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New England Journal of Medicine· 2020Q1

Covid-19'da Pulmoner Vasküler Endotelit, Trombozis ve Anjiyogenez

Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19

Maximilian Ackermann, Stijn E. Verleden, Mark Kuehnel, Axel Haverich ve diğerleri

Kısa özet

7 ölümcül Covid-19 hastasından alınan otopsi akciğerleri, hücre içi virüs ile birlikte şiddetli endotel hasarı, yaygın mikrotrombi (%9 kat daha yaygın influenza'ya göre) ve artmış intussuseptif anjiyogenez (%2.7 kat daha yüksek influenza'ya göre) gösterdi.

Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.

Ana noktalar

  • Ölümcül Covid-19 akciğerleri, hücre içi virüs ve bozulmuş hücre zarları ile birlikte şiddetli endotel hasarı sergiler.
  • Pulmoner mikrotrombi, Covid-19 hastalarında influenza hastalarına göre 9 kat daha yaygındı.
  • İntussuseptif anjiyogenez yoluyla yeni damar büyümesi, Covid-19 akciğerlerinde influenza akciğerlerine göre 2.7 kat daha yüksekti.
  • Perivasküler T-hücre infiltrasyonu ile birlikte diffüz alveolar hasar, hem Covid-19 hem de influenza'ya bağlı solunum yetmezliğinde yaygındı.

Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.

Özet (abstract)

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.).

Yazarların özeti; kaynağından alınmıştır. New England Journal of Medicine, 2020 · DOI ↗

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Infectious DiseasesMedicine