The effect of lockdown during SARS-CoV-2 pandemic on maxillofacial injuries in a level I trauma centre: a comparative study.

INTRODUCTION: The SARS-CoV-2 pandemic forced many governments to impose nation-wide lockdowns. Government legislation forced limited travel on the population with restrictions on the normal way of life to limit spread of the SARS-CoV-2 virus. The aim of this study is to explore the effects of lockdown on the presentation of maxillofacial trauma in a level I trauma centre. METHODS: Comparative analysis was carried out using prospective and retrospective review of all consecutive patients admitted with any maxillofacial fracture in the lockdown period between 15th March and 15th June 2020 with the same period in 2019 to a Regional Trauma Maxillofacial Surgery Unit. Data included basic demographics and mechanism of injury including alcohol/drug influence, polytrauma, site of injury and treatment modality including escalation of care. RESULTS: Across both periods, there were a total of one hundred and five (n = 105) recorded episodes of traumatic fractures with fifty-three (n = 53) in the pre-lockdown cohort and fifty-two (n = 52) in the lockdown. Included patients were significantly (p = 0.024) older during lockdown (mean age 41.44 years SD 20.70, range 5-96) with no differences in gender distribution between cohorts (p = 0.270). Patients in lockdown were more likely to be involved in polytrauma (p < 0.05) and have sustained their injury by cycling/running or any outdoor related activity (p = 0.013). Lockdown saw a significant reduction in alcohol and drug related violence (p < 0.05). Significantly more patients required operative management (p = 0.038). CONCLUSION: Local lockdowns form part of the governments public health strategy for managing future outbreaks of SARS-CoV-2. Our study showed no significant reduction in volume of trauma during lockdown. It is vital that hospitals maintain trauma capacity to ensure that patients are treated in a timely manner.

Frailty score before admission as risk factor for mortality of renal patients during the first wave of the COVID pandemic in London

Background: Frailty is a known predictor of mortality and poor outcomes during hospital admission. In this large renal retrospective cohort study, we investigated whether frailer COVID-19 positive renal patients had worse outcomes. Design: All SARS-Cov-2 positive renal patients aged >=18 years who presented to the emergency department at the Royal Free Hospital or at the satellite dialysis centres from 10th of March until the 10th of May 2020, with recent data on frailty, were included. The follow up was until 26th of May 2020. Age, gender, ethnicity, body mass index, chronic kidney disease stage, modality of renal replacement therapy, co-morbidities, Rockwood clinical frailty score (CFS), C reactive protein and the neutrophil-to-lymphocyte count were collected at presentation. The primary outcome was the overall mortality rate following COVID-19 diagnosis. Secondary outcomes included the need for hospital admission.

Integrative genomic analysis highlights potential genetic risk factors for COVID-19

RATIONALE: The genes that influence the pathophysiology of COVID-19 have yet to be identified. Association analysis has found genetic loci for COVID-191. We used integrative genomics (IG) to combine gene expression and proteomic information with COVID-19 susceptibility loci in order to identify candidate genes for this disease. METHODS: For these analyses we used the COVID-19 Host Genetics Initiative genome-wide association (GWA) meta-analysis version 4 (COVID-19 positive versus COVID-19 negative), the Lung eQTL study2 (n=1,038), eQTLGen3 study (n=31,784) and the INTERVAL4 study (n=3,301). We conducted two IG methods (Bayesian Colocalization [coloc] and Summary Based Mendelian Randomization) to link gene and protein expression in lung and blood tissues with COVID-19 susceptibility loci. We identified the most consistently colocalized gene and conducted a Mendelian Randomization (MR) to assess the causal association of its protein ('exposure') with COVID-19 susceptibility ('outcomes'). Significant MR was set as P<0.05. RESULTS: The expression of 6 genes in lung and 12 in blood colocalized with COVID-19 susceptibility loci. SMR results demonstrated that the expression levels of 6 genes in lung tissue and 5 in blood were associated with COVID-19. Out of the candidate genes identified, two (ABO and SLC6A20) were within previously identified loci (Figure 1). Based on the SMR we found that the expression of SLC6A20 in lung was associated with a higher risk of COVID-19. Novel discovered associations included ERMP1, FCER1G, and CA11, genes which have been previously linked with respiratory diseases (i.e.: asthma) and host immune responses (i.e.: neutrophil and eosinophil counts). COVID-19 susceptibility also colocalized with plasma protein levels of ABO. Based on MR, ABO demonstrated a significant causal association (P = 2.10 × 10-5) with the risk of COVID-19 with increased levels of this protein in plasma associated with an increased risk of COVID-19. The top variant in the MR test (rs505922) was in complete linkage disequilibrium with the variant responsible for the blood O genotype, conferring reduced risk. CONCLUSIONS: This multi-omics approach led to the discovery of novel genes associated with COVID-19. We found that the ABO protein is a causal risk factor for COVID-19, with blood group O being protective against COVID-19. REFERENCES: 1. Ellinghaus, D. et al. N. Engl. J. Med. (2020). 2. Hao, K. et al. PLoS Genet. (2012). 3. Ṽsa, U. et al. bioRxiv. (2018). 4. Sun, B. B. et al. Nature. (2018) .