Background and aims: COVID-19 is an emerging pandemic due to droplet infection of 2019-novel coronavirus (2019-nCoV). Due to its rapid transmission and high case-fatality rate, recognition of its risk and prognostic factor is important. Obesity has been associated with impaired immune system, increasing the susceptibility for 2019-nCoV infection. We aimed to study the impact of obesity to the prognosis and disease severity of COVID-19. Methods: A systematic search and handsearching was conducted in four databases: Cochrane, MEDLINE, EMBASE, and PubMed. The identified articles were screened using the chosen eligibility criteria. We obtained three retrospective cohort studies (Wu J et al., Lighter J et al., and Simonnet A et al.) to be critically appraised using Newcastle Ottawa Scale. Results: The findings of all included studies were consistent in stating the contribution of obesity as a risk factor to increase the requirement for advanced medical care. Study with the highest quality, Simonnet A et al., reported an increase need of invasive mechanical ventilation in COVID-19 patients with body mass index higher than 35 kg/m 2 , OR: 7.36 (1.63e33.14; p ¼ 0.021). This is associated with a higher mortality rate in obese population infected with COVID-19. Conclusion: Obesity is an independent risk and prognostic factor for the disease severity and the requirement of advanced medical care in COVID-19. This systematic review highlights a particularly vulnerable group e obese, and emphasises on the importance of treatment aggression and disease prevention in this population group.

Highlights Admission fasting blood glucose (AFBG) independently predicts poor COVID-19 outcomes. Risk of COVID-19 severity rises by 33% for each 1 mmol/L increase in AFBG. There is high-quality evidence on the independent link between AFBG and severity. We found moderate-quality evidence linking AFBG with mortality and poor outcomes. Further researches on the independent prognostic value of admission random BG are required.

No abstract

Background: Multiple reports suggested disproportionate impact of Covid-19 on ethnic minorities. Whether ethnicity is an independent risk factor for severe Covid-19 illness is unclear. Purpose: Review the association between ethnicity and poor Covid-19 outcomes including all-cause mortality, hospitalisation, critical care admission, respiratory and kidney failure. Data Sources: MEDLINE, EMBASE, Cochrane COVID-19 Study Register, WHO COVID-19 Global Research Database up to 15/06/2020, and preprint servers. No language restriction. Study Selection: All studies providing ethnicity-aggregated data on the pre-specified outcomes, except case reports or interventional trials Data Extraction: Pairs of investigators independently extracted data, assessed risk of bias using Newcastle-Ottawa scale (NOS), and rated certainty of evidence following GRADE framework. Data Synthesis: Seventy-two articles (59 cohort studies with 17,950,989 participants; 13 ecological studies; 54 US-based and 15 UK-based; 41 peer-reviewed) were included for systematic review and 45 for meta-analyses. Risk of bias was low, with median NOS of 7 (interquartile range 6-8). In the unadjusted analyses, compared to white ethnicity, all-cause mortality risk was similar in Black (RR:0.96 [95%CI: 0.83-1.08]), Asian (RR:0.99 [0.85-1.16]) but reduced in Hispanic ethnicity (RR:0.69 [0.57-0.84]). Age and sex-adjusted-risks were significantly elevated for Black (HR:1.38 [1.09-1.75]) and Asian (HR:1.42 [1.15-1.75]), but not for Hispanic (RR:1.14 [0.93-1.40]). Further adjusting for comorbidities attenuated these association to non-significance; Black (HR:0.95 [0.72-1.25]); Asian (HR:1.17 [0.84-1.63]); Hispanic (HR:0.94 [0.63-1.44]). Similar results were observed for other outcomes. In subgroup analysis, there is a trend towards greater disparity in outcomes for UK ethnic minorities, especially hospitalisation risks. Limitations: Paucity of evidence on native ethnic groups, and studies outside US and UK. Conclusions: Currently available evidence cannot confirm ethnicity as an independent risk factor for severe Covid-19 illness, but indicates that disparity may be partially attributed to greater burden of comorbidities. Registration: PROSPERO, CRD42020188421 Funding source: none

Cardiovascular disease (CVD) correlates with inflammation and a reduction in circulating endothelial progenitor cells (cEPCs). Recently, CVD was shown to be the main cause of mortality in individuals with type 1 diabetes (T1DM). In animals, miR-342 was shown to exert an anti-inflammatory effect in CVD. Hypothesis: miR-342-3p/-5p are downregulated in subclinical CVD (T1DM), whereas inflammatory cytokines are upregulated. We studied miR -342 -3p/5p in plasma/peripheral blood mononuclear cells (PBMCs) in 29 T1DM and 20 controls (HC). Vascular health was measured by fibronectin adhesion assay (FAA), cEPCs (CD45dimCD34+133+ cells) and by assessing inflammation and tissue inhibition of metalloproteases (TIMP-1). In T1DM IL-7, IL-8, TNFα and VEGF-C were increased in plasma. MiR-342-3p/-5p were downregulated in PBMCs in T1DM, but not in plasma. PANX2, chemokine receptors CXCR1/2 mRNAs, were increased in PBMCs in T1DM. MiR-342-3p was negatively correlated with TIMP-1, IL-6, IL-8, TNF-α, HbA1c and CXCR2, whilst miR-342-5p was negatively correlated with TIMP-1, IL-6, IL-8 and HbA1c. There was a positive correlation among miR-342-3p, FAA and cEPCs, and between miR-342-5p and cEPCs. ROC curve analyses showed significant downregulation of miR-342-3p/-5p at HbA1c > 46.45 mmol/mol, indicating their potential as biomarkers for subclinical CVD. Our findings validated animal studies and confirmed the proangiogenic properties of miR-342-3p/-5p. MiR-342-3p/-5p-based intervention or monitoring may prove to be beneficial in managing CVD.