PLoS Med. 2020 Sep 8;17(9):e1003308. doi: 10.1371/journal.pmed.1003308. eCollection 2020 Sep.

ABSTRACT

BACKGROUND: Concerns over the safety of non-steroidal anti-inflammatory drug (NSAID) use during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been raised. We studied whether use of NSAIDs was associated with adverse outcomes and mortality during SARS-CoV-2 infection.

METHODS AND FINDINGS: We conducted a population-based cohort study using Danish administrative and health registries. We included individuals who tested positive for SARS-CoV-2 during the period 27 February 2020 to 29 April 2020. NSAID users (defined as individuals having filled a prescription for NSAIDs up to 30 days before the SARS-CoV-2 test) were matched to up to 4 non-users on calendar week of the test date and propensity scores based on age, sex, relevant comorbidities, and use of selected prescription drugs. The main outcome was 30-day mortality, and NSAID users were compared to non-users using risk ratios (RRs) and risk differences (RDs). Secondary outcomes included hospitalization, intensive care unit (ICU) admission, mechanical ventilation, and acute renal replacement therapy. A total of 9,236 SARS-CoV-2 PCR-positive individuals were eligible for inclusion. The median age in the study cohort was 50 years, and 58% were female. Of these, 248 (2.7%) had filled a prescription for NSAIDs, and 535 (5.8%) died within 30 days. In the matched analyses, treatment with NSAIDs was not associated with 30-day mortality (RR 1.02, 95% CI 0.57 to 1.82, p = 0.95; RD 0.1%, 95% CI -3.5% to 3.7%, p = 0.95), risk of hospitalization (RR 1.16, 95% CI 0.87 to 1.53, p = 0.31; RD 3.3%, 95% CI -3.4% to 10%, p = 0.33), ICU admission (RR 1.04, 95% CI 0.54 to 2.02, p = 0.90; RD 0.2%, 95% CI -3.0% to 3.4%, p = 0.90), mechanical ventilation (RR 1.14, 95% CI 0.56 to 2.30, p = 0.72; RD 0.5%, 95% CI -2.5% to 3.6%, p = 0.73), or renal replacement therapy (RR 0.86, 95% CI 0.24 to 3.09, p = 0.81; RD -0.2%, 95% CI -2.0% to 1.6%, p = 0.81). The main limitations of the study are possible exposure misclassification, as not all individuals who fill an NSAID prescription use the drug continuously, and possible residual confounding by indication, as NSAIDs may generally be prescribed to healthier individuals due to their side effects, but on the other hand may also be prescribed for early symptoms of severe COVID-19.

CONCLUSIONS: Use of NSAIDs was not associated with 30-day mortality, hospitalization, ICU admission, mechanical ventilation, or renal replacement therapy in Danish individuals who tested positive for SARS-CoV-2.

TRIAL REGISTRATION: The European Union electronic Register of Post-Authorisation Studies EUPAS34734.

PMID:32898149 | DOI:10.1371/journal.pmed.1003308

Eur Heart J. 2020 Sep 1;41(32):3038-3044. doi: 10.1093/eurheartj/ehaa623.

ABSTRACT

The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.

PMID:32882706 | DOI:10.1093/eurheartj/ehaa623

Stress Health. 2020 Aug 6. doi: 10.1002/smi.2975. Online ahead of print.

ABSTRACT

The COVID-19 outbreak has caused unprecedented social disruption. This collective trauma has resulted in school closures, shuttered businesses, rising unemployment, and a spike in emotional distress from the pandemic and related secondary stressors. In this time of crisis, and due to sweeping stay-at-home orders across the United States and internationally, billions of individuals are engaging in work and school from home. This has resulted in an increasing reliance on technology to accomplish these tasks. Moreover, there has been a substantial rise in the use of technology as a way to stay connected to loved ones, for entertainment, for telehealth services, and to engage in at-home-fitness. This commentary reviews literature that discusses the potential harm of increased technology use as well as its benefits. If mindfully leveraged, technology can be harnessed to promote increased social connectedness, work productivity, and leisure time. Mental health services may be more widely distributed through telehealth and related services, improving access and reducing health disparities. Recommendations about how technology can promote effective coping and improve physical and mental health during and after the COVID-19 pandemic are discussed. This article is protected by copyright. All rights reserved.

PMID:32762116 | DOI:10.1002/smi.2975

Ozaras R, et al. J Med Virol 2020.

ABSTRACT

In their study, Yue et al. reported influenza co-infection among COVID-19 patients as 57.3%. The study included a period of January 12-February 21, 2020 in Wuhan, China. We have recently detected this rate as 0.54% in Turkey. This difference between rates of co-infection can be explained by the seasonality of the influenza virus. Our study included the period of March 10-May 10. Another study from Wuhan, including the period of 28 January-29 February 2020, reported the rate of influenza co-infection among critically ill COVID-19 patients as 49.5%. Zhu et al. reported 2.7% influenza co-infections among COVID-19 patients, in their study from January 22-February 2. Two studies from USA reported low rates of 0.08% in March 16-April 20, and 0.9% in March 3-March 25. Therefore, studies from the influenza season reported very high rates of co-infection. When the COVID-19 came to Europe and America, the influenza season was almost over and thus the co-infection rates are low. A recent research found moderate to strong correlation between higher influenza vaccine uptake in the elderly and lower COVID-19 deaths in Italy. This might be explained by the prevention of influenza co-infection. In elderly, both influenza and COVID-19 have higher rates of mortality. The impact of prevention of influenza in this fragile group is higher. Current influenza-COVID-19 co-infection reports suggest that co-infection rates are as high as 57% when influenza is circulating. Pending the new waves of COVID-19, it is reasonable to recommend influenza vaccination especially for elderly, but most probably, to general population. This article is protected by copyright. All rights reserved.

PMID:32639643 | DOI:10.1002/jmv.26272