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Coronavirus disease 2019 (COVID-19) has become a serious threat to global public health. Unfortunately, to date, there are no specific vaccines or targeted drugs, and the number of patients with positivity for systemic acute respiratory syndrome-novel coronavirus-2 infection is growing worldwide. Patients with COVID-19 may be at risk for liver injury, but the mechanism and clinical significance of injury remains unclear. Proposed mechanisms include direct virus-induced insults, immune-mediated damage (due to excessive inflammatory response), and drug-induced injury. COVID-19-related liver dysfunction is now gaining widespread attention; however, liver injury’s impact on the outcome of COVID-19 patients is not clearly understood. We have evaluated the impact of liver insults on the hospitalization outcome of COVID-19 patients admitted to a suburban New York safety-net hospital and would like to share our preliminary results in a Letter to the Editor instead of an Original Article for rapid dissemination to the worldwide audience. In our retrospective, unmatched, single-center analysis, we have identified the first 639 confirmed COVID-19 patients (ages $18 years) admitted to our facility from March 2020 to May 2020. Elevated liver-related enzymes [serum alanine aminotransferase (commonly referred to as ALT) >40 U/L, aspartate aminotransferase (commonly referred to as AST) >40 U/L, or alkaline phosphatase (commonly referred to as ALP) >120] were used to stratify patients with or without liver injury. The primary outcome was all-cause in-hospital mortality; other in-patient outcomes, including cardiac arrest, acute respiratory distress syndrome, arrhythmia, shock, and intubation rate, were also measured. The Pearson’s chi-square test and Student’s t-test were used for evaluating categorical and continuous variables, respectively. A two-step hierarchical multivariate regression model was performed to assess the risk of in-patient mortality and other hospitalization outcomes after adjusting for baseline characteristics and comorbidities. All statistical analyses were performed using SPSS Corp. Version 22 (Armonk, NY, USA). This analysis was approved by the Institutional Review Board (IRB) of Nassau Health Care Corporation (NHCC) at Nassau University Medical Center (NUMC), under IRB reference # 20-277. Out of the total 639 COVID-19 patients, 476 (74.5%) [mean age of 58.89±15.61 years, 63.0%male] had evidence of liver injury. COVID-19 liver injury cohorts had statistically significant higher rates of all cause in-patient mortality [35.5% vs. 22.7%; adjusted odds ratio (aOR): 2.84; 95% confidence interval (CI): 1.71-4.71; p<0.001). COVID-19 liver injury was observed more often in our Hispanic patient population (38.2%). The COVID-19 liver injury group showed higher risk of other in-patient outcomes, such as cardiac arrest (26.1% vs. 14.1%; aOR: 2.65; 95% CI: 1.52-4.59; p#0.001), requirement of intubation (30% vs. 14.7%; aOR: 2.87; 95% CI: 1.70-4.85; p<0.001), acute respiratory distress syndrome (43.1% vs. 30.7%; aOR: 1.89; 95% CI: 1.23-2.91; p=0.004), arrhythmia (5.2% vs. 0.6%; aOR: 3.16; 95% CI: 0.95-10.33; p=0.05) and shock (15% vs. 2.8%; aOR: 2.06; 95% CI: 1.15-3.70; p=0.016) compared to COVID-19 patients without evidence of liver injury (Tables 1 and 2). The infection of liver cells with the systemic acute respiratory syndrome-novel coronavirus-2 (SARS-CoV-2) may directly cause liver dysfunction. Other indirect mechanisms of liver injury are also plausible. Chen et al. showed that more than one-third of COVID-19 patients have some liver dysfunction; in most cases, patients had mild-to-moderate elevations of ALT or AST levels. Our analysis has shown that approximately every fourth patient presented evidence of liver injury. It is postulated that SARS-CoV-2 binds to host ACE-2 receptors (ACE2) on target cells to gain entry. Interestingly, ACE2 receptors are also highly expressed within the biliary tree. However, the cholestatic liver disease is not a common feature of COVID-19. Chau et al. demonstrated in their study that liver biopsies of SARS patients showed a significant increase in mitotic cells, eosinophils and balloon-like liver cells, which indicated that SARS-CoV-2 might induce liver cell apoptosis and thus lead to liver damage. The study by Tan et al. showed that SARS-CoV-2 specific protein 7a could induce cell apoptosis in different organs (including lung, kidney, and liver) through the caspase-dependent

Impact of Liver Injury in COVID-19 Patients: Single-center Retrospective Cohort Analysis