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Objectives: COVID-19 viral pneumonia can result in increased arterial stiffness, along with cardiac and systemic inflammatory responses. This study aimed to investigate the association between arterial stiffness, inflammation severity, and all-cause mortality in patients with COVID-19., Methods: In this study, anthropometric data, pneumonia infection severity, and blood tests were analyzed. Arterial stiffness was assessed using the non-invasive assessment indices, including arterial velocity pulse index (AVI) and central arterial pulse pressure (CAPP). Infection volumes and percentages for the whole lungs, most lobes, and most segments were extracted from CT images using artificial intelligence-based quantitative analysis software. The relationship between arterial stiffness, central hemodynamics, and all-cause mortality was investigated., Results: In multivariable Cox regression analysis, high CAPP was significantly associated with all-cause mortality (hazard ratio: 0.263, 95% CI, 0.073-0.945, p = 0.041). Whole lung infection percentages were independently associated with high CAPP, with an area under the curve (AUC) of 0.662 and a specificity of 89.09%., Conclusions: High CAPP, but not high AVI, demonstrated independent prognostic value for all-cause mortality in patients due to COVID-19 pneumonia infection. Evaluating this parameter could help in risk assessment and improve diagnostic and therapeutic strategies in viral pneumonia infections., (© 2024. The Author(s).)

This work proposes a modelling framework to analyse flow and pressure distributions throughout the lung of mechanically ventilated COVID-19 patients. The methodology involves: segmentation of the lungs and major airways from patient CT images; a volume filling algorithm that creates a dichotomous airway network in the remaining volume of the lung; an estimate of resistance and compliance within the lung based on Hounsfield unit values from the CT scan; and a computational fluid dynamics model to analyse flow, lung inflation, and pressure throughout the airway network. Mechanically ventilated patients with differing progression and severity of the disease were simulated. The results indicate that the flow distribution within the lung can be significantly affected when there are competing types of lung damage. These competing types are primarily fibrosis-like lung damage that creates higher resistance and lower compliance in that region; and emphysema, which causes a decrease in resistance and increase in compliance. In a patient with severe disease, the model predicted an increase in inflation by 33% in an area affected by emphysema-like conditions. This could increase the risk of alveolar rupture. The framework could readily be adapted to study other respiratory diseases. Early interventions in critical respiratory care could be facilitated through such efficient patient-specific modelling approaches., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interests., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Objectives: Identifying voice handicap and voice-related quality of life in patients presenting pulmonary impairment associated with COVID-19 infection, comparing pulmonary parameters between these patients and individuals in the control group, as well as correlating pulmonary parameters to self-assessment questionnaires (IDV-10 and QVV)., Methods: Thirty-five (35) patients presenting pulmonary impairment with COVID-19 infection were herein selected and compared to 35 individuals who were not affected by COVID-19 infection. Two self-assessment questionnaires were applied (vocal handicap index and voice quality of life protocol). Maximum phonation time Forced Expiratory Pressure (PEF) and Forced Inspiratory Pressure (PIF) were measured and videolaryngoscopy was performed., Results: There was statistically significant difference in scores recorded in voice self-assessment questionnaires (IDV-10 and QVV), Expiratory Pressure (PEF) and Forced Inspiratory Pressure (PIF) between patients with pulmonary impairment associated with COVID-19 infection and those in the control group. Correlation between PEF/PIF and scores recorded in voice self-assessment questionnaires was also observed., Conclusion: Pulmonary impairment associated with COVID-19 infection has worsened voice handicap and voice-related quality of life in the assessed patients, as well as reduced their forced expiratory and inspiratory pressure in comparison to the control group., (Copyright © 2024 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier España S.L.U. All rights reserved.)

Objective: While coronavirus disease 2019 (COVID-19) is generally considered to exhibit a less severe clinical course in children than in adults, studies have demonstrated that respiratory symptoms can endure for more than 3 months following infection in at least one-third of pediatric cases. The present study evaluates the respiratory functions of children aged 3-15 years within 3-6 months of their recovery from COVID-19 using impulse oscillometry (IOS) and compares them with the values of healthy children., Methods: Included in this prospective cross-sectional study were 63 patients (patient group) aged 3-15 years who contracted COVID-19 between December 2021 and May 2022, as well as 57 healthy children as a control group, matched for age and sex. The demographic, clinical, and laboratory data of the patients were recorded, and respiratory function was assessed based on airway resistance (zR5, zR20, R5-20) and reactance (zX5, zX20, reactance area [AX], resonant frequency [Fres]) using an IOS device., Results: There were no significant differences in the age, weight, height, and body weight z score values of the two groups (p > .05). While the zR5 and R5-20 levels of the patient group were higher (p = .008 and p < .001, respectively) than those of the controls, the zR20, AX, and Fres values did not differ significantly between the groups (p > .05). The parameters indicating the reactance, including zX5 and zX20, were significantly lower in the patient group than in the control group (p = .028 and p < .001, respectively)., Conclusion: Total and peripheral airway resistances were found to be elevated in children who had recovered from COVID-19 in the preceding 3-6 months., (© 2024 The Authors. Pediatric Pulmonology published by Wiley Periodicals LLC.)

Importance: Self-report surveys suggest that long-lasting taste deficits may occur after SARS-CoV-2 infection, influencing nutrition, safety, and quality of life. However, self-reports of taste dysfunction are inaccurate, commonly reflecting deficits due to olfactory not taste system pathology; hence, quantitative testing is needed to verify the association of post-COVID-19 condition with taste function., Objective: To use well-validated self-administered psychophysical tests to investigate the association of COVID-19 with long-term outcomes in taste and smell function., Design, Setting, and Participants: This nationwide cross-sectional study included individuals with and without a prior history of COVID-19 recruited from February 2020 to August 2023 from a social media website (Reddit) and bulletin board advertisements. In the COVID-19 cohort, there was a mean of 395 days (95% CI, 363-425 days) between diagnosis and testing., Exposure: History of COVID-19., Main Outcomes and Measures: The 53-item Waterless Empirical Taste Test (WETT) and 40-item University of Pennsylvania Smell Identification Test (UPSIT) were used to assess taste and smell function. Total WETT and UPSIT scores and WETT subtest scores of sucrose, citric acid, sodium chloride, caffeine, and monosodium glutamate were assessed for groups with and without a COVID-19 history. The association of COVID-19 with taste and smell outcomes was assessed using analysis of covariance, χ2, and Fisher exact probability tests., Results: Tests were completed by 340 individuals with prior COVID-19 (128 males [37.6%] and 212 females [62.4%]; mean [SD] age, 39.04 [14.35] years) and 434 individuals with no such history (154 males [35.5%] and 280 females [64.5%]; mean (SD) age, 39.99 [15.61] years). Taste scores did not differ between individuals with and without previous COVID-19 (total WETT age- and sex-adjusted mean score, 33.41 [95% CI, 32.37-34.45] vs 33.46 [95% CI, 32.54-34.38]; P = .94). In contrast, UPSIT scores were lower in the group with previous COVID-19 than the group without previous COVID-19 (mean score, 34.39 [95% CI, 33.86-34.92] vs 35.86 [95% CI, 35.39-36.33]; P < .001]); 103 individuals with prior COVID-19 (30.3%) and 91 individuals without prior COVID-19 (21.0%) had some degree of dysfunction (odds ratio, 1.64 [95% CI, 1.18-2.27]). The SARS-CoV-2 variant present at the time of infection was associated with smell outcomes; individuals with original untyped and Alpha variant infections exhibited more loss than those with other variant infections; for example, total to severe loss occurred in 10 of 42 individuals with Alpha variant infections (23.8%) and 7 of 52 individuals with original variant infections (13.5%) compared with 12 of 434 individuals with no COVID-19 history (2.8%) (P < .001 for all)., Conclusions and Relevance: In this study, taste dysfunction as measured objectively was absent 1 year after exposure to COVID-19 while some smell loss remained in nearly one-third of individuals with this exposure, likely explaining taste complaints of many individuals with post-COVID-19 condition. Infection with earlier untyped and Alpha variants was associated with the greatest degree of smell loss.

Background: Coronavirus disease 2019 (COVID-19) has spread worldwide determining dramatic impacts on healthcare systems. Early identification of high-risk parameters is required in order to provide the best therapeutic approach. Coronary, thoracic aorta and aortic valve calcium can be measured from a non-gated chest computer tomography (CT) and are validated predictors of cardiovascular events and all-cause mortality. However, their prognostic role in acute systemic inflammatory diseases, such as COVID-19, has not been investigated., Objectives: The aim was to evaluate the association of coronary artery calcium and total thoracic calcium on in-hospital mortality in COVID-19 patients., Methods: 1093 consecutive patients from 16 Italian hospitals with a positive swab for COVID-19 and an admission chest CT for pneumonia severity assessment were included. At CT, coronary, aortic valve and thoracic aorta calcium were qualitatively and quantitatively evaluated separately and combined together (total thoracic calcium) by a central Core-lab blinded to patients' outcomes., Results: Non-survivors compared to survivors had higher coronary artery [Agatston (467.76 ​± ​570.92 vs 206.80 ​± ​424.13 ​mm 2 , p ​< ​0.001); Volume (487.79 ​± ​565.34 vs 207.77 ​± ​406.81, p ​< ​0.001)], aortic valve [Volume (322.45 ​± ​390.90 vs 98.27 ​± ​250.74 mm 2 , p ​< ​0.001; Agatston 337.38 ​± ​414.97 vs 111.70 ​± ​282.15, p ​< ​0.001)] and thoracic aorta [Volume (3786.71 ​± ​4225.57 vs 1487.63 ​± ​2973.19 mm 2 , p ​< ​0.001); Agatston (4688.82 ​± ​5363.72 vs 1834.90 ​± ​3761.25, p ​< ​0.001)] calcium values. Coronary artery calcium (HR 1.308; 95% CI, 1.046-1.637, p ​= ​0.019) and total thoracic calcium (HR 1.975; 95% CI, 1.200-3.251, p ​= ​0.007) resulted to be independent predictors of in-hospital mortality., Conclusion: Coronary, aortic valve and thoracic aortic calcium assessment on admission non-gated CT permits to stratify the COVID-19 patients in-hospital mortality risk., (Copyright © 2021 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

Background: The aim of the study is to estimate the prevalence of atelectasis assessed with computer tomography (CT) in SARS-CoV-2 pneumonia and the relationship between the amount of atelectasis with oxygenation impairment, Intensive Care Unit admission rate and the length of in-hospital stay., Patients and Methods: Two-hundred thirty-seven patients admitted to the hospital with SARS-CoV-2 pneumonia diagnosed by clinical, radiology and molecular tests in the nasopharyngeal swab who underwent a chest computed tomography because of a respiratory worsening from Apr 1 to Apr 30, 2020 were included in the study. Patients were divided into three groups depending on the presence and amount of atelectasis at the computed tomography: no atelectasis, small atelectasis (< 5% of the estimated lung volume) or large atelectasis (> 5% of the estimated lung volume). In all patients, clinical severity, oxygen-therapy need, Intensive Care Unit admission rate, the length of in-hospital stay and in-hospital mortality data were collected., Results: Thirty patients (19%) showed small atelectasis while eight patients (5%) showed large atelectasis. One hundred and seventeen patients (76%) did not show atelectasis. Patients with large atelectasis compared to patients with small atelectasis had lower SatO 2 /FiO 2 (182 vs 411 respectively, p = 0.01), needed more days of oxygen therapy (20 vs 5 days respectively, p = 0,02), more frequently Intensive Care Unit admission (75% vs 7% respectively, p < 0.01) and a longer period of hospitalization (40 vs 14 days respectively p < 0.01)., Conclusion: In patients with SARS-CoV-2 pneumonia, atelectasis might appear in up to 24% of patients and the presence of larger amount of atelectasis is associated with worse oxygenation and clinical outcome., (© 2021. The Author(s).)

Objective: Respiratory failure is the leading cause of mortality in COVID-19 patients, characterized by a generalized disbalance of inflammation. The aim of this study was to investigate the relationship between immune-inflammatory index and mortality in PSI IV-V patients with COVID-19., Methods: We retrospectively reviewed the medical records of COVID-19 patients from Feb. to Apr. 2020 in the Zhongfa Xincheng Branch of Tongji Hospital, Wuhan, China. Patients who presented high severity of COVID-19-related pneumonia were enrolled for further analysis according to the Pneumonia Severity Index (PSI) tool., Results: A total of 101 patients diagnosed with COVID-19 were identified at initial research. The survival analysis revealed that mortality of the PSI IV-V cohort was significantly higher than the PSI I-III group ( p = 0.0003). The overall mortality in PSI IV-V patients was 32.1% (9/28). The fatal cases of the PSI IV-V group had a higher level of procalcitonin ( p = 0.022) and neutrophil-to-lymphocyte ratio ( p = 0.033) compared with the survivors. Procalcitonin was the most sensitive predictor of mortality for the severe COVID-19 population with area under receiver operating characteristic curve of 0.78, higher than the neutrophil-to-lymphocyte ratio (0.75) and total lymphocyte (0.68) and neutrophil (0.67) counts., Conclusion: Procalcitonin and neutrophil-to-lymphocyte ratio may potentially be effective predictors for mortality in PSI IV-V patients with COVID-19. Increased procalcitonin and neutrophil-to-lymphocyte ratio were associated with greater risk of mortality., Competing Interests: The authors declare that this research was conducted in the absence of commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Rui Han et al.)

Previous studies have suggested that COVID-19 pneumonia is associated with an increased risk of venous thromboembolism (VTE). This study aimed to investigate the incidence of VTE among mechanically ventilated adults with COVID-19 pneumonia, compared to patients with respiratory failure related to other causes. Prospective study that enrolled critically ill adults with suspected COVID-19 pneumonia between June 2, 2020 and August 11, 2020. Critically ill adults with suspected COVID-19 pneumonia who required mechanical ventilation within 24 h after hospital admission were followed until death or hospital discharge. Sequential ultrasonography screening of the lower extremities and catheter insertion sites, as well as testing for plasma biochemical markers, were performed at the intensive care unit admission, day 3, day 7, and day 14. The primary outcome was a composite of deep venous thrombosis, pulmonary embolism, and thrombosis at the central catheter insertion sites. We enrolled 70 patients, including 57 patients with COVID-19 and 13 patients without COVID-19, and all patients completed follow-up. The incidence of the primary outcome was higher among patients with COVID-19 than among patients with respiratory failure related to other etiologies (36.8% vs. 0%, p = 0.023). Multivariate regression analysis revealed that VTE was independently associated with a COVID-19 diagnosis (odds ratio: 6.28, 95% confidence interval: 1.19-68.07) and D-dimer concentration (1-ng/mL increase, odds ratio: 1.15, 95% confidence interval: 1.05-1.30). The incidence of VTE was higher among critically ill mechanically ventilated patients, relative to among patients with respiratory failure related to other causes., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.)

During the second wave of the COVID-19 pandemic in South Africa, a recurrent pattern of prolonged recovery after acute COVID-19 pneumonia, characterised by low oxygen saturation levels for &gt;2 weeks, was observed in an intermediate-care facility in Cape Town. A case study together with a series of 12 patients is presented to illustrate this phenomenon, and two types of 'sats gap' are described, which were used by physiotherapists and doctors to monitor daily progress. We attempt to explain this prolonged recovery in terms of the possible pathophysiology, and suggest a number of learning points to guide further research.

Introduction: The novel coronavirus SARS-Cov-2 can infect the respiratory tract causing a spectrum of disease varying from mild to fatal pneumonia, and known as COVID-19. Ongoing clinical research is assessing the potential for long-term respiratory sequelae in these patients. We assessed the respiratory function in a cohort of patients after recovering from SARS-Cov-2 infection, stratified according to PaO 2 /FiO 2 (p/F) values., Method: Approximately one month after hospital discharge, 86 COVID-19 patients underwent physical examination, arterial blood gas (ABG) analysis, pulmonary function tests (PFTs), and six-minute walk test (6MWT). Patients were also asked to quantify the severity of dyspnoea and cough before, during, and after hospitalization using a visual analogic scale (VAS). Seventy-six subjects with ABG during hospitalization were stratified in three groups according to their worst p/F values: above 300 (n = 38), between 200 and 300 (n = 30) and below 200 (n = 20)., Results: On PFTs, lung volumes were overall preserved yet, mean percent predicted residual volume was slightly reduced (74.8 ± 18.1%). Percent predicted diffusing capacity for carbon monoxide (DLCO) was also mildly reduced (77.2 ± 16.5%). Patients reported residual breathlessness at the time of the visit (VAS 19.8, p < 0.001). Patients with p/F below 200 during hospitalization had lower percent predicted forced vital capacity (p = 0.005), lower percent predicted total lung capacity (p = 0.012), lower DLCO (p < 0.001) and shorter 6MWT distance (p = 0.004) than patients with higher p/F., Conclusion: Approximately one month after hospital discharge, patients with COVID-19 can have residual respiratory impairment, including lower exercise tolerance. The extent of this impairment seems to correlate with the severity of respiratory failure during hospitalization., (© 2021. The Author(s).)

Recent publications on the probable role of heparin-binding protein (HBP) as a biomarker in sepsis prompted us to investigate its diagnostic and prognostic performance in severe COVID-19. HBP and IL-6 were measured by immunoassays at admission and on day 7 in 178 patients with pneumonia by SARS-CoV-2. Patients were classified into non-sepsis and sepsis as per the Sepsis-3 definitions and were followed up for the development of severe respiratory failure (SRF) and for outcome. Results were confirmed by multivariate analyses. HBP was significantly higher in patients classified as having sepsis and was negatively associated with the oxygenation ratio and positively associated with creatinine and lactate. Logistic regression analysis evidenced admission HBP more than 18 ng/ml and IL-6 more than 30 pg/ml as independent risk factors for the development of SRP. Their integration prognosticated SRF with respective sensitivity, specificity, positive predictive value, and negative predictive 59.1%, 96.3%, 83.9%, and 87.8%. Cox regression analysis evidenced admission HBP more than 35 ng/ml and IL-6 more than 30 pg/ml as independent risk factors for 28-day mortality. Their integration prognosticated 28-day mortality with respective sensitivity, specificity, positive predictive value, and negative predictive value 69.2%, 92.7%, 42.9%, and 97.5%. HBP remained unchanged over-time course. A prediction score of the disposition of patients with COVID-19 is proposed taking into consideration admission levels of IL-6 and HBP. Using different cut-offs, the score may predict the likelihood for SRF and for 28-day outcome.

Abstract: The coronavirus disease 2019 pandemic has escalated clinical needs while interrupting regular processes and straining resources. Striving to deliver optimal care to infected patients with respiratory failure, Rush University Medical Center in Chicago created a multidisciplinary team to provide manual prone positioning safely and efficiently. Team members' experiences, which they shared through a survey, help to illustrate the advantages of a multidisciplinary approach and suggest opportunities to enhance the effectiveness of such a team., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

It has been reported that myocardial damage and heart failure are more common in COVID-19 patients with severe symptoms. The aim of our study was to measure the right ventricular functions of COVID-19 patients 30 days after their discharge, and compare them to the right ventricular functions of healthy volunteers. Fifty one patients with COVID-19 and 32 healthy volunteers who underwent echocardiographic examinations were enrolled in our study. 29 patients were treated for severe and 22 patients were treated for moderate COVID-19 pneumonia. The study was conducted prospectively, in a single center, between 15 May 2020 and 15 July 2020. We analyzed the right ventricular functions of the patients using conventional techniques and two-dimensional speckle-tracking. Right ventricular end-diastolic and end-systolic area were statistically higher than control group. The right ventricular fractional area change (RVFAC) was significantly lesser in the patient group compared to the control group. Tricuspid annular plane systolic motion (TAPSE) was within normal limits in both groups, it was lower in the patient group compared to the control group. Pulmonary artery pressure was found to be significantly higher in the patient group. Right ventricular global longitudinal strain (RV-GLS) was lesser than the control group (- 15.7 [(- 12.6)-(- 18.7)] vs. - 18.1 [(- 14.8)-(- 21)]; p 0.011). Right ventricular free wall strain (RV-FWS) was lesser in the patient group compared to the control group (- 16 [(- 12.7)-(- 19)] vs - 21.6 [(- 17)-(- 25.3)]; p < 0.001). We found subclinical right ventricular dysfunction in the echocardiographies of COVID-19 patients although there were no risk factors.

Background: Knowledge about SARS-CoV-2 infection in pregnancy and newborns is scarce. The objective of this study is to analyse clinical and epidemiological characteristics of a cohort of women infected with SARS-CoV-2 during pregnancy and their newborns exposed to SARS-CoV-2 during gestation., Methods: Multicentric observational study of Spanish hospitals from the GESNEO-COVD cohort, participants in RECLIP (Spanish Network of Paediatric Clinical Assays). Women with confirmed SARS-CoV-2 infection by PCR and/or serology during pregnancy, diagnosed and delivering during the period 15/03/2020-31/07/2020 were included. Epidemiological, clinical, and analytical data was collected., Results: A total of 105 pregnant women with a median of 34.1 years old (IQR: 28.8-37.1) and 107 newborns were included. Globally, almost 65% of pregnant women had some COVID-19 symptoms and more than 43% were treated for SARS-COV-2. Overall, 30.8% of pregnant women had pneumonia and 5 (4.8%) women were admitted to the intensive care unit needing invasive mechanical ventilation. There was a rate of 36.2% of caesarean sections, which was associated with pneumonia during pregnancy (OR: 4.203, CI 95%: 1.473-11.995) and lower gestational age at delivery (OR: 0.724, CI 95%: 0.578-0.906). The prevalence of preterm birth was 20.6% and prematurity was associated with pneumonia during gestation (OR: 6.970, CI95%: 2.340-22.750) and having a positive SARS-CoV-2 PCR at delivery (OR: 6.520, CI95%: 1.840-31.790). All nasopharyngeal PCR in newborns were negative at birth and one positivized at 15 days of life. Two newborns died, one due to causes related to prematurity and another of unexpected sudden death during early skin-to-skin contact after delivery., Conclusions: Although vertical transmission has not been reported in this cohort, the prognosis of newborns could be worsened by SARS-CoV-2 infection during pregnancy as COVID-19 pneumonia increased the risk of caesarean section deliveries and preterm births.

Background: Platypnea-orthodeoxia syndrome (POS) is a rare condition characterized by dyspnoea (platypnea) and arterial desaturation in the upright position resolved in the supine position (orthodeoxia). Intracardiac shunt, pulmonary ventilation-perfusion mismatch and others intrapulmonary abnormalities are involved., Case Presentation: We report a case of POS associated with two pathophysiological issues: one, cardiac POS caused by a patent foramen ovale (PFO) and second, pulmonary POS due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) interstitial pneumonia. POS has resolved after recovery of coronavirus disease 2019 (COVID-19) pneumonia., Conclusions: Right-to-left interatrial shunt and intrapulmonary shunt caused by SARS-CoV-2 pneumonia contributed to refractory hypoxemia and POS. Therefore, in case of COVID-19 patient with unexplained POS, the existence of PFO must be investigated.

Rationale: Northern Italy has been particularly hit by the current Covid-19 pandemic. Italian deceased patients have a mean age of 78.5 years and only 1.2% have no comorbidities. These data started a public debate whether patients die "with" or "from" Covid-19. If on one hand the public opinion has been persuaded to believe that Covid-19 infection has poor outcomes just in elderly and/or fragile subjects, on the other hand, hospitals are admitting an increasing number of healthy young patients needing semi-intensive or intensive care units., Patient Concerns: At the end of March 2020, a 79-year-old patient (M.G.) was admitted to the emergency department of our hospital with a 5 days history of fever, dyspnea, and cough. He was known for hypertension and coronary artery disease with a previous coronary artery stenting. Both the comorbidities were carried out without complications and the patient was previously asymptomatic and in good health. At admission, he was febrile and showed signs of respiratory failure with hypoxia and hypocapnia at blood gas analysis., Diagnosis: The day after, he was tested for SARS-CoV-2 with a real-time reverse transcriptase-polymerase chain reaction assay of nasopharyngeal swab, which turned positive and a chest CT-Scan was consistent with the diagnosis of interstitial pneumonia., Interventions: He was treated with i.v. diuretics, paracetamol, prolonged noninvasive ventilation (CPAP), and empiric antibiotic therapy on top of his chronic treatment., Outcomes: A treatment with heparin and corticosteroids was started; however, he developed irreversible respiratory failure. Invasive ventilation was not considered appropriate due to his comorbidities, low chances of recovery, and intensive care unit overcrowding. The patient died 9 days after admission., Lessons: Health conditions that are most reported as risk factors are common cardiovascular diseases that can be managed in modern clinical practice. Through a brief illustrative clinical case, we would like to underline how Covid-19 can be per se the cause of death in patients that would otherwise have had an acceptable life expectancy., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection has rapidly spread throughout the world since December 2019 to become a global public health emergency for the elevated deaths and hospitalizations in Intensive Care Units. The severity spectrum of SARS-CoV-2 pneumonia ranges from mild to severe clinical conditions. The clinical course of SARS-CoV-2 disease is correlated with multiple factors including host characteristics (genetics, immune status, age, and general health), viral load and, above all, the host distribution of the airways and lungs of the viral receptor cells. In this review, we will briefly summarize the current knowledge of the characteristics and management of coronavirus disease 2019-pneumonia. However, other studies are needed to better understand the pathogenetic mechanisms induced by SARS-Cov-2 infection, and to evaluate the long-term consequences of the virus on the lungs., (© 2020 Wiley Periodicals LLC.)

Older adults are far more vulnerable to adverse health outcomes and mortality after contracting COVID-19. There are likely multiple age-related biological, clinical, and environmental reasons for this increased risk, all of which are exacerbated by underlying age-associated changes to the immune system as well as increased prevalence of chronic disease states in older adults. Innate immune system overactivity, termed the cytokine storm, appears to be critical in the development of the worst consequences of COVID-19 infection. Pathophysiology suggests that viral stimulation of the innate immune system, augmented by inflammatory signals sent from dying cells, ramps up into a poorly controlled outpouring of inflammatory mediators. Other aging-related changes in cells such as senescence as well as higher prevalence of chronic disease states also likely ramp up inflammatory signaling. This in turn drives downstream pathophysiological changes to pulmonary, cardiovascular, skeletal muscle, and brain tissues that drive many of the adverse health outcomes observed in older adults. This article provides an overview of the underlying etiologies of innate immune system activation and adaptive immune system dysregulation in older adults and how they potentiate the consequences of the COVID-19-related cytokine storm, and possible uses of this knowledge to develop better risk assessment and treatment monitoring strategies., (© The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: COVID-19 has had a disproportionate impact on older adults. Mexico's population is younger, yet COVID-19's impact on older adults is comparable to countries with older population structures. Here, we aim to identify health and structural determinants that increase susceptibility to COVID-19 in older Mexican adults beyond chronological aging., Methods: We analyzed confirmed COVID-19 cases in older adults using data from the General Directorate of Epidemiology of Mexican Ministry of Health. We modeled risk factors for increased COVID-19 severity and mortality, using mixed models to incorporate multilevel data concerning healthcare access and marginalization. We also evaluated structural factors and comorbidity profiles compared to chronological age for COVID-19 mortality risk prediction., Results: We analyzed 20 804 confirmed SARS-CoV-2 cases in adults aged 60 and older. Male sex, smoking, diabetes, and obesity were associated with pneumonia, hospitalization, and intensive care unit (ICU) admission in older adults, CKD and COPD were associated with hospitalization. High social lag indexes and access to private care were predictors of COVID-19 severity and mortality. Age was not a predictor of COVID-19 severity in individuals without comorbidities and combination of structural factors and comorbidities were better predictors of COVID-19 lethality and severity compared to chronological age alone. COVID-19 baseline lethality hazards were heterogeneously distributed across Mexican municipalities, particularly when comparing urban and rural areas., Conclusions: Structural factors and comorbidity explain excess risk for COVID-19 severity and mortality over chronological age in older Mexican adults. Clinical decision-making related to COVID-19 should focus away from chronological aging onto more a comprehensive geriatric care approach., (© The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

The current pandemic of COVID-19 caused thousands of deaths and healthcare professionals struggle to properly manage infected patients. This review summarizes information about SARS-CoV-2 receptor binding dynamics and intricacies, lung autopsy findings, immune response patterns, evidence-based explanations for the immune response, and COVID-19-associated hypercoagulability.

Abstract: In this cross-sectional study, we evaluated skeletal muscle strength and physical performance (1-min sit-to-stand and short physical performance battery tests), dyspnea, fatigue, and single-breath counting at discharge from a postacute COVID department, in patients recovering from COVID-19 pneumonia who had no locomotor disability before the infection.Quadriceps and biceps were weak in 86% and 73% of the patients, respectively. Maximal voluntary contraction for quadriceps was 18.9 (6.8) kg and for biceps 15.0 (5.5) kg (i.e., 54% and 69% of the predicted normal value, respectively). The number of chair rises in the 1-min sit-to-stand test was 22.1 (7.3 corresponding to 63% of the predicted normal value), whereas the short physical performance battery score was 7.9 (3.3 corresponding to 74% of the predicted normal value). At the end of the 1-min sit-to-stand test, 24% of the patients showed exercise-induced desaturation. The single-breath counting count was 35.4 (12.3) corresponding to 72% that of healthy controls. Mild-to-moderate dyspnea and fatigue were found during activities of daily living (Borg scale score, median value = 0.5 [0-2] and 1 [0-2]) and after the 1-min sit-to-stand (Borg scale score, median value = 3 [2-5] and 1 [0-3]). Significant correlations were observed between muscle strength and physical performance indices (R = 0.31-0.69).The high prevalence of impairment in skeletal muscle strength and physical performance in hospitalized patients recovering from COVID-19 pneumonia without previous locomotor disabilities suggests the need for rehabilitation programs after discharge., Competing Interests: Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Human adenoviruses (HAdV) infection caused pneumonia remains a major threat to global children health. Currently, diagnosis of severe HAdV pneumonia in children is hampered by the lack of specific biomarkers. Also, the severity of adenovirus pneumonia in pediatric patients is generally based on clinical features and existing biomarkers do not reliably correlate to clinical severity. Here, we asked whether local and systemic inflammatory mediators could act as biomarkers predicting severe HAdV pneumonia in children., Methods: Totally 37 common inflammatory protein levels were determined by Luminex assay in plasma and bronchoalveolar lavage (BAL) from pediatric patients who were diagnosed with HAdV pneumonia, and their correlation with the disease severity and lung lesion were assessed using statistical and bioinformatic analysis., Results: Among 37 inflammatory cytokines, the protein levels of 4 TNF superfamily (TNFSF) members and their receptors (TNF receptor superfamily, TNFRSF) [TNFSF13B, TNFSF14, sTNF-R1 and sTNF-R2] in the plasma and 7 TNFSF/TNFRSF members [TNFSF12, TNFSF13, TNFSF13B, TNFSF14, TNFRSF8, sTNF-R1, and sTNF-R2] in the BAL were enhanced in patients with HAdV pneumonia compared with control subjects with airway foreign body. Moreover, the protein levels of all the tested TNFSF/TNFRSF members (except TNFSF12) were elevated in the BAL of severe group compared with non-severe HAdV pneumonia patients, while only TNFSF13B and TNFSF14 were dramatically increased in the plasma of severe cases, and positively related to the plasma CRP levels. In addition, ROC analysis indicated that TNFSF13B and TNFSF14 displayed a great potential to predict severe HAdV pneumonia., Conclusion: In pediatric HAdV pneumonia, TNFSF/TNFRSF members function as key molecules in local and systemic inflammatory network, and the plasma TNFSF13B and TNFSF14 may be the potential local and systemic inflammatory indicators of severe HAdV pneumonia in pediatric patients., 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 © 2021 Fan, Lu, Cao, Li, Yang, Huang, Ding, Wu and Lu.)

COVID-19, a novel coronavirus-related illness, has spread worldwide. Patients with apparently mild/moderate symptoms can suddenly develop severe pneumonia. Therefore, almost all COVID-19 patients require hospitalization, which can reduce limited medical resources in addition to overwhelming medical facilities. To identify predictive markers for the development of severe pneumonia, a comprehensive analysis of serum chemokines and cytokines was conducted using serial serum samples from COVID-19 patients. The expression profiles were analyzed along the time axis. Serum samples of common diseases were enrolled from a BioBank to confirm the usefulness of predictive markers. Five factors, IFN-λ3, IL-6, IP-10, CXCL9, and CCL17, were identified as predicting the onset of severe/critical symptoms. The factors were classified into two categories. Category A included IFN-λ3, IL-6, IP-10, and CXCL9, and their values surged and decreased rapidly before the onset of severe pneumonia. Category B included CCL17, which provided complete separation between the mild/moderate and the severe/critical groups at an early phase of SARS-CoV-2 infection. The five markers provided a high predictive value (area under the receiver operating characteristic curve (AUROC): 0.9-1.0, p < 0.001). Low expression of CCL17 was specifically observed in pre-severe COVID-19 patients compared with other common diseases, and the predictive ability of CCL17 was confirmed in validation samples of COVID-19. The factors identified could be promising prognostic markers to distinguish between mild/moderate and severe/critical patients, enabling triage at an early phase of infection, thus avoiding overwhelming medical facilities., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Rationale: Coronavirus disease 2019 (COVID-19) has caused a global pandemic. A classifier combining chest X-ray (CXR) with clinical features may serve as a rapid screening approach. Methods: The study included 512 patients with COVID-19 and 106 with influenza A/B pneumonia. A deep neural network (DNN) was applied, and deep features derived from CXR and clinical findings formed fused features for diagnosis prediction. Results: The clinical features of COVID-19 and influenza showed different patterns. Patients with COVID-19 experienced less fever, more diarrhea, and more salient hypercoagulability. Classifiers constructed using the clinical features or CXR had an area under the receiver operating curve (AUC) of 0.909 and 0.919, respectively. The diagnostic efficacy of the classifier combining the clinical features and CXR was dramatically improved and the AUC was 0.952 with 91.5% sensitivity and 81.2% specificity. Moreover, combined classifier was functional in both severe and non-serve COVID-19, with an AUC of 0.971 with 96.9% sensitivity in non-severe cases, which was on par with the computed tomography (CT)-based classifier, but had relatively inferior efficacy in severe cases compared to CT. In extension, we performed a reader study involving three experienced pulmonary physicians, artificial intelligence (AI) system demonstrated superiority in turn-around time and diagnostic accuracy compared with experienced pulmonary physicians. Conclusions: The classifier constructed using clinical and CXR features is efficient, economical, and radiation safe for distinguishing COVID-19 from influenza A/B pneumonia, serving as an ideal rapid screening tool during the COVID-19 pandemic., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

Given the coronavirus disease 2019 (COVID-19) pandemic, investigations into host susceptibility to infectious diseases and downstream sequelae have never been more relevant. Pneumonia is a lung disease that can cause respiratory failure and hypoxia and is a common complication of infectious diseases, including COVID-19. Few genome-wide association studies (GWASs) of host susceptibility and severity of pneumonia have been conducted. We performed GWASs of pneumonia susceptibility and severity in the Vanderbilt University biobank (BioVU) with linked electronic health records (EHRs), including Illumina Expanded Multi-Ethnic Global Array (MEGA EX )-genotyped European ancestry (EA, n= 69,819) and African ancestry (AA, n = 15,603) individuals. Two regions of large effect were identified: the CFTR locus in EA (rs113827944; OR = 1.84, p value = 1.2 × 10 -36 ) and HBB in AA (rs334 [p.Glu7Val]; OR = 1.63, p value = 3.5 × 10 -13 ). Mutations in these genes cause cystic fibrosis (CF) and sickle cell disease (SCD), respectively. After removing individuals diagnosed with CF and SCD, we assessed heterozygosity effects at our lead variants. Further GWASs after removing individuals with CF uncovered an additional association in R3HCC1L (rs10786398; OR = 1.22, p value = 3.5 × 10 -8 ), which was replicated in two independent datasets: UK Biobank (n = 459,741) and 7,985 non-overlapping BioVU subjects, who are genotyped on arrays other than MEGA EX . This variant was also validated in GWASs of COVID-19 hospitalization and lung function. Our results highlight the importance of the host genome in infectious disease susceptibility and severity and offer crucial insight into genetic effects that could potentially influence severity of COVID-19 sequelae., (Copyright © 2020. Published by Elsevier Inc.)

Objective: To analyze the current scientific literature to document, in an integrative review, the main findings that correlate Kawasaki disease (KD) to COVID-19., Data Sources: The search was carried out in June 2020 in the following databases: Biblioteca Virtual em Saúde (BVS), periódico da CAPES and U.S National Library of Medicine (PubMed). The combination of descriptors used was [(COVID-19 OR SARS-CoV-2) AND (Kawasaki disease)], and the inclusion criteria stipulated were studies published from January 2019 to June 2020, without restriction of language or location, and available online in full. News, editorials, comments, and letters, as well as duplicates and articles that did not answer the guiding question were excluded., Data Synthesis: A total of 97 articles were identified, of which seven comprised this review. The association of KD to the new coronavirus appears to trigger a severe clinical condition of vasculitis. Different from the usual, in this inflammatory syndrome, patients are older, and prevalence is higher in children from African or Caribbean ancestry; clinical and laboratory manifestations are also atypical, with a predominance of abdominal complaints and exaggerated elevation of inflammatory markers. In addition, there was a greater report of rare complications and greater resistance to the recommended treatment for KD., Conclusions: Pediatric COVID-19 and its potential association to severe KD, still unfamiliar to health professionals, reinforces the importance of testing patients with vasculitis for the new coronavirus and the need to wage high surveillance and preparation of the health system during the current pandemic.

Objective: To investigate the relationship between maximal exercise capacity measured before severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and hospitalization due to coronavirus disease 2019 (COVID-19)., Methods: We identified patients (≥18 years) who completed a clinically indicated exercise stress test between January 1, 2016, and February 29, 2020, and had a test for SARS-CoV-2 (ie, real-time reverse transcriptase polymerase chain reaction test) between February 29, 2020, and May 30, 2020. Maximal exercise capacity was quantified in metabolic equivalents of task (METs). Logistic regression was used to evaluate the likelihood that hospitalization secondary to COVID-19 is related to peak METs, with adjustment for 13 covariates previously identified as associated with higher risk for severe illness from COVID-19., Results: We identified 246 patients (age, 59±12 years; 42% male; 75% black race) who had an exercise test and tested positive for SARS-CoV-2. Among these, 89 (36%) were hospitalized. Peak METs were significantly lower (P<.001) among patients who were hospitalized (6.7±2.8) compared with those not hospitalized (8.0±2.4). Peak METs were inversely associated with the likelihood of hospitalization in unadjusted (odds ratio, 0.83; 95% CI, 0.74-0.92) and adjusted models (odds ratio, 0.87; 95% CI, 0.76-0.99)., Conclusion: Maximal exercise capacity is independently and inversely associated with the likelihood of hospitalization due to COVID-19. These data further support the important relationship between cardiorespiratory fitness and health outcomes. Future studies are needed to determine whether improving maximal exercise capacity is associated with lower risk of complications due to viral infections, such as COVID-19., (Copyright © 2020 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.)

Background: The SARS-CoV-2 pneumonia infection is associated with high rates of hospitalization and mortality and this has placed healthcare systems under strain. Our study provides a novel method for the progress prediction, clinical treatment and prognosis of NCP, and has important clinical value for timely treatment of severe NCP patients., Objective: To summarize the clinical features and severe illness risk factors of the patients with novel coronavirus pneumonia (NCP), in order to provide support for the progression prediction, clinical treatment and prognosis of NCP patients., Materials and Methods: A total of 196 NCP patients treated in our hospital from January 25, 2020 to June 21, 2020 were divided into the severe group and the mild group. The clinical features of the two groups were analyzed and compared. The risk factors were explored by using multivariate logistic regression, and the receiver operating characteristic (ROC) curve was obtained. The correlations of the risk factors with the prognosis of NCP were investigated combined with the lung function test., Results: The primary clinical symptoms of 196 cases of NCP included fever in 167 cases (85.2%) and cough in 121 cases (61.73%). The chest computed tomography (CT) scans of the 178 cases (90.81%) showed a typical ground-glass opacification. In 149 cases, the lymphocyte count was decreased, while the levels of creatine kinase (CK), lactate dehydrogenase (LDH), c-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and D-dimer (D-D) increased. 44 cases (22.45%) were found to be severely ill. The multivariate logistic regression analysis demonstrated that age, underlying disease, length of hospital stay, body mass index (BMI), LDH, chest CT visual score, absolute lymphocyte count (ALC) and CRP were risk factors for severe.

The long-term sequelae of coronavirus disease 2019 (COVID-19) are still unknown. Lessons from past viral epidemics reveal that, after recovery, patients with viral pulmonary infections can suffer from irreversible pulmonary dysfunction and demonstrate residual imaging or functional abnormalities. Residual ground glass opacities, consolidations, reticular and linear opacities, residual crazy paving pattern, melted sugar sign, and parenchymal fibrotic bands are several features found in the late or remission stages of COVID-19. These radiologic findings have been observed weeks after symptom onset, even after hospital discharge, and they may or may not correlate with clinical manifestations. High-resolution CT may be indicated to establish new baselines and track changes in residual impairments. In our previous review, we observed significant pulmonary sequelae in some COVID-19 survivors at follow-up. In this update, we review the current literature on the clinical and radiologic manifestations of post-recovery COVID-19 toward the end of hospital admission and after discharge.

Background: Globally, the current medical emergency for novel coronavirus 2019 (COVID-19) leads to respiratory distress syndrome and death., Purpose: This review highlighted the effect of COVID-19 on systemic multiple organ failure syndromes. This review is intended to fill a gap in information about human physiological response to COVID-19 infections. This review may shed some light on other potential mechanisms and approaches in COVID -19 infections towards systemic multiorgan failure syndromes., Finding: SARS-CoV-2 intervened mainly in the lung with progression to pneumonia and acute respiratory distress syndrome (ARDS) via the angiotensin-converting enzyme 2(ACE2) receptor. Depending on the viral load, infection spread through the ACE2 receptor further to various organs such as heart, liver, kidney, brain, endothelium, GIT, immune cell, and RBC (thromboembolism). This may be aggravated by cytokine storm with the extensive release of proinflammatory cytokines from the deregulating immune system., Conclusion: The widespread and vicious combinations of cytokines with organ crosstalk contribute to systemic hyper inflammation and ultimately lead to multiple organ dysfunction (Fig. 1). This comprehensive study comprises various manifestations of different organs in COVID-19 and may assist the clinicians and scientists pertaining to a broad approach to fight COVID 19., (Copyright © 2020 Elsevier B.V. All rights reserved.)

COVID-19 pneumonia has a significant case fatality rate and no effective antiviral drugs are available even after 9 months of the pandemic. The spectrum of COVID-19 disease ranges from asymptomatic cases to severe ARDS with myriad manifestations. Here we report a case of a male patient with severe COVID-19 ARDS who improved after receiving standard therapy but again 'deteriorated' after being stepped down to ward. He complained of worsening shortness of breath and hypoxemia which was found to be mainly positional. After ruling out other causes, he was labeled as a case of platypnea-orthodeoxia syndrome due to underlying lung involvement.  It is important to be aware of this condition in the context of COVID-19 which can be easily diagnosed bedside with pulse oximetry.

Background: The clinical characteristics of patients with confirmed 2019 novel coronavirus disease (COVID-19) in Jilin Province, China were investigated., Methods: Clinical, laboratory, radiology, and treatment data of 41 hospitalized patients with confirmed COVID-19 were retrospectively collected. The population was stratified by disease severity as mild, moderate, or severe, based on guidelines of the National Health and Medical Commission of China., Results: The 41 hospitalized patients with COVID-19 were studied, and the median age was 45 years (interquartile range [IQR], 31-53; range, 10-87 years) and 18 patients (43.9%) were female. All of the patients had recently visited Wuhan or other places (ie, Beijing, Thailand) or had Wuhan-related exposure. Common symptoms included fever (32[78%]) and cough (29[70.7%]). All patients were without hepatitis B/C virus hepatitis. CRP (C-reactive protein, 11.3 mg/L [interquartile range {IQR}, 2.45-35.2]) was elevated in 22 patients (53.7%), and cardiac troponin I (1.5 ng/mL [IQR, 0.8-5.0]) was elevated in 41 patients (100%). Chest computed tomographic scans showed bilateral ground glass opacity (GGO) or GGO with consolidation in the lungs of 27(65.9%) patients. 31(75.6%) patients had an abnormal electrocardiograph (ECG). Comparing the three groups, the levels of CRP and cardiac troponin I, GGO distribution in bilateral lungs, and electrocardiogram changes were statistically significant (p < 0.05). Cardiac troponin I had a strong positive correlation with CRP (r = 0.704, p = 0.042) and LDH (r = 0.738, p = 0.037)., Conclusion: Significant differences among the groups suggest that several clinical parameters may serve as biomarkers of COVID-19 severity at hospital admission. Elevated cTnI could be considered as a predictor of severe COVID-19, reflecting the prognosis of patients with severe COVID-19. The results warrant further inspection and confirmation.

A role for the renin-angiotensin-aldosterone-system in Severe Acute Respiratory Syndrome-Coronavirus-2 infection and in the development of COronaVIrus Disease-19 disease has generated remarkable concerns among physicians and patients. Even though a suggestive pathophysiological link between renin-angiotensin-aldosterone-system and the virus has been proposed, its pathogenic role remains very difficult to be defined. Although COronaVIrus Disease-19 targets preferentially older people with high prevalence of hypertension and extensive use of renin-angiotensin-aldosterone-system inhibitors, an independent role for hypertension and its therapies is not defined. In this article, we scrutinize evidence from the most representative available studies in which the potential role of renin-angiotensin system inhibitors, specifically angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, was evaluated in the COronaVIrus Disease-19 disease course, with regard to severity of the disease and mortality. We conclude that at this time, the overall available evidence fails to support a pathogenetic speaks against any harmful role for of renin-angiotensin-aldosterone-system inhibitors in COronaVIrus Disease-19. Consequently, we conclude that treatment with renin-angiotensin-aldosterone-system inhibitors should not be discontinued and, therefore, these therapies should not be interrupted., (Copyright © 2020 Elsevier B.V. All rights reserved.)

During the COVID-19 outbreak, the mobile cabin hospital has effectively isolated and treated patients diagnosed as mild-moderate disease. However, a detailed clinical course has not been well described. We included 483 patients who were isolated and treated from Feb 6, 2020, to Feb 15, 2020, including definite outcome (discharge or deterioration). Sixty-two patients were transferred to severe cases, of whom were trasfered to designated hospital for intensive care. By March 9, 2020, all patients were discharged without dead. The mobile cabin hospital provides feasible strategy of isolation of mild-moderate cases and timely intervention during the virus outbreak.

Background: COVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy., Methods: The authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19., Results: The primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed., Conclusion: The endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease.

: Coronavirus disease is a highly contagious disease caused by systemic acute respiratory syndrome coronavirus 2 with high mortality rates. We aimed to evaluate the relationship between serum D-dimer levels and tomography findings at the time of admission in patients diagnosed with coronavirus disease 2019 (COVID-19). This study included 94 patients, 48 women (51%) and 46 men (49%), diagnosed by PCR method. Patients without any suspicious findings on thorax tomography and having oxygen saturation above 90% at the time of presentation were included as the first group. Patients with suspicious tomography findings but having oxygen saturation above 90% were designed as the second group, and patients with both suspicious tomography findings for COVID-19 and low oxygen saturation levels (<90%) at the time of admission were taken as the third group. Patients with oxygen desaturation were significantly older than the patients with normal oxygen saturations (P = 0.001). Patients with thorax tomography findings were having significantly higher D-dimer levels (P = 0.001). Patients with oxygen desaturation were having significantly higher D-dimer levels than the patients with normal oxygen saturations (P = 0.001). There was a significant negative correlation between oxygen saturation and D-dimer levels in all patients with and without tomography findings (r = -0.301, P = 0.016). Similarly, there was a significant positive correlation between the oxygen saturation and the lymphocyte count (r = 0.300, P < 0.017). Thorax tomography and D-dimer levels significantly correlate in patients with suspected COVID-19 admission. It should be kept in mind that patients with low oxygen saturation and high D-dimer levels may have serious lung involvement.

Background: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) epidemic has been emerged as a cardinal public health problem. Children have their own specific clinical features; notably, they seem to be escaping the severe respiratory adverse effects. The international scientific community is rapidly carrying out studies, driving to the need to reassess knowledge of the disease and therapeutic strategies., Aim: To assess the characteristics of COVID-19 infected children worldwide of all ages, from neonates to children and adolescents, and how they differ from their adult counterparts., Search Strategy: An electronic search in PubMed was conducted, using combinations of the following keywords: coronavirus, SARS-CoV-2, COVID-19, children. The search included all types of articles written in English between January 1, 2019 until August 15, 2020., Results: The search identified 266 relevant articles. Children were mainly within family clusters of cases and have relatively milder clinical presentation compared with adults; children were reported to have better outcomes with a significantly lower mortality rate. Cough and fever were the most common symptoms while pneumonia was the cardinal respiratory manifestation of infected children. Laboratory results and thoracic imaging give varying results., Conclusions: Children were mainly family cluster cases and usually presented with a mild infection, although cases presented with the multisystem inflammatory syndrome are becoming more apparent. Studies determining why the manifestations of SARS-CoV-2 infection are so variable may help to gain a better understanding of the disease and accelerate the development of vaccines and therapies., (© 2020 Wiley Periodicals LLC.)

Objective: Coronavirus disease 2019 (COVID-19) is a global health problem that can result in serious complications. The aim of this study was to investigate the prevalence and clinical importance of vitamin D deficiency in children with COVID-19., Material and Methods: This study includes 40 patients who were diagnosed to have COVID-19 and hospitalized with the real-time reverse transcription polymerase chain reaction method, 45 healthy matched control subjects with vitamin D levels. The age of admission, clinical and laboratory data, and 25-hydroxycholecalciferol (25-OHD) levels were recorded. Those with vitamin D levels which are below 20 ng/ml were determined as Group 1 and those with ≥20 ng/ml as Group 2., Results: Patients with COVID-19 had significantly lower vitamin D levels 13.14 μg/L (4.19-69.28) than did the controls 34.81 (3.8-77.42) μg/L (p < .001). Patients with COVID-19 also had significantly lower serum phosphorus (4.09 ± 0.73 vs. 5.06 ± 0.93 vs. (U/L) (p < .001)) values compared with the controls. The symptom of fever was significantly higher in COVID- 19 patients who had deficient and insufficient vitamin D levels than in patients who had sufficient vitamin D levels (p = .038). There was a negative correlation found between fever symptom and vitamin D level (r = -0.358, p = .023)., Conclusion: This is the first to evaluate vitamin D levels and its relationship with clinical findings in pediatric patients with COVID-19. Our results suggest that vitamin D values may be associated with the occurrence and management of the COVID-19 disease by modulating the immunological mechanism to the virus in the pediatric population., (© 2020 Wiley Periodicals LLC.)

This study aims to analyze the different clinical characteristics between children and their families infected with severe acute respiratory syndrome coronavirus 2. Clinical data from nine children and their 14 families were collected, including general status, clinical, laboratory test, and imaging characteristics. All the children were detected positive result after their families onset. Three children had fever (22.2%) or cough (11.2%) symptoms and six (66.7%) children had no symptom. Among the 14 adult patients, the major symptoms included fever (57.1%), cough (35.7%), chest tightness/pain (21.4%), fatigue (21.4%) and sore throat (7.1%). Nearly 70% of the patients had normal (71.4%) or decreased (28.6%) white blood cell counts, and 50% (7/14) had lymphocytopenia. There were 10 adults (71.4%) showed abnormal imaging. The main manifestations were pulmonary consolidation (70%), nodular shadow (50%), and ground glass opacity (50%). Five discharged children were admitted again because their stool showed positive result in SARS-CoV-2 PCR. COVID-19 in children is mainly caused by family transmission, and their symptoms are mild and prognosis is better than adult. However, their PCR result in stool showed longer time than their families. Because of the mild or asymptomatic clinical process, it is difficult to recognize early for pediatrician and public health staff.

Since the outbreak of coronavirus disease 2019 (COVID-19) in Wuhan, China, it has rapidly spread across many other countries. While the majority of patients were considered mild, critically ill patients involving respiratory failure and multiple organ dysfunction syndrome are not uncommon, which could result death. We hypothesized that cytokine storm is associated with severe outcome. We enrolled 102 COVID-19 patients who were admitted to Renmin Hospital (Wuhan, China). All patients were classified into moderate, severe and critical groups according to their symptoms. 45 control samples of healthy volunteers were also included. Inflammatory cytokines and C-Reactive Protein (CRP) profiles of serum samples were analyzed by specific immunoassays. Results showed that COVID-19 patients have higher serum level of cytokines (TNF-α, IFN-γ, IL-2, IL-4, IL-6 and IL-10) and CRP than control individuals. Within COVID-19 patients, serum IL-6 and IL-10 levels are significantly higher in critical group ( n  = 17) than in moderate ( n  = 42) and severe ( n  = 43) group. The levels of IL-10 is positively correlated with CRP amount ( r  = 0.41, P  < 0.01). Using univariate logistic regression analysis, IL-6 and IL-10 are found to be predictive of disease severity and receiver operating curve analysis could further confirm this result (AUC = 0.841, 0.822 respectively). Our result indicated higher levels of cytokine storm is associated with more severe disease development. Among them, IL-6 and IL-10 can be used as predictors for fast diagnosis of patients with higher risk of disease deterioration. Given the high levels of cytokines induced by SARS-CoV-2, treatment to reduce inflammation-related lung damage is critical.

Coronavirus disease 2019 (COVID-19) has a clinical course predominated by acute respiratory failure due to viral pneumonia with possible acute respiratory distress syndrome. However, nearly one third of infected patients, especially those with preexisting cardiovascular (CV) disease, are reported to present with some combination of acute cardiac injury, myocarditis, heart failure, cardiogenic shock, or significant dysrhythmias. In addition, COVID-19 infections are also associated with high rates of thromboembolic and disseminated intravascular coagulation complications. Severe myocarditis and heart failure have both been reported as the initial presenting conditions in COVID-19 infection. This review highlights the important considerations related to the CV manifestations of COVID-19 infections, describes the mechanisms and clinical presentation of CV injury, and provides practical management and therapy suggestions. This narrative review is based primarily on the multiple case series and cohorts from the largest initial COVID-19 outbreak centers (ie, Wuhan, China, and Italy); hence, nearly all presented data and findings are retrospective in nature with the attendant limitations of such reports.

The global pandemic of novel coronavirus disease 2019 (COVID-19) has taken the entire human race by surprise and led to an unprecedented number of mortalities worldwide so far. Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). In addition, ACE2 is the major component of the renin-angiotensin system. ACE2 deteriorates angiotensin II, a peptide that is responsible for the promotion of stroke. The downregulation of ACE2 further activates an immunological cascade. Thus, researchers need to explore and examine the possible links between COVID-19 and ischemic stroke (IS). Human ACE2 expression level and pattern in various tissues might be decisive for the vulnerability, symptoms, and treatment outcomes of the SARS-CoV-2 infection. The swift increase in the knowledge of SARS-CoV-2 has given creditable evidence that SARS-CoV-2 infected patients also encounter neurological deficits. As the SARS-CoV-2 binds to ACE2, it will hamper the activity of ACE2 in providing neuroprotection, especially in the case of stroke patients. Due to the downregulation of ACE2, the inflammatory response is activated in the ischemic penumbra. The COVID-19 pandemic has affected people with various pre-existing diseases, including IS, in such a way that these patients need special care and attention for their survival. Several clinical trials are currently ongoing worldwide as well as many other projects are in different stages of conceptualization and planning to facilitate the effective management of stroke patients with COVID-19 infection.

Recent innovations in translational research have ushered an exponential increase in the discovery of novel biomarkers, thereby elevating the hope for deeper insights into "personalized" medicine approaches to disease phenotyping and care. However, a critical gap exists between the fast pace of biomarker discovery and the successful translation to clinical use. This gap underscores the fundamental biomarker conundrum across various acute and chronic disorders: how does a biomarker address a specific unmet need? Additionally, the gap highlights the need to shift the paradigm from a focus on biomarker discovery to greater translational impact and the need for a more streamlined drug approval process. The unmet need for biomarkers in acute respiratory distress syndrome (ARDS) is for reliable and validated biomarkers that minimize heterogeneity and allow for stratification of subject selection for enrollment in clinical trials of tailored therapies. This unmet need is particularly highlighted by the ongoing SARS-CoV-2/COVID-19 pandemic. The unprecedented numbers of COVID-19-induced ARDS cases has strained health care systems across the world and exposed the need for biomarkers that would accelerate drug development and the successful phenotyping of COVID-19-infected patients at risk for development of ARDS and ARDS mortality. Accordingly, this review discusses the current state of ARDS biomarkers in the context of the drug development pipeline and highlight gaps between biomarker discovery and clinical implementation while proposing potential paths forward. We discuss potential ARDS biomarkers by category and by context of use, highlighting progress in the development continuum. We conclude by discussing challenges to successful translation of biomarker candidates to clinical impact and proposing possible novel strategies., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Competing Interests: Competing interests: The authors completed the ICMJE Unified Competing Interest form (available upon request from the corresponding author), and declare no conflicts of interest.