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Eur Rev Med Pharmacol Sci ; 26(1): 270-277, 2022 01.
Article in English | MEDLINE | ID: covidwho-1631285


Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare new syndrome occurring after the ChAdOx1 nCoV-19 vaccine immunization. Patients with VITT are characterized by a variable clinical presentation, likewise also the outcome of these patients is very variable. Here we report the lung ultrastructural findings in the course of VITT of a 58-year-old male patient. Alveoli were mainly dilated, irregular in shape, and occupied by a reticular network of fibrin, while interalveolar septa appeared thickened. The proliferation of small capillaries gave rise to plexiform structures and pulmonary capillary hemangiomatosis-like features. Near the alveoli occupied by a dense fibrin network, the medium-sized arteries showed a modified wall and an intraluminal thrombus. This scenario looks quite similar to that found during COVID-19, where the lungs suffer from the attack of the antigen-antibodies complexes and the virus respectively. In both diseases, the final outcome is a severe inflammation, activation of the haemostatic system and fibrinolysis.

/adverse effects , Lung Injury/etiology , Lung Injury/pathology , Purpura, Thrombocytopenic, Idiopathic/chemically induced , Vaccination/adverse effects , COVID-19/prevention & control , Fibrin , Humans , Lung Injury/diagnostic imaging , Lung Injury/immunology , Male , Microscopy, Electron, Scanning , Middle Aged , Parenchymal Tissue/pathology , Purpura, Thrombocytopenic, Idiopathic/diagnosis , Purpura, Thrombocytopenic, Idiopathic/immunology
European Review for Medical and Pharmacological Sciences ; 25(24):7997-8003, 2021.
Article in English | Web of Science | ID: covidwho-1589477


OBJECTIVE: The ongoing Coronavirus pandemic (COVID-19) showed similar characteristics with the severe acute respiratory syndrome (SARS). In the most compromised cases, COVID-19 infection leads to death due to severe respiratory complications. COVID-19-related acute respiratory distress syndrome (ARDS) is the primary cause of death in these patients. In the present study, we show an ultrastructural analysis on the lungs of a patient affected by COVID-19. PATIENTS AND METHODS: Lung specimens obtained at autopsy from a 63-years old patient affected by COVID-19 were fixed in 1% paraformaldehyde. Slices of 300 mu m thickness were dehydrated and dried by Critical Point Drying in CO2. Slices were covered with a conductive gold film approximately 30 nm thick and observed at a Zeiss Sigma 300 SEM FEG in the secondary electron (SE) and backscattered electron (BSE) modes. As case control a lung biopsy from a 60-year-old man was considered. RESULTS: At low power in all COVID-19 lung specimens severe changes in the pulmonary architecture were found, due to the collapse of air spaces. Moreover, alveolar cavities were covered by large membranes. At high power, alveolar membranes showed a fibrillar structure, suggestive of a loose network of fibrin. It has been also found that intra-alveolar red blood cells were frequently present in the alveolar spaces, surrounded by a reticular fibrin network, suggestive for fibrin-hemorrhagic alveolitis. Alveolar changes were constantly associated with pathological features related to the pulmonary vessels. Vascular changes were prominent, including endothelial damage and thrombosis of large pulmonary vessels. Fibrinous microthrombi were frequently detected in the inter-alveolar septal capillaries. In addition, it has been frequently detected capillary proliferation in the alveolar septa with finding suggestive for intussusceptive neo-angiogenesis. CONCLUSIONS: In conclusion, our electron microscopy analysis showed that COVID-19-related lung disease is characterized by a substantial architectural distortion, with the interactions between alveolar and vascular changes. Intra-alveolar hyaline membranes are associated with macro-and micro-thrombotic angiopathy, ending with capillary proliferation. The new blood vessel formation originates from the septa and extends into the surrounding parenchyma. Our findings confirm previous reports on the specificity of the multiple and complex morphological pattern typical, and apparently specific, of COVID-19-related lung disease.

HemaSphere ; 5(SUPPL 2):373-374, 2021.
Article in English | EMBASE | ID: covidwho-1393423


Background: Knowledge on the immunopathobiology of COVID-19 is rapidly increasing but most studies analyzed relatively small series of patients and immune features predictive of fatal outcome are unavailable for routine stratification. Furthermore, an increased risk of death in patients with hematological cancer infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been identified, but it remains unknown if this is related to possible immunosuppression caused by cancer itself and cytotoxic treatment. Aims: Characterize the immune response to SARS-CoV-2 in a large cohort of patients to identify high-risk immune biomarkers and evaluate the association between COVID-19 severity and immunosuppression in patients with hematological cancer. Methods: Multidimensional flow cytometry was used to conduct holistic and unbiased analyses of17 immune cell types on 780 peripheral blood samples obtained from 513 COVID-19 patients, 24 cases with non-SARS-CoV-2 infection and 36 age-matched healthy adults.167 COVID-19 patients had 207 longitudinal samples collected over time. RNA sequencing on FACSorted cells and high-resolution flow cytometry were used to perform a deeper characterization of various myeloid and lymphoid subsets in14 COVID-19 patients and4 healthy adults. Results: Immune profiles of COVID-19 patients were generally similar to those of age-matched patients with non-SARS-CoV-2 infection, but significantly different from those of age-matched healthy adults. When compared to the later, COVID-19 patients showed increased percentages of neutrophils, CD4+CD56+ T-cells, and plasmablasts, whereas levels of basophils, eosinophils, and non-classical monocytes, as well as double-negative, CD8loCD56-, CD8-/loCD56+ and CD8hiCD56- T-cells, and B-cells were decreased. Both transcriptional and immunophenotypic data in myeloid and lymphoid subsets suggested an association between COVID-19 severity and neutrophil activation, as well as significantly reduced levels of specific adaptive immune cell types. Unsupervised clustering analysis of 513 patients revealed three immunotypes in response to SARS-CoV-2 infection. One of them, present in14% of patients (n=74), was characterized by significantly lower percentages of all immune cell types except neutrophils and plasmablasts, and was significantly associated with more severe disease. Of note, 50% of COVID-19 patients with blood cancer displayed this immunotype. Accordingly, hematological patients showed a significantly higher frequency of admission into intensive care units (50% vs 5%, P<.001) and death (30% vs4%, P<.001) than patients without tumor did. On multivariate analysis incorporating age and comorbidities, the frequency of B-cells and non-classical monocytes were independent prognostic factors for overall survival. Indeed, <1% B-cells in peripheral blood was most strongly associated with risk of death. Among patients with immune monitoring during follow-up, significant changes in the relative distribution of eight immune cell types, including basophils, CD8loCD56- T-cells, and B-cells, were observed from the first to last peripheral blood sample between patients who survived or died. Summary/Conclusion: Our results accelerate our understanding of the immunopathobiology of COVID-19 and unveil an association between altered immune profiles in patients with hematological cancer and their poorer outcome. Reduced percentages of B-cells and non-classical monocytes are high-risk immune biomarkers that could be readily implemented in routine practice for risk-stratification of COVID-19.