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SARS-CoV-2 effects on sperm parameters: a meta-analysis study.
Xie, Y, Mirzaei, M, Kahrizi, MS, Shabestari, AM, Riahi, SM, Farsimadan, M, Roviello, G
Journal of assisted reproduction and genetics. 2022;39(7):1555-1563
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Infertility is a reproductive system disorder. Viruses as a major cause of fertility problems can potentially interfere with reproductive function in men. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was found to be the causing viral pathogen of COVID-19 and capable of affecting human health. The aim of this study was to evaluate the effects of SARS-CoV-2 on different semen parameters including sperm count, sperm concentration, volume, motility, and progressive motility. This study is a meta-analysis of twelve studies of which seven were case control studies and five were retrospective cohort studies. Results show that SARS-CoV-2 infection could lead to significant impairments of male reproductive function through exerting negative influences on different semen parameters namely semen volume, sperm concentration, sperm count, and sperm motility. Authors conclude that their findings revealed the vulnerability of semen quality to SARS-CoV-2 infection.
Abstract
AIM: The rapid outbreak of the coronavirus disease 2019 (COVID-19) pandemic posed challenges across different medical fields, especially reproductive health, and gave rise to concerns regarding the effects of SARS-CoV-2 on male infertility, owing to the fact that the male reproductive system indicated to be extremely vulnerable to SARS-CoV-2 infection. Only a small number of studies have investigated the effects of SARS-CoV-2 on male reproduction, but the results are not consistent. So, we performed this meta-analysis to draw a clearer picture and evaluate the impacts of COVID-19 on male reproductive system. METHOD We searched Embase, Web of Science, PubMed, and Google Scholar databases to identify the potentially relevant studies. Standardized mean difference (SMD) with 95% confidence interval (CI) was applied to assess the relationship. Heterogeneity testing, sensitivity analysis, and publication bias testing were also performed. RESULTS A total of twelve studies including 7 case control investigations and 5 retrospective cohort studies were found relevant and chosen for our research. Our result showed that different sperm parameters including semen volume [SMD = - 0.27 (- 0.46, - 1.48) (p = 0.00)], sperm concentration [SMD = - 0.41 (- 0.67, - 0.15) (p = 0.002)], sperm count [SMD = - 0.30 (- 0.44, - 0.17) (p = 0.00)], sperm motility [SMD = - 0.66 (- 0.98, - 0.33) (p = 0.00)], and progressive motility [SMD = - 0.35 (- 0.61, - 0.08) (p = 0.01)] were negatively influenced by SARS-CoV-2 infection. However, sperm concentration (p = 0.07) and progressive motility (p = 0.61) were not found to be significantly associated with SARS-CoV-2 infection in case control studies. No publication bias was detected. CONCLUSION The present study revealed the vulnerability of semen quality to SARS-CoV-2 infection. Our data showed a strong association of different sperm parameters with SARS-CoV-2 infection. The results suggested that SARS-CoV-2 infection in patients may negatively influence their fertility potential in a short-term period, but more studies are needed to decide about the long-term effects.
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Vasculitis changes in COVID-19 survivors with persistent symptoms: an [18F]FDG-PET/CT study.
Sollini, M, Ciccarelli, M, Cecconi, M, Aghemo, A, Morelli, P, Gelardi, F, Chiti, A
European journal of nuclear medicine and molecular imaging. 2021;48(5):1460-1466
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The SARS-CoV-2 infection manifests with a broad spectrum of clinical patterns ranging from minimally or asymptomatic cases to mild illness, to severe infection, to critical disease. The aim of this study was to evaluate whether the radiopharmaceutical, 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG), was able to demonstrate a persistent inflammatory process in the vascular epithelium or in any other site. The study included Covid-19 patients who recovered but complained of unexplained persisting symptoms for more than 30 days during the follow-up visits. The patients where divided into two groups; the long Covid and control group. Results indicate that although the total vascular score was similar in the two groups, the target-to-blood pool ratio was significantly higher in three vascular regions (thoracic aorta, right iliac artery, and femoral arteries) in the long Covid than in controls. Authors conclude that their findings suggest that SARS-CoV-2 induces vascular inflammation, which may be responsible for persisting symptoms.
Abstract
PURPOSE Several patients experience unexplained persistent symptoms after SARS-CoV-2 recovering. We aimed at evaluating if 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) was able to demonstrate a persistent inflammatory process. METHODS Recovered adult COVID-19 patients, who complained unexplained persisting symptoms for more than 30 days during the follow-up visits, were invited to participate in the study. Patients fulfilling inclusion criteria were imaged by [18F]FDG positron emission tomography/computed tomography ([18F]FDG-PET/CT). Whole-body [18F]FDG-PET/CT, performed according to good clinical practice, was qualitatively (comparison with background/liver) and semi-quantitatively (target-to-blood pool ratio calculated as average SUVmax artery/average SUVmean inferior vena cava) analyzed. Negative follow-up [18F]FDG-PET/CT images of oncologic patients matched for age/sex served as controls. Mann-Whitney test was used to test differences between groups. SPSS version 26 was used for analyses. RESULTS Ten recovered SARS-CoV-2 patients (seven male and three females, median age 52 years, range 46-80) with persisting symptoms were enrolled in the study. Common findings at visual analysis were increased [18F]FDG uptake in bone marrow and blood vessels (8/10 and 6/10 cases, respectively). [18F]FDG uptake in bone marrow did not differ between cases and controls (p = 0.16). The total vascular score was similar in the two groups (p = 0.95). The target-to-blood pool ratio resulted higher in recovered SARS-CoV-2 patients than in controls. CONCLUSION Although the total vascular score was similar in the two groups, the target-to-blood pool ratio was significantly higher in three vascular regions (thoracic aorta, right iliac artery, and femoral arteries) in the recovered COVID-19 cohort than in controls, suggesting that SARS-CoV-2 induces vascular inflammation, which may be responsible for persisting symptoms.
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Historical Insight into Infections and Disorders Associated with Neurological and Psychiatric Sequelae Similar to Long COVID.
Stefano, GB
Medical science monitor : international medical journal of experimental and clinical research. 2021;27:e931447
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Literature shows that there are long-term symptoms and organ damage in patients with confirmed coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 that persist after the acute illness. The aim of this review was to present a historical overview of infections and disorders associated with the neurological and psychiatric sequelae that have shown similarities with long COVID. Historically, the common symptom of altered cognition has been reported during earlier pandemics. Pandemics discussed in this review include; influenza pandemics of 1889 and 1892 (Russian flu), Spanish flu pandemic (1918-1919), encephalitis lethargica, diphtheria, and myalgic encephalomyelitis (chronic fatigue syndrome or post-viral fatigue syndrome). Furthermore, literature shows that there are similarities between the symptoms of chronic fatigue syndrome and the brain fog of long COVID. Viral infection, cerebral hypoxia [reduced supply of oxygen to the brain), cognitive dysfunction, or brain fog may occur along a common pathway in the long-term pathogenesis of epidemic and pandemic infections, including COVID-19. Authors conclude that utilising data from past epidemics and pandemics may help to identify common acute and chronic syndromes, including neurological and psychiatric sequelae with similarities to the conditions currently described in patients with long COVID.
Abstract
Long-term sequelae of coronavirus disease 2019 (COVID-19) due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are now recognized. However, there is still a lack of consensus regarding the terminology for this emerging chronic clinical syndrome, which includes long COVID, chronic COVID syndrome, post-COVID-19 syndrome, post-acute COVID-19, and long-hauler COVID-19. In this review, I will use the term "long COVID". A review of the medical history and epidemiology of past pandemics and epidemics in modern literature review identifies common long-term post-infectious disorders, with the common finding of altered cognition. In the brain, the cerebral hypoxia induced by SARS-CoV-2 infection may be caused by mitochondrial dysfunction, resulting in "brain fog". Historically, the common symptom of altered cognition has been reported during earlier pandemics, which include the influenza pandemics of 1889 and 1892 (Russian flu), the Spanish flu pandemic (1918-1919), encephalitis lethargica, diphtheria, and myalgic encephalomyelitis (chronic fatigue syndrome or post-viral fatigue syndrome). There are similarities between chronic fatigue syndrome and the "brain fog" described in long COVID. During past viral epidemics and pandemics, a commonality of neural targets may have increased viral survival by conformational matching. The neurological and psychiatric sequelae of SARS-CoV-2 infection, or long COVID, may have emerged from neural effects that have emerged from an invertebrate and vertebrate virosphere. This review aims to present a historical overview of infections and disorders associated with neurological and psychiatric sequelae that have shown similarities with long COVID.
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SARS-CoV-2 and immune-microbiome interactions: Lessons from respiratory viral infections.
Cyprian, F, Sohail, MU, Abdelhafez, I, Salman, S, Attique, Z, Kamareddine, L, Al-Asmakh, M
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases. 2021;105:540-550
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped RNA beta-coronavirus. This virus caused the coronavirus disease 2019 (COVID-19) pandemic. The aim of this review was to investigate the relationship between microbiota, immunity, and COVID-19, with particular focus on how microbiome-associated immune crosstalk can shape outcome of COVID-19. The study included 118 articles which investigated or reviewed COVID-19 or coronavirus and the microbiome of the gut or respiratory tract. Findings indicate that: - an over-activated immune system leads to massive pulmonary damage in COVID-19 patients. - the effect of aging and comorbidities, and the use of antibiotics have an effect on the diversity of the microbiota. - the milieu of gut flora can exert influence on pulmonary immune responses. - a unique cross-talk exists between the pulmonary and gut microbial compartments. Authors conclude by highlighting the need of further studies that delineate the role of the microbiota and their products in the immune dysregulation observed in SARS-CoV-2 infections.
Abstract
By the beginning of 2020, infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) had rapidly evolved into an emergent worldwide pandemic, an outbreak whose unprecedented consequences highlighted many existing flaws within public healthcare systems across the world. While coronavirus disease 2019 (COVID-19) is bestowed with a broad spectrum of clinical manifestations, involving the vital organs, the respiratory system transpires as the main route of entry for SARS-CoV-2, with the lungs being its primary target. Of those infected, up to 20% require hospitalization on account of severity, while the majority of patients are either asymptomatic or exhibit mild symptoms. Exacerbation in the disease severity and complications of COVID-19 infection have been associated with multiple comorbidities, including hypertension, diabetes mellitus, cardiovascular disorders, cancer, and chronic lung disease. Interestingly, a recent body of evidence indicated the pulmonary and gut microbiomes as potential modulators for altering the course of COVID-19, potentially via the microbiome-immune system axis. While the relative concordance between microbes and immunity has yet to be fully elucidated with regards to COVID-19, we present an overview of our current understanding of COVID-19-microbiome-immune cross talk and discuss the potential contributions of microbiome-related immunity to SARS-CoV-2 pathogenesis and COVID-19 disease progression.
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Understanding Viral Infection Mechanisms and Patient Symptoms for the Development of COVID-19 Therapeutics.
Choi, HM, Moon, SY, Yang, HI, Kim, KS
International journal of molecular sciences. 2021;22(4)
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The outbreak of a novel coronavirus was reported in Wuhan, in the Hubei province of China, in December 2019. This virus was officially designated as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) because of its phylogenetic and taxonomic similarities to other coronaviruses. The aim of this review was to understand the viral infection mechanisms of SARS-CoV-2, the clinical features of Covid-19 and the mechanisms through which Covid-19 can be effectively treated with existing drugs. Literature shows that: • SARS-CoV-2 is usually transmitted by inhalation or contact with infected droplets. Inhaled droplets or aerosol carrying the virus then infect and spread through the respiratory tracts. • Severe inflammatory response is a remarkable feature of Covid-19 symptoms. This is caused by delayed viral clearance, which induces chronic systemic inflammation and widespread tissue damage, even leading to cytokine storms. • The incubation period is generally 5-6 days, but it ranges from one day to as much as two weeks. • Interstitial pneumonia and subsequent acute respiratory distress syndrome are the leading causes of death in patients with Covid-19. • There is no licensed treatment for Covid-19, only a combination of antiviral and anti-inflammatory drug treatments are being used. Authors conclude that their finding may provide new insights into the development of therapeutics by understanding the various clinical and basic research studies currently underway.
Abstract
Coronavirus disease 2019 (COVID-19), caused by the SARS-CoV-2 virus, has become a worldwide pandemic. Symptoms range from mild fever to cough, fatigue, severe pneumonia, acute respiratory distress syndrome (ARDS), and organ failure, with a mortality rate of 2.2%. However, there are no licensed drugs or definitive treatment strategies for patients with severe COVID-19. Only antiviral or anti-inflammatory drugs are used as symptomatic treatments based on clinician experience. Basic medical researchers are also trying to develop COVID-19 therapeutics. However, there is limited systematic information about the pathogenesis of COVID-19 symptoms that cause tissue damage or death and the mechanisms by which the virus infects and replicates in cells. Here, we introduce recent knowledge of time course changes in viral titers, delayed virus clearance, and persistent systemic inflammation in patients with severe COVID-19. Based on the concept of drug reposition, we review which antiviral or anti-inflammatory drugs can effectively treat COVID-19 patients based on progressive symptoms and the mechanisms inhibiting virus infection and replication.
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Ross River Virus Immune Evasion Strategies and the Relevance to Post-viral Fatigue, and Myalgic Encephalomyelitis Onset.
Lidbury, BA
Frontiers in medicine. 2021;8:662513
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Ross river virus (RRV) is a mosquito borne virus that is thought to be the trigger of myalgic encephalomyelitis (ME) in many Australians. Viruses like RRV are thought to be so successful due to their ability to avoid and often manipulate the hosts immune response. This review of 75 studies aimed to discuss immune evasion strategies employed by RRV and understand the relevance to post viral fatigue and the development of ME. The authors began by explaining how RRV manipulates the hosts immune system to gain entry to cells and replicate. Once the virus has entered the cells, it is thought that it disrupts inflammatory pathways and decreases anti-viral genes. Disruption of inflammation has also been reported to affect energy production in individuals with ME. It was concluded that viruses such as RRV can manipulate the hosts immune system resulting in disruption of energy production. Understanding these pathways and interactions may explain why some individuals go on to develop ME post infection and others do not. Findings may also help to understand ME like symptoms reported by some patients who have recovered from Covid-19. This paper could be used by healthcare professionals to understand the development of ME and fatigue symptoms in individuals who have recovered from viruses such as RRV and Covid-19.
Abstract
Ross River virus (RRV) is an endemic Australian arbovirus, and member of the Alphavirus family that also includes Chikungunya virus (CHIK). RRV is responsible for the highest prevalence of human disease cases associated with mosquito-borne transmission in Australia, and has long been a leading suspect in cases of post-viral fatigue syndromes, with extrapolation of this link to Myalgic Encephalomyelitis (ME). Research into RRV pathogenesis has revealed a number of immune evasion strategies, impressive for a virus with a genome size of 12 kb (plus strand RNA), which resonate with insights into viral pathogenesis broadly. Drawing from observations on RRV immune evasion, mechanisms of relevance to long term idiopathic fatigue are featured as a perspective on infection and eventual ME symptoms, which include considerations of; (1) selective pro-inflammatory gene suppression post antibody-dependent enhancement (ADE) of RRV infection, (2) Evidence from other virus families of immune disruption and evasion post-ADE, and (3) how virally-driven immune evasion may impact on mitochondrial function via target of rapamycin (TOR) complexes. In light of these RRV measures to counter the host immune - inflammatory responses, links to recent discoveries explaining cellular, immune and metabolomic markers of ME will be explored and discussed, with the implications for long-COVID post SARS-CoV-2 also considered. Compelling issues on the connections between virally-induced alterations in cytokine expression, for example, will be of particular interest in light of energy pathways, and how these perturbations manifest clinically.
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'Long COVID': persistent COVID-19 symptoms in survivors managed in Lagos State, Nigeria.
Osikomaiya, B, Erinoso, O, Wright, KO, Odusola, AO, Thomas, B, Adeyemi, O, Bowale, A, Adejumo, O, Falana, A, Abdus-Salam, I, et al
BMC infectious diseases. 2021;21(1):304
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The spectrum of clinical presentation of COVID-19 ranges from the asymptomatic, to symptomatic with varying levels of severity depending on age, comorbid conditions, and basal metabolic index. The aim of this study was to highlight associations between socio-demographic characteristics and comorbidities with persistent symptoms in COVID-19 survivors. This study is a retrospective study using de-identified data of 274 COVID-19 survivors. A thorough clinical history and physical assessment was conducted for all patients. Results indicate that: - the most common symptom manifested by survivors was easy fatigability. - neurologic symptoms were found in 39.1% of the COVID-19 survivors. Symptoms included headaches, insomnia, and attention deficits. - there was no significant association between demographic factors and comorbidities such as hypertension or diabetes and the presence of persistent symptoms in COVID-19 survivors. Authors conclude these findings, together with evidence from other studies, can guide policies and interventions aimed at improving the quality of life of survivors and return to usual health.
Abstract
BACKGROUND Coronavirus disease once thought to be a respiratory infection is now recognised as a multi-system disease affecting the respiratory, cardiovascular, gastrointestinal, neurological, immune, and hematopoietic systems. An emerging body of evidence suggests the persistence of COVID-19 symptoms of varying patterns among some survivors. This study aimed to describe persistent symptoms in COVID-19 survivors and investigate possible risk factors for these persistent symptoms. METHODS The study used a retrospective study design. The study population comprised of discharged COVID-19 patients. Demographic information, days since discharge, comorbidities, and persistent COVID-19 like symptoms were assessed in patients attending the COVID-19 outpatient clinic in Lagos State. Statistical analysis was done using STATA 15.0 software (StataCorp Texas) with significance placed at p-value < 0.05. RESULTS A total of 274 patients were enrolled in the study. A majority were within the age group > 35 to ≤49 years (38.3%), and male (66.1%). More than one-third (40.9%) had persistent COVID-19 symptoms after discharge, and 19.7% had more than three persistent COVID-like symptoms. The most persistent COVID-like symptoms experienced were easy fatigability (12.8%), headaches (12.8%), and chest pain (9.8%). Symptomatic COVID-19 disease with moderate severity compared to mild severity was a predictor of persistent COVID-like symptoms after discharge (p < 0.05). CONCLUSION Findings from this study suggests that patients who recovered from COVID-19 disease may still experience COVID-19 like symptoms, particularly fatigue and headaches. Therefore, careful monitoring should be in place after discharge to help mitigate the effects of these symptoms and improve the quality of life of COVID-19 survivors.
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Clinical Characteristics and Outcomes of Hospitalized and Critically Ill Children and Adolescents with Coronavirus Disease 2019 at a Tertiary Care Medical Center in New York City.
Chao, JY, Derespina, KR, Herold, BC, Goldman, DL, Aldrich, M, Weingarten, J, Ushay, HM, Cabana, MD, Medar, SS
The Journal of pediatrics. 2020;223:14-19.e2
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Epidemiologic studies have consistently demonstrated that children are at lower risk of developing severe symptoms or critical illness compared with adults. The aim of this study was to describe the clinical profiles and risk factors for critical illness in hospitalised children and adolescents with COVID-19. The study is a retrospective review of 67 children aged between 1 month to 21 years with COVID-19 from a single tertiary care children’s hospital. Out of the 44 children who tested positive, 33 (72%) were admitted to the general paediatric medical unit and 13 (28%) to the paediatric intensive care unit (PICU). Results showed that patients admitted to the PICU were noted to have more severe symptoms and markers of inflammatory response. The most common symptoms at admission were cough (63%) and fever (60.9%). Of the 13 patients in the PICU, 8 (61.5%) were discharged home, and 4 (30.7%) patients remain hospitalized on ventilatory support at day 14. Authors conclude that their study showed a higher rate of PICU admission per hospitalization (28.2%), which they believe may be a reflection of a variety of social determinants that influence health outcomes.
Abstract
OBJECTIVE To describe the clinical profiles and risk factors for critical illness in hospitalized children and adolescents with coronavirus disease 2019 (COVID-19). STUDY DESIGN Children 1 month to 21 years of age with COVID-19 from a single tertiary care children's hospital between March 15 and April 13, 2020 were included. Demographic and clinical data were collected. RESULTS In total, 67 children tested positive for COVID-19; 21 (31.3%) were managed as outpatients. Of 46 admitted patients, 33 (72%) were admitted to the general pediatric medical unit and 13 (28%) to the pediatric intensive care unit (PICU). Obesity and asthma were highly prevalent but not significantly associated with PICU admission (P = .99). Admission to the PICU was significantly associated with higher C-reactive protein, procalcitonin, and pro-B type natriuretic peptide levels and platelet counts (P < .05 for all). Patients in the PICU were more likely to require high-flow nasal cannula (P = .0001) and were more likely to have received Remdesivir through compassionate release (P < .05). Severe sepsis and septic shock syndromes were observed in 7 (53.8%) patients in the PICU. Acute respiratory distress syndrome was observed in 10 (77%) PICU patients, 6 of whom (46.2%) required invasive mechanical ventilation for a median of 9 days. Of the 13 patients in the PICU, 8 (61.5%) were discharged home, and 4 (30.7%) patients remain hospitalized on ventilatory support at day 14. One patient died after withdrawal of life-sustaining therapy because of metastatic cancer. CONCLUSIONS We describe a higher than previously recognized rate of severe disease requiring PICU admission in pediatric patients admitted to the hospital with COVID-19.
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Prevalence, Severity and Mortality associated with COPD and Smoking in patients with COVID-19: A Rapid Systematic Review and Meta-Analysis.
Alqahtani, JS, Oyelade, T, Aldhahir, AM, Alghamdi, SM, Almehmadi, M, Alqahtani, AS, Quaderi, S, Mandal, S, Hurst, JR
PloS one. 2020;15(5):e0233147
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This meta-analysis reviewed 15 studies covering a total of 2473 confirmed COVID-19 patients to summarise the potential risk factors for smokers and patients with chronic obstructive pulmonary disease (COPD), a dysfunction of the lung associated with limitation in airflow. They found that neither COPD or smoking increased the initial risk of contracting COVID-19 with only 2% and 9% respectively of the cases falling into these categories. However, both groups had increased risk of developing more servere forms of COVID-19 requiring hospitalisation, admission to Intensive Care Units (ICU), mechanical ventilation, and ultimately death, with a much higher mortality rate of 60% versus other patients. Current smokers were also shown to have double the risk of complications versus ex-smokers. The most severe cases were generally in the older age brackets, with coexisting comorbidities and a hypothesized greater amount of lung damage. Both groups showed signs of acute inflammation and had a much slower recovery compared to non-smokers and patients without COPD. Despite the low prevalence of these groups contracting COVID-19, these people should be considered vulnerable because of the severity of symptoms and greater burden on healthcare.
Abstract
BACKGROUND Coronavirus disease 2019 (COVID-19) is an evolving infectious disease that dramatically spread all over the world in the early part of 2020. No studies have yet summarized the potential severity and mortality risks caused by COVID-19 in patients with chronic obstructive pulmonary disease (COPD), and we update information in smokers. METHODS We systematically searched electronic databases from inception to March 24, 2020. Data were extracted by two independent authors in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Study quality was assessed using a modified version of the Newcastle-Ottawa Scale. We synthesized a narrative from eligible studies and conducted a meta-analysis using a random-effects model to calculate pooled prevalence rates and 95% confidence intervals (95%CI). RESULTS In total, 123 abstracts were screened and 61 full-text manuscripts were reviewed. A total of 15 studies met the inclusion criteria, which included a total of 2473 confirmed COVID-19 patients. All studies were included in the meta-analysis. The crude case fatality rate of COVID-19 was 7.4%. The pooled prevalence rates of COPD patients and smokers in COVID-19 cases were 2% (95% CI, 1%-3%) and 9% (95% CI, 4%-14%) respectively. COPD patients were at a higher risk of more severe disease (risk of severity = 63%, (22/35) compared to patients without COPD 33.4% (409/1224) [calculated RR, 1.88 (95% CI, 1.4-2.4)]. This was associated with higher mortality (60%). Our results showed that 22% (31/139) of current smokers and 46% (13/28) of ex-smokers had severe complications. The calculated RR showed that current smokers were 1.45 times more likely [95% CI: 1.03-2.04] to have severe complications compared to former and never smokers. Current smokers also had a higher mortality rate of 38.5%. CONCLUSION Although COPD prevalence in COVID-19 cases was low in current reports, COVID-19 infection was associated with substantial severity and mortality rates in COPD. Compared to former and never smokers, current smokers were at greater risk of severe complications and higher mortality rate. Effective preventive measures are required to reduce COVID-19 risk in COPD patients and current smokers.
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The COVID-19 Pandemic: a Call to Action to Identify and Address Racial and Ethnic Disparities.
Laurencin, CT, McClinton, A
Journal of racial and ethnic health disparities. 2020;7(3):398-402
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The severe acute respiratory syndrome coronavirus 2 virus was first identified in late 2019 in Wuhan, China. Various unsubstantiated reports emerged declaring that the genetic constitution of Blacks or even the presence of melanin rendered Blacks immune to the virus. This study is a call of action which reviews preliminary data on race and ethnicity in the peer-reviewed literature for citizens in America affected by COVID-19. Findings demonstrate that communities of colour (Blacks) have a higher rate of infection and death in comparison to their population percentage in the state of Connecticut. However, authors are unable to draw conclusions since race and ethnicity data is missing and the data in this paper is the earliest data available. Therefore, the authors call for action to identify and address racial and ethnic health disparities in the COVID-19 crisis.
Abstract
The Coronavirus disease 2019 (COVID-19) pandemic has significantly impacted and devastated the world. As the infection spreads, the projected mortality and economic devastation are unprecedented. In particular, racial and ethnic minorities may be at a particular disadvantage as many already assume the status of a marginalized group. Black Americans have a long-standing history of disadvantage and are in a vulnerable position to experience the impact of this crisis and the myth of Black immunity to COVID-19 is detrimental to promoting and maintaining preventative measures. We are the first to present the earliest available data in the peer-reviewed literature on the racial and ethnic distribution of COVID-19-confirmed cases and fatalities in the state of Connecticut. We also seek to explode the myth of Black immunity to the virus. Finally, we call for a National Commission on COVID-19 Racial and Ethnic Health Disparities to further explore and respond to the unique challenges that the crisis presents for Black and Brown communities.