ABSTRACT
The search for sensitive and specific markers enabling timely identification of patients with a life-threat-ening novel coronavirus infection (COVID-19) is important for a successful treatment. The aim of the study was to examine the association of molecular biomarkers of air-blood barrier damage, surfactant proteins SP-A and SP-D and Club cell protein CC16, with the outcome of patients with COVID-19. Materials and methods. A cohort of 109 patients diagnosed with COVID-19 was retrospectively divided into two groups. Group 1 comprised survivor patients discharged from the ICU (n=90). Group 2 included the patients who did not survive (n=19). Association of disease outcome and SP-A, SP-D, and CC16 levels in blood serum, clinical, and laboratory data were examined taking into account the day of illness at the time of bio-material collection. Results. The non-survivors had higher SP-A (from days 1 to 10 of symptoms onset) and lower CC16 (from days 11 to 20 of symptoms onset) levels vs survivors discharged from ICU. No significant differences in SP-D levels between the groups were found. Conclusion. According to the study results, the surfactant protein SP-A and Club cell protein CC16 are associated with increased COVID-19 mortality.
ABSTRACT
The aim of the study was to identify the pathomorphology of brain damage in patients who died of COVID-19. Material and methods. Autopsy reports and autopsy brain material of 17 deceased patients with pre-mortem confirmed COVID-19 infection were analyzed. Fatal cases in which COVID-19 was the major cause of death were included in the study. Five people were diagnosed with cerebral infarction. Organ samples were taken for histological examination during autopsy. Sections were stained with hematoxylin and eosin and by Nissl to assess brain histopathology. To study the vascular basal membranes the PAS reaction was used, to detect fibrin in vessels phosphotungstic acid-hematoxylin (PTAH) staining was used, to determine DNA in nuclei sections were stained according to Feulgen, to detect RNA in neuronal nuclei and cytoplasm sections were stained with methyl green-pyronin. Immunohistochemical study of a neuronal marker, nuclear protein NeuN, was performed to assess neuronal damage. Results. The signs of neuronal damage found in patients who died of COVID-19 included nonspecific changes of nerve cells (acute swelling, retrograde degeneration, karyolysis and cytolysis, ‘ghost' cells, neuronophagia and satellitosis) and signs of circulatory disorders (perivascular and pericellular edema, diapedesis, congested and engorged microvasculature). Conclusion. Brain histopathological data indicate damage to the central nervous system in COVID-19 patients. Ischemic stroke in patients with COVID-19 is mostly caused by a combination of hypoxia resulting from respiratory failure and individual risk factors, including cerebrovascular atherosclerosis and hypertension.
ABSTRACT
The aim of the study was to evaluate the histopathological changes in the lungs of patients who died of a new coronavirus infection (COVID-19) in relation to the length of hospital stay. We evaluated lung autopsy material, autopsy reports, and death summaries of 39 patients who died of COVID-19. The length of hospital stay ranged from a few hours to 25 days. At all stages of the disease, lung alterations (desquamation of bronchial and alveolar epithelium), circulatory disorders (alveolar edema and hemorrhages, congestion in small blood vessels, thrombosis), compensatory response (fibrosis) were identified. The patients who died during the first week of hospitalization demonstrated predominant signs of circulatory disorders (alveolar edema, hyaline membranes, alveolar hemorrhages, congestion in small blood vessels). Fibrosis, usually not typical for the first week of acute respiratory distress syndrome, was detected in 46% of the deceased during the first week of hospitalization, which may be due to late hospitalization or patterns of fibrosis development in COVID-19. For those who died in the 2nd and 3rd weeks of hospitalization, the compensatory response and progression of fibrosis were noted. By the 3rd week, pulmonary fibrosis was detected in 91% of patients. Thrombotic complications (thrombosis, pulmonary artery thromboembolism) were observed in almost half of fatalities occurring during weeks 2-3. Hemorrhagic infarction was found in 43% (6 patients) who died during week 2 of hospitalization, three of them were diagnosed with pulmonary embolism, indicating progression of pulmonary vascular damage.