed:
- Widespread thrombosis with microangiopathy.
- Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza.
- 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.

Conclusively, In this 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 these observations require further research to define.

Source: https://www.nejm.org/doi/full/10.1056/NEJMoa2015432?query=featured_home
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How long for the approval?
May 24, 2020Like
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May 25, 2020Like