BACKGROUND There is little evidence about the association of pre-existing hepatitis C infection (HCV) with outcomes in patients with coronavirus disease 2019 (COVID-19). AIM To assess the prevalence of history of HCV among patients with COVID-19 and to study the relationship of in-hospital mortality in relation with other predictors of poor outcomes in the presence or absence of COVID-19 induced acute liver injury. METHODS In a retrospective single-center study design, 1193 patients with COVID-19 infection were studied. Patients were then classified into those with and without a history of HCV, 50 (4.1%) and 1157 (95.9%) respectively. RESULTS Multivariate cox-regression models showed that age, HCV, D-Dimer, and ferritin were the only predictors of in-hospital mortality. Acute liver injury and fibrosis score (Fib-4 score) were not different between both groups. Multivariate cox-regression model for liver profile revealed that aspartate aminotransferase/ alanine aminotransferase ratio, Fib-4 score, and HCV were predictors of in-hospital mortality. After propensity score matching HCV was the only predictor of mortality in the multivariate cox-regression model. A model including HCV was found to add predictive value to clinical and laboratory parameters. CONCLUSION In patients with COVID-19, history of HCV infection leads to an accentuated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virulence, irrespective of baseline comorbidities, admission laboratory variables, or COVID-19-induced liver injury, which may be related to extrahepatic effects of HCV leading to enhanced ACE-2/TMPRSS mechanisms of SARS-CoV-2 viral entry, baseline cytokine-mediated pro-inflammation, and endothelial dysfunction.

IntroductionSmoking causes inflammation of the lung epithelium by releasing cytokines and impairing mucociliary clearance. Some studies have linked smoking with severity of illness of COVID-19 whereas others have found no such association.MethodsThis was a retrospective analysis of all adults hospitalised with COVID-19 from 9 March to 18 May 2020.Results1173 patients met the study criteria. 837 patients never smoked whereas 336 patients were either current smokers or past smoker and were grouped together in smokers group. Patients in smokers group were more likely to be male and had higher incidence of underlying chronic obstructive pulmonary disease (19% vs 6%, p<0.001), HIV infection (11% vs 5%,p<0.001), cancer (11% vs 6%, p=0.005), congestive heart failure (15% vs 8%, p<0.001), coronary artery disease (15% vs 9%, p=0.3), chronic kidney disease (11% vs 8%, p=0.037) and end-stage renal disease (10% vs 6%, p=0.009) compared with non-smokers. Outcome analysis showed that smokers were more likely to develop critical illness requiring mechanical ventilation (47% vs 37% p=0.005). Univariate Cox model for survival analysis by smoking status showed that among smokers only current smokers had higher risk of death compared with never smokers (HR 1.61, 95% CI 1.22 to 2.12, p<0.001). In the multivariate approach, Cox model for the survival, female sex, young age, low serum lactate dehydrogenase and systemic steroid use were associated with overall improved survival.ConclusionIn our large single-centre retrospective database of patients hospitalised with COVID-19, smoking was associated with development of critical illness and higher likelihood of death.

Objective: Coronavirus disease 2019 (COVID-19) can infect patients in any age group including those with no comorbid conditions. Understanding the demographic, clinical, and laboratory characteristics of these patients is important toward developing successful treatment strategies. Approach and Results: In a retrospective study design, consecutive patients without baseline comorbidities hospitalized with confirmed COVID-19 were included. Patients were subdivided into ≤55 and >55yearsof age. Predictors of in-hospital mortality or mechanical ventilation were analyzed in this patient population, as well as subgroups. Stable parameters in overall and subgroup models were used to construct a cluster model for phenotyping of patients. Of 1207 COVID-19–positive patients, 157 met the study criteria (80≤55 and 77>55 years of age). Most reliable predictors of outcomes overall and in subgroups were age, initial and follow-up d -dimer, and LDH (lactate dehydrogenase) levels. Their predictive cutoff values were used to construct a cluster model that produced 3 main clusters. Cluster 1 was a low-risk cluster and was characterized by younger patients who had low thrombotic, coagulopathic, and inflammatory features. Cluster 2 was intermediaterisk that also consisted of younger population that had moderate level of thrombosis, higher inflammatory cells, and inflammatory markers. Cluster 3 was a high-risk cluster that had the most aggressive thrombotic, inflammatory, coagulopathic feature. Conclusions: In healthy patient population, COVID-19 remains significantly associated with morbidity and mortality. While age remains the most important predictor of in-hospital outcomes, thromboinflammatory interactions are also associated with worse clinical outcomes regardless of age in healthy patients.

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Cystic lesions of the liver are a heterogeneous group of disorders with varied etiology, prevalence, and clinical manifestations. Fibropolycystic liver disease encompasses a spectrum of related liver and biliary tract lesions caused by abnormal embryologic development of the ductal plates. These disorders include congenital hepatic fibrosis, biliary hamartomas, polycystic liver disease (PCLD), choledochal cysts, and Carolis disease. PCLD is arbitrarily defined as a liver that contains &#x3e;20 cysts. Most liver cysts are incidentally found on imaging studies, and the majority of the patients with liver cysts are asymptomatic. Rarely, complications such as compression, infection, and bleeding within the cyst can occur. Under the effect of the increased pressure, the epithelial lining of the cyst undergoes necrosis and sloughing, causing injury of the fragile blood vessels, leading to intracystic bleeding. The bleeding within or from the cyst can be precipitated by anticoagulation. We present a patient with PCLD who developed intracystic bleeding after he was started on apixaban for the prevention of thromboembolism.