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Purpose: We quantified lung glycolytic metabolic activity, clinical symptoms and inflammation, coagulation, and endothelial activation biomarkers in 2019 coronavirus disease (COVID-19) pneumonia survivors., Methods: Adults previously hospitalized with moderate to severe COVID-19 pneumonia were prospectively included. Subjects filled out a questionnaire on clinical consequences, underwent chest CT and 18 F-FDG PET/CT, and provided blood samples on the same day. Forty-five volunteers served as control subjects. Analysis of CT images and quantitative voxel-based analysis of PET/CT images were performed for both groups. 18 F-FDG uptake in the whole-lung volume and in high- and low-attenuation areas was calculated and normalized to liver values. Quantification of plasma markers of inflammation (interleukin 6), d -dimer, and endothelial cell activation (angiopoietins 1 and 2, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1) was also performed., Results: We enrolled 53 COVID-19 survivors (62.3% were male; median age, 50 years). All survivors reported at least 1 persistent symptom, and 41.5% reported more than 6 symptoms. The mean lung density was greater in survivors than in control subjects, and more metabolic activity was observed in normal and dense lung areas, even months after symptom onset. Plasma proinflammatory, coagulation, and endothelial activation biomarker concentrations were also significantly higher in survivors., Conclusion: We observed more metabolic activity in areas of high and normal lung attenuation several months after moderate to severe COVID-19 pneumonia. In addition, plasma markers of thromboinflammation and endothelial activation persisted. These findings may have implications for our understanding of the in vivo pathogenesis and long-lasting effects of COVID-19 pneumonia., Competing Interests: Conflicts of interest and sources of funding: The authors declare that they have no conflicts of interest. This work was supported by grants from the D'Or Institute for Research and Education, Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (numbers E-26/202.751/2018, E-26/202.785/2017, E-26/203.001/2018, E-26/203.279/2017, and E-26/211.867/2016), and Conselho Nacional de Desenvolvimento Científico e Tecnológico (numbers 02839/2017-8, 302702/2017-2, and 312410/2017-4)., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Liver test abnormalities are frequently observed in patients with coronavirus disease 2019 (COVID-19) and are associated with worse prognosis. However, information is limited about pathological changes in the liver in this infection, so the mechanism of liver injury is unclear. Here we describe liver histopathology and clinical correlates of 27 patients who died of COVID-19 in Manaus, Brazil. There was a high prevalence of liver injury (elevated alanine aminotransferase and aspartate aminotransferase in 44% and 48% of patients, respectively) in these patients. Histological analysis showed sinusoidal congestion and ischemic necrosis in more than 85% of the cases, but these appeared to be secondary to systemic rather than intrahepatic thrombotic events, as only 14% and 22% of samples were positive for CD61 (marker of platelet activation) and C4d (activated complement factor), respectively. Furthermore, the extent of these vascular findings did not correlate with the extent of transaminase elevations. Steatosis was present in 63% of patients, and portal inflammation was present in 52%. In most cases, hepatocytes expressed angiotensin-converting enzyme 2 (ACE2), which is responsible for binding and entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), even though this ectoenzyme was minimally expressed on hepatocytes in normal controls. However, SARS-CoV-2 staining was not observed. Most hepatocytes also expressed inositol 1,4,5-triphosphate receptor 3 (ITPR3), a calcium channel that becomes expressed in acute liver injury. Conclusion: The hepatocellular injury that commonly occurs in patients with severe COVID-19 is not due to the vascular events that contribute to pulmonary or cardiac damage. However, new expression of ACE2 and ITPR3 with concomitant inflammation and steatosis suggests that liver injury may result from inflammation, metabolic abnormalities, and perhaps direct viral injury., (© 2021 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of American Association for the Study of Liver Diseases.)

Background: Coronavirus disease (COVID-19) is caused by SARS-COV2, a highly transmissible and pathogenic viral infection, and was identified in December 2019 in Wuhan, China. Three months later, it became a severe pandemic., Objective: To identify scientific evidence on the use of face shields by health professionals during the COVID-19 pandemic period., Method: An integrative literature review of articles obtained from PubMed, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science databases was undertaken. For the search, controlled, non-controlled descriptors and specific keywords: "face shield," "fluid resistance procedure," "respiratory infections," "healthcare workers," "COVID-19," "aerosols," and "personal protection infection" were used., Results: The sample comprised seven studies. The available evidence has shown that face shields do not have a defined standard for their production-their effectiveness depends on the quality of the visor, structure, and fixation system. They must be used as adjuvants to other personal protective equipment (PPE), and their isolated use is not recommended due to the fragilities of peripheral face sealing, especially during the COVID-19 pandemic period., Conclusion: Due to the shortage of this equipment, domestic face shields can be indicated if they meet production requirements, based on scientific evidence for their efficient use.

The COVID-19 pandemic brings to light the reality of the Brazilian health system. The underreporting of COVID-19 deaths in the state of Minas Gerais (MG), where the second largest population of the country is concentrated, reveals government unpreparedness, as there is a low capacity of testing in the population, which prevents the real understanding of the general panorama of SARS-CoV-2 dissemination. The goals of this research are to analyze the causes of deaths in different Brazilian government databases (Civil Registry Transparency Portal and InfoGripe) and to assess whether there are sub-records showing an unexpected increase in the frequency of deaths from causes clinically similar to COVID-19. A descriptive and quantitative analysis of the number of deaths by COVID-19 and similar causes was performed in different databases. Our results demonstrate that different official sources had a discrepancy of 109.45% between these data referring to the same period. There was also a 758.57% increase in SARI deaths in 2020, when compared to the average of previous years. Finally, it was shown that there was an increase in the rate of pneumonia and respiratory insufficiency (RI) by 6.34 and 6.25%, respectively. In conclusion, there is an underreporting of COVID-19 deaths in MG due to the unexplained excess of deaths caused by SARI, respiratory insufficiency, and pneumonia compared to previous years., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2020 Alves, Souza, Silva, Ramos and Oliveira.)