COVID-19 Newest and Interesting Articles

Coronavirus disease 2019 (COVID-19) causes a spectrum of disease; some patients develop a severe proinflammatory state which can be associated with a unique coagulopathy and procoagulant endothelial phenotype. Initially, COVID-19 infection produces a prominent elevation of fibrinogen and D-dimer/fibrin(ogen) degradation products. This is associated with systemic hypercoagulability and frequent venous thromboembolic events. The degree of D-dimer elevation positively correlates with mortality in COVID-19 patients. COVID-19 also leads to arterial thrombotic events (including strokes and ischemic limbs) as well as microvascular thrombotic disorders (as frequently documented at autopsy in the pulmonary vascular beds). COVID-19 patients often have mild thrombocytopenia and appear to have increased platelet consumption, together with a corresponding increase in platelet production. Disseminated intravascular coagulopathy (DIC) and severe bleeding events are uncommon in COVID-19 patients. Here, we review the current state of knowledge of COVID-19 and hemostasis.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SAR2-COV-2) and was first identified in Wuhan, China, in December of 2019, but quickly spread to the rest of the world, causing a pandemic. While some studies have found no link between smoking status and severe COVID-19, others demonstrated a significant one. The present study aimed to determine the relationship between smoking and clinical COVID-19 severity via a systematic meta-analysis approach.

We searched the Google Scholar, PubMed, Scopus, Web of Science, and Embase databases to identify clinical studies suitable for inclusion in this meta-analysis. Studies reporting smoking status and comparing nonsevere and severe patients were included. Nonsevere cases were described as mild, common type, nonintensive care unit (ICU) treatment, survivors, and severe cases as critical, need for ICU, refractory, and nonsurvivors.

A total of 16 articles detailing 11322 COVID-19 patients were included. Our meta-analysis revealed a relationship between a history of smoking and severe COVID-19 cases (OR = 2.17; 95% CI: 1.37-3.46; < .001). Additionally, we found an association between the current smoking status and severe COVID-19 (OR = 1.51; 95% CI: 1.12-2.05; < .008). In 10.7% (978/9067) of nonsmokers, COVID-19 was severe, while in active smokers, severe COVID-19 occurred in 21.2% (65/305) of cases.

Active smoking and a history of smoking are clearly associated with severe COVID-19. The SARS-COV-2 epidemic should serve as an impetus for patients and those at risk to maintain good health practices and discontinue smoking. The trial is registered with the International Prospective Register of Systematic Reviews (PROSPERO) CRD42020180173.

The mortality rate associated with Covid-19 varies considerably among studies and determinants of this variability are not well characterized.

A systematic review of peer-reviewed literature published through March 31, 2020 was performed to estimate the mortality rate among hospitalized patients in China with a confirmed diagnosis of Covid-19. Hospital mortality rates were estimated using an inverse variance-weighted random-effects meta-analysis model. Funnel plot symmetry was evaluated for small-study effects, a one-study removed sensitivity analysis assessed the influence of individual studies on the pooled mortality rate, and metaregression assessed the association of potential confounding variables with mortality rates.

The review included 16 observational studies involving 1832 hospitalized patients with a diagnosis of Covid-19. The surveillance period among studies ranged from December 16, 2019 to February 23, 2020. The median patient age was 53 years and 53% were males. A total of 38.5% of patients presented with at least 1 comorbidity, most commonly hypertension (24.0%), cardiac disease (15.1%), and diabetes mellitus (14.4%). Fever and cough, reported in 84.8% and 61.7% of patients respectively, were the most common patient symptoms. The pooled mortality rate was 9.9% (95% confidence interval 6.1% to 14.5%). Funnel plot asymmetry was not observed and the meta-analysis results were not substantially influenced by any single study since the pooled mortality rate ranged from 8.9% to 11.1% following iterative removal of one study at a time. Substantial heterogeneity in the mortality rate was identified among studies (I = 87%; P < .001). In a metaregression that included demographics, patient risk factors, and presenting symptoms, only a higher prevalence of diabetes mellitus was associated with a higher mortality rate (P = .03).

In a meta-analysis of hospitalized patients in China with a diagnosis of Covid-19, the mortality rate was 9.9% and a higher diabetes mellitus prevalence was independently associated with a worse prognosis. The independent influence of diabetes mellitus with Covid-19 mortality should be viewed as hypothesis-generating and warrants further study.

Background: To date, several clinical laboratory parameters associated with Coronavirus disease 2019 (COVID-19) severity have been reported. However, these parameters have not been observed consistently across studies. The aim of this review was to assess clinical laboratory parameters which may serve as markers or predictors of severe or critical COVID-19.

Methods and findings: We conducted a systematic search of MEDLINE, Embase, Web of Science, CINAHL and Google Scholar databases from 2019 through April 18, 2020, and reviewed bibliographies of eligible studies, relevant systematic reviews, and the medRxiv pre-print server. We included hospital-based observational studies reporting clinical laboratory parameters of confirmed cases of COVID-19 and excluded studies having large proportions (>10%) of children and pregnant women. Two authors independently carried out screening of articles, data extraction and quality assessment. Meta-analyses were done using random effects model. Meta-median difference (MMD) and 95% confidence interval (CI) was calculated for each laboratory parameter. Forty-five studies in 6 countries were included. Compared to non-severe COVID-19 cases, severe or critical COVID-19 was characterised by higher neutrophil count (MMD: 1.23 [95% CI: 0.58 to 1.88] ×109 cells/L), and lower lymphocyte, CD4 and CD8 T cell counts with MMD (95% CI) of -0.39 (-0.47, -0.31) ×109 cells/L, -204.9 (-302.6, -107.1) cells/μl and -123.6 (-170.6, -76.6) cells/μl, respectively. Other notable results were observed for C-reactive protein (MMD: 36.97 [95% CI: 27.58, 46.35] mg/L), interleukin-6 (MMD: 17.37 [95% CI: 4.74, 30.00] pg/ml), Troponin I (MMD: 0.01 [0.00, 0.02] ng/ml), and D-dimer (MMD: 0.65 [0.45, 0.85] mg/ml).

Conclusions: Relative to non-severe COVID-19, severe or critical COVID-19 is characterised by increased markers of innate immune response, decreased markers of adaptive immune response, and increased markers of tissue damage and major organ failure. These markers could be used to recognise severe or critical disease and to monitor clinical course of COVID-19.

COVID-19, caused by a novel coronavirus, is a persistent global pandemic. It is crucial to examine existing reports to effectively summarize and characterize its clinical course. We used a large-scale meta-analysis to establish prevalence rates for loss of olfaction and gustation in COVID-19 positive patients. PubMed/Medline, Embase, and Web of Sciences were searched for articles published until April 30, 2020. Furthermore, to avoid missing papers, more searches were carried out in the reference lists of covered studies. Articles that mentioned olfactory and/or gustatory disorder in patients with COVID-19 were included for further analysis. Articles that did not report the aforementioned information were excluded. Duplicated articles, reviews, and meta-analysis were excluded as well. The quality of the references was assessed according to the checklist provided by JBI (Joanna Briggs Institute). We used independent extraction of data by multiple observers. The pooled frequency with 95% confidence intervals (CI) was assessed using random effect model. The main outcome measures reported were the pooled frequency of olfaction and pooled frequency of gustation disorder in patients with COVID-19 calculated using a random effect model weighted by the study population. The 15 included studies had 3,739 participants which all had confirmed COVID-19. Olfactory and gustatory disorders were assessed and a total number of 1,354 and 1,729 were reported to have taste or smell impairment, respectively. The estimated rate of taste disorder in patients with COVID-19 was 49.0% [95% confidence interval (CI) 34.0-64.0, I2: 96%] (Figure 2). The estimated rate of olfactory disorder in patients with COVID-19 was 61.0% (95% CI 44.0%-75.0%). Our meta-analysis demonstrated high rates of taste (49.0%) and smell (61.0%) disorders in patients with confirmed COVID-19. Results increase the power of recent reports-loss of olfactory and loss of gustation should now routinely be considered in the setting of COVID-19 infection.

The purpose of this systematic review and meta-analysis was to explore the literature and collate data comparing the mortality of coronavirus disease 2019 (COVID-19) patients with and without asthma. The databases PubMed, Scopus, Embase, Google Scholar, and medRxiv.org were searched for studies comparing the clinical outcomes of asthmatic patients with those of nonasthmatic patients diagnosed with COVID-19. Mortality data were summarized using the Mantel-Haenszel OR with 95% CI in a random-effects model. Five retrospective studies met the inclusion criteria. A meta-analysis of data from 744 asthmatic patients and 8,151 nonasthmatic patients indicated that the presence of asthma had no significant effect on mortality (OR = 0.96; 95% CI 0.70-1.30; I2 = 0%; p = 0.79). Results were stable in a sensitivity analysis. A descriptive analysis of other clinical outcomes indicated no difference in the duration of hospitalization and the risk of intensive care unit (ICU) transfer between asthmatic and nonasthmatic patients. To conclude, preliminary data indicates that asthma as a comorbidity may not increase the mortality of COVID-19. Data on the influence of asthma on the risk of hospitalization, the duration of hospitalization, the requirement of ICU admission, and disease severity is still too limited to draw any strong conclusions. Further studies with a larger sample size are required to establish strong evidence.