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English Abstract
Journal Article
[Lung pathology in children with a long-term novel coronavirus infection COVID-19].
Arkhiv Patologii 2024
UNLABELLED: New coronavirus infection is registered less frequently in children than in adults. Among all patients with COVID-19, the share of children is 8.6%. Clinical practice shows that in children, COVID-19 can be severe and even fatal. Articles have been published reflecting the clinical manifestations of Long Covid in children, while data on pathomorphological examination of the lungs during long-term COVID-19 in children are not available in the literature. On the basis of the Department of Pathological Anatomy with a course of Forensic Medicine and the Pathological-Anatomical Department of the Clinic of St. Petersburg State Pediatric Medical University, an analysis of medical documentation was carried out, autopsy materials were selected from 3 observations of the death of children from COVID-19. The selection criterion was the duration of the disease. A histological examination using standard methods and IHC analysis using antibodies to the nucleocapsid of SARS-Cov-2, CD95, CD31 were carried out on the lung tissue of 3 children aged 2 months to 2 years who died from a new coronavirus infection. Microscopically, all three patients showed microvessels damage, their thrombosis, angiogenesis, as well as signs of diffuse alveolar damage The combination of expression of the SARS-CoV-2 nucleocapsid and the apoptosis marker on the vascular endothelium of the MCR is of interest.
CONCLUSION: The data obtained indicate infection with coronavirus and death of endothelial cells due to apoptosis. Endothelial damage in the microvessels of the lungs is the initiating factor in the development of capillary-alveolar block, tissue hypoxia, and disseminated intravascular coagulation syndrome, leading in some cases to respiratory/multiple organ failure and death.
CONCLUSION: The data obtained indicate infection with coronavirus and death of endothelial cells due to apoptosis. Endothelial damage in the microvessels of the lungs is the initiating factor in the development of capillary-alveolar block, tissue hypoxia, and disseminated intravascular coagulation syndrome, leading in some cases to respiratory/multiple organ failure and death.
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