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Radu Crisan-Dabija

Bio: Radu Crisan-Dabija is an academic researcher from Grigore T. Popa University of Medicine and Pharmacy. The author has contributed to research in topics: Medicine & Pandemic. The author has an hindex of 5, co-authored 15 publications receiving 65 citations.

Papers
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Journal ArticleDOI
TL;DR: Because viral respiratory infections and TB impede the host's immune responses, it can be assumed that their lethal synergism may contribute to more severe clinical evolution.
Abstract: Background. The threat of contagious infectious diseases is constantly evolving as demographic explosion, travel globalization, and changes in human lifestyle increase the risk of spreading pathogens, leading to accelerated changes in disease landscape. Of particular interest is the aftermath of superimposing viral epidemics (especially SARS-CoV-2) over long-standing diseases, such as tuberculosis (TB), which remains a significant disease for public health worldwide and especially in emerging economies. Methods and Results. The PubMed electronic database was systematically searched for relevant articles linking TB, influenza, and SARS-CoV viruses and subsequently assessed eligibility according to inclusion criteria. Using a data mining approach, we also queried the COVID-19 Open Research Dataset (CORD-19). We aimed to answer the following questions: What can be learned from other coronavirus outbreaks (focusing on TB patients)? Is coinfection (TB and SARS-CoV-2) more severe? Is there a vaccine for SARS-CoV-2? How does the TB vaccine affect COVID-19? How does one diagnosis affect the other? Discussions. Few essential elements about TB and SARS-CoV coinfections were discussed. First, lessons from past outbreaks (other coronaviruses) and influenza pandemic/seasonal outbreaks have taught the importance of infection control to avoid the severe impact on TB patients. Second, although challenging due to data scarcity, investigating the pathological pathways linking TB and SARS-CoV-2 leads to the idea that their coexistence might yield a more severe clinical evolution. Finally, we addressed the issues of vaccination and diagnostic reliability in the context of coinfection. Conclusions. Because viral respiratory infections and TB impede the host’s immune responses, it can be assumed that their lethal synergism may contribute to more severe clinical evolution. Despite the rapidly growing number of cases, the data needed to predict the impact of the COVID-19 pandemic on patients with latent TB and TB sequelae still lies ahead. The trial is registered with NCT04327206 , NCT01829490 , and NCT04121494 .

43 citations

Journal ArticleDOI
TL;DR: It is found that there is a complexity of interactions between coexisting idiopathic pulmonary fibrosis/interstitial lung disease (ILD) and COVID-19 disease, and patients recovering from severe COVID -19 disease are at serious risk of developing PF.
Abstract: The COVID-19 pandemic rapidly became a worldwide healthcare emergency affecting millions of people, with poor outcomes for patients with chronic conditions and enormous pressure on healthcare systems. Pulmonary fibrosis (PF) has been cited as a risk factor for a more severe evolution of COVID-19, primarily because its acute exacerbations are already associated with high mortality. We reviewed the available literature on biochemical, pathophysiological, and pharmacological mechanisms of PF and COVID-19 in an attempt to foresee the particular risk of infection and possible evolution of PF patients if infected with SARS-COV-2. We also analyzed the possible role of medication and risk factors (such as smoking) in the disease's evolution and clinical course. We found out that there is a complexity of interactions between coexisting idiopathic pulmonary fibrosis/interstitial lung disease (ILD) and COVID-19 disease. Also, patients recovering from severe COVID-19 disease are at serious risk of developing PF. Smokers seem to have, in theory, a chance for a better outcome if they develop a severe form of COVID-19 but statistically are at much higher risk of dying if they become critically ill.

33 citations

Journal ArticleDOI
TL;DR: Higher levels of mortality/morbidity due to “CO VID-19 versus non-COVID-19” polarisation oblige the healthcare community to find ways to provide proper care for its elders, and various religious practices provide resources for coping with isolation/overcoming loneliness.
Abstract: Since epidemiological arguments favouring self-isolation during the COVID-19 pandemic are widely recommended, the consequences of social isolation/loneliness of older people considered to be at higher risk for severe illness are neglected. We identified and described medical, social, psychological, and religious issues, indirectly generated by the COVID-19 lockdown. Mortality induced by SARS-CoV-2 and death from other "neglected" issues were put in balance. Arguments for strict lockdown from most European countries are compared with a relaxed approach, as has been applied in Sweden. Social isolation affects disproportionally the elderly, transforming it into a public health concern. One witnesses openly ageist discourse, while painful decisions to prioritising ventilation for younger patients deepens the sense of hopelessness. Fear has led to anxiety disorders and depression. Various religious practices provide resources for coping with isolation/overcoming loneliness. Higher levels of mortality/morbidity due to "COVID-19 versus non-COVID-19" polarisation oblige the healthcare community to find ways to provide proper care for its elders.

24 citations

Journal ArticleDOI
TL;DR: The purpose of this Editorial is to raise the alarm about certain thrombophilic patterns that would predispose toThrombosis in the context of COVID-19 infection, and to explore and propose new ways of research in this regard, with the obvious aim of optimizing treatment and limiting thromBotic complications in the contexts of SARS-CoV-2 infection.
Abstract: The purpose of this Editorial is 2-fold: to raise the alarm about certain thrombophilic patterns that would predispose to thrombosis in the context of COVID-19 infection, and to explore and propose new ways of research in this regard, with the obvious aim of optimizing treatment and limiting thrombotic complications in the context of SARS-CoV-2 infection. Our assumption is advocated by a theory validated in a reasonably related condition such as sepsis, according to which thrombophilic mutations in patients with sepsis can affect their clinical response. The similarity between these 2 conditions is sustained by autopsy studies findings, documented immune pathogenesis, and microcirculation dysfunctions, the ability of SARS-CoV-2 to disseminate the infection in other organs and by the fact that many critically ill COVID-19 patients developed clinical symptoms of shock following a process called “viral sepsis.” A recent paper dealing with SARS-CoV-2 and “viral sepsis” raised alarm signals that despite the huge percentage of 71,4% of non-survivors of COVID-19 who matched the grade of overt disseminated intravascular coagulation, the concrete mechanisms of vascular thrombosis are not yet known. Far fewer studies have addressed the matter of identifying non-viral, predisposing factors (genetic, environmental) for thrombotic events in COVID-19, despite the crucial impact this could have on risk stratification, more precise therapies, and less adverse events. The issue of thrombosis (both arterial and venous) in COVID-19 is intensely debated due to its deleterious and often fatal consequences. The International Society on Thrombosis and Haemostasis guidance issued at the end of May 2020 recommended that all hospitalized patients with COVID-19, including non-critically ill, should be considered for thromboprophylaxis with either unfractionated heparin or low-molecular-weight heparin unless they have contraindications, although no level of evidence was stated. Although thromboprophylaxis for any hospitalized COVID-19 patient is generally accepted, there is an ongoing debate about the exact dosage to be administered. Furthermore, the World Health Organization advises for a pharmacological prophylaxis of thromboembolism in hospitalized COVID-19 patients but warns on carefully considering the significant side-effects and drug-drug interactions that may affect COVID-19 symptomatology. Especially among critically ill patients or patients developing acute respiratory distress syndrome (ARDS) shortly after COVID-19 onset, the need for anticoagulation is justified by the mechanism and the consequences of the alveolar injuries that occur during the viral attack when characteristically neutrophil–platelet aggregates are formed. Aside from increasing the pulmonary vascular permeability to proteins, these aggregates emerge from the endothelial cell activation. This process increases the vascular permeability furthermore in a positivefeedback loop. The pathophysiology of the thrombotic events during viral aggression begins with the increased expression of the tissue factor (TF), induced by proinflammatory cytokines in the alveolar macrophages and alveolar epithelial cells which is a membrane protein of the fibroblasts present in the lungs that become exposed to the bloodstream during the endothelial

13 citations

Posted ContentDOI
01 May 2020-medRxiv
TL;DR: Investigating the pathological pathways linking TB and SARS-CoV-2 leads to the idea that their coexistence might yield a more severe clinical evolution, and the issues of vaccination and diagnostic reliability in the context of coinfection are addressed.
Abstract: Background The threat of contagious infectious diseases is constantly evolving, as demographic explosion, travel globalization and changes in human lifestyle increase the risk of spreading pathogens, leading to accelerated changes in disease landscape. Of particular interest is the aftermath of superimposing viral epidemics (especially SARS-CoV-2) over long-standing diseases, such as tuberculosis (TB), which remains a significant disease for public health worldwide and especially in emerging economies. Methods and Results PubMed electronic database was requested for relevant articles linking TB, influenza and SARS-CoV viruses and subsequently assessed eligibility according to inclusion criteria. Using a data mining approach, we also queried the COVID-19 Open Research Dataset (CORD-19). We aimed to answer the following questions: What can be learned from other coronavirus outbreaks (with a focus on TB patients)? Is coinfection (TB and SARS-CoV-2) more severe? Is there a vaccine for SARS-CoV-2? How does the TB vaccine affect COVID19? How does one diagnosis affect the other? Discussions Few essential elements about TB and SARS-CoV coinfections were discussed. First, lessons from the past outbreaks (other coronaviruses), as well as influenza pandemic / seasonal outbreaks have taught the importance of infection control to avoid the severe impact on TB patients. Second, although challenging due to data scarcity, investigating the pathological pathways linking TB and SARS-CoV-2 leads to the idea that their coexistence might yield a more severe clinical evolution. Finally, we addressed the issues of vaccination and diagnostic reliability in the context of coinfection. Conclusions Because viral respiratory infections and TB impede the host’s immune responses, it can be assumed that their harmful synergism may contribute to more severe clinical evolution. Despite the rapidly growing number of cases, the data needed to predict the impact of the COVID-19 pandemic on patients with latent TB and TB sequelae still lies ahead.

11 citations


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01 Jan 2020
TL;DR: Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future.
Abstract: Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.

4,408 citations

Posted Content
TL;DR: The mechanics of dataset construction are described, highlighting challenges and key design decisions, an overview of how CORD-19 has been used, and several shared tasks built around the dataset are described.
Abstract: The Covid-19 Open Research Dataset (CORD-19) is a growing resource of scientific papers on Covid-19 and related historical coronavirus research. CORD-19 is designed to facilitate the development of text mining and information retrieval systems over its rich collection of metadata and structured full text papers. Since its release, CORD-19 has been downloaded over 75K times and has served as the basis of many Covid-19 text mining and discovery systems. In this article, we describe the mechanics of dataset construction, highlighting challenges and key design decisions, provide an overview of how CORD-19 has been used, and preview tools and upcoming shared tasks built around the dataset. We hope this resource will continue to bring together the computing community, biomedical experts, and policy makers in the search for effective treatments and management policies for Covid-19.

565 citations

Journal ArticleDOI
Camilla Lindan1, Kshitij Mankad2, D. Ram3, Larry K. Kociolek4, V. Michelle Silvera5, Nathalie Boddaert6, Stavros Stivaros7, Stavros Stivaros8, Stavros Stivaros9, Susan Palasis4, Sameen Akhtar, Douglas Alden, Suraj Amonkar, Pascale Aouad, Mélodie Aubart, Jose Alejandro Bacalla, Alcino A Barbosa, Romain Basmaci, Laureline Berteloot, Thomas Blauwblomme, Gilles Brun, Olivia Carney, Judith Chareyre, Gérard Chéron, Pablo Picasso De Araujo Coimbra, Volodia Dangouloff-Ros, Felice D'Arco, Robert A. Dineen, Loic De-Pontual, Isabelle Desguerre, Wissam Elfallal, D. Gareth Evans, Suely Fazio Ferraciolli, Nadine Girard, Fabrício Guimarães Gonçalves, Ivan A. Gonzalez, P. Ellen Grant, David Grevent, Carolina Valduga de Alencastro Guimaraes, Jane Hassell, Fabiana C.C. Hirata, Ian Kamaly-Asl, Jeffrey Jacob, Kandise Jackson, Blaise V. Jones, Robin Joseph, Ah Young Jung, Amna Kashgari, John-Paul Kilday, Alyssa Kirsch, Manoelle Kossorotoff, Anant Krishnan, Shilpa Kulkarni, Marianne Leruez-Vill, Fabrice Lesage, Raphaël Levy, Yi Li, Carol Cavalcante de Vasconcelos Lima, Lokesh Lingappa, Ulrike Löbel, Roberto Lopez-Alberola, Leandro Tavares Lucato, Daniela Duarte Moreira, Jonathan G. Murnick, Sarah Nahmani, Shubra Pagariya, Julija Pavaine, Bryan Philbrook, Ana Cláudia Piovesan, Kelsey E. Poisson, Nihaal Reddy, Phil Riley, A Romsauerova, Charlies-Joris Roux, Carlos Rugilo, Gaurav Saigal, Gabriel Lucca de Oliveira Salvador, David Seidenwurm, Isabelle Sermet-Gaudelus, Jai Sidpra, Sniya Valsa Sudhakar, María Sol Toronchik, Gilbert Vézina 
TL;DR: Recurring patterns of disease and atypical neuroimaging manifestations can be found and should be recognised being as potentially due to SARS-CoV-2 infection as an underlying aetiological factor.

156 citations

Journal ArticleDOI
TL;DR: In this paper, the authors report the available evidence on the interaction between these two infections and discuss the differences and similarities of TB and COVID-19, their immunological features, diagnostics, epidemiological and clinical characteristics and public health implications.

116 citations

Journal ArticleDOI
TL;DR: Quality of life, life satisfaction, and well-being during the pandemic is affected by age, trait anxiety, and Coronavirus threat.
Abstract: Introduction Psychological studies undertaken during the COVID-19 pandemic rarely include people in their 60s. In our study, we studied the predictors of the quality of life, wellbeing, sleep and life satisfaction during the pandemic in older people from Germany and Poland, including factors such as risk behaviour, trait anxiety, feeling of threat, sleep quality, optimism, comparing them to three different age groups. Methods 494 adults in four groups: 60+ (N=60), 50-60 (N=139), 36-49 (N=155), <35 (N=140) completed validated self-report questionnaires assessing: socio-demographic data, quality of life, trait anxiety, risk tolerance, coronavirus threat, optimism regarding the pandemic, difficulty relaxing, life satisfaction, wellbeing, sleep quality during the pandemic period. Results Older people rated higher their quality higher of life than younger (mean difference = .74, SE = .19, p < .01) and middle-aged (mean difference = .79, SE = .18, p < .01), life satisfaction than younger (mean difference = 1.23, SE = .31, p < .01) and middle-aged (mean difference = .92, SE = .30, p < .05) as well as wellbeing higher than younger (mean difference = 1.40, SE = .31, p < .01) and middle-aged participants (mean difference = .91, SE = .31, p < .05), but experienced lower levels of trait anxiety and Coronavirus threat (mean difference = -9.19, SE = 1.90, p < .01), compared to younger age groups. They experienced greater risk tolerance (mean difference = 1.38, SE = .33, p < .01), as well as sleep quality (F=1.25; eta2=.01), optimism regarding the pandemic (F=1.96; eta2=.01), and had less difficulty relaxing during the pandemic (F=3.75; eta2=.02) than middle-aged respondents. Conclusions The findings show that the assessed quality of life, life satisfaction and wellbeing during pandemic is affected by the respondent’s age, trait anxiety and the threat of Coronavirus. Older people rated their quality higher of life, life satisfaction and wellbeing during pandemic higher than younger people, but experienced lower levels of trait anxiety and Coronavirus threat compared to younger age groups. They experienced greater risk tolerance, as well as sleep quality, optimism regarding the pandemic, and had less difficulty relaxing during the pandemic than middle-aged respondents.

101 citations