Background and Aim There is a paucity of data on the clinical presentations and outcomes of Corona Virus Disease-19 (COVID-19) in patients with underlying liver disease. We aimed to summarize the presentations and outcomes of COVID-19-positive patients and compare with historical controls. Methods Patients with known chronic liver disease who presented with superimposed COVID-19 (n = 28) between 22 April 2020 and 22 June 2020 were studied. Seventy-eight cirrhotic patients without COVID-19 were included as historical controls for comparison. Results A total of 28 COVID-19 patients (two without cirrhosis, one with compensated cirrhosis, sixteen with acute decompensation [AD], and nine with acute-on-chronic liver failure [ACLF]) were included. The etiology of cirrhosis was alcohol (n = 9), non-alcoholic fatty liver disease (n = 2), viral (n = 5), autoimmune hepatitis (n = 4), and cryptogenic cirrhosis (n = 6). The clinical presentations included complications of cirrhosis in 12 (46.2%), respiratory symptoms in 3 (11.5%), and combined complications of cirrhosis and respiratory symptoms in 11 (42.3%) patients. The median hospital stay was 8 (7-12) days. The mortality rate in COVID-19 patients was 42.3% (11/26), as compared with 23.1% (18/78) in the historical controls (p = 0.077). All COVID-19 patients with ACLF (9/9) died compared with 53.3% (16/30) in ACLF of historical controls (p = 0.015). Mortality rate was higher in COVID-19 patients with compensated cirrhosis and AD as compared with historical controls 2/17 (11.8%) vs. 2/48 (4.2%), though not statistically significant (p = 0.278). Requirement of mechanical ventilation independently predicted mortality (hazard ratio 13.68). Both non-cirrhotic patients presented with respiratory symptoms and recovered uneventfully. Conclusion COVID-19 is associated with poor outcomes in patients with cirrhosis, with worst survival rates in ACLF. Mechanical ventilation is associated with a poor outcome.

Background: Family history of bladder cancer confers an increased risk for concordant and discordant cancers in relatives. However, previous studies investigating this relationship lack any correction for smoking status of family members. We conducted a population-based study of cancer risks in relatives of bladder cancer patients and matched controls with exclusion of variant subtypes to improve the understanding of familial cancer clustering. Methods: Case subjects with urothelial carcinoma were identified using the Utah Cancer Registry and matched 1:5 to cancerfree controls from the Utah Population Database. Cox regression was used to determine the risk of cancer in first-degree relatives, second-degree relatives, first cousins, and spouses. A total of 229 251 relatives of case subjects and 1 197 552 relatives of matched control subjects were analyzed. To correct for smoking status, we performed a secondary analysis excluding families with elevated rates of smoking-related cancers. All statistical tests were two-sided. Results: First-and second-degree relatives of case subjects had an increased risk for any cancer diagnosis (hazard ratio [HR] ¼ 1.06, 95% confidence interval [CI] ¼ 1.03 to 1.09, P < .001; HR ¼ 1.04, 95% CI ¼ 1.02 to 1.07, P ¼ .001) and urothelial cancer (HR ¼ 1.73, 95% CI ¼ 1.50 to 1.99, P < .001; HR ¼ 1.35, 95% CI ¼ 1.21 to 1.51, P < .001). Site-specific analysis found increased risk for bladder (HR ¼ 1.69, 95% CI ¼ 1.47 to 1.95, P < .001), kidney (HR ¼ 1.30, 95% CI ¼ 1.08 to 1.57, P ¼ .006), cervical (HR ¼ 1.25, 95% CI ¼ 1.06 to 1.49, P ¼ .01), and lung cancer (HR ¼ 1.34, 95% CI ¼ 1.19 to 1.51, P < .001) in first-degree relatives. Second-degree relatives had increased risk for bladder (HR ¼ 1.35, 95% CI ¼ 1.2 to 1.5, P < .001) and thyroid cancer (HR ¼ 1.18, 95% CI ¼ 1.03 to 1.35, P ¼ .02). Spouses showed an increased risk for laryngeal (HR ¼ 2.68, 95% CI ¼ 1.02 to 7.05, P ¼ .04) and cervical cancer (HR ¼ 1.57, 95% CI ¼ 1.13 to 2.17, P ¼ .007). These results did not substantively change after correction for suspected smoking behaviors. Conclusion: Our results suggest familial urothelial cancer clustering independent of smoking, with increased risk in relatives for both concordant and discordant cancers, suggesting shared genetic or environmental roots. Identifying families with statistically significant risks for non-smoking-related urothelial cancer would be extremely informative for genetic linkage studies.

Background Acute‐on‐chronic liver failure (ACLF) is associated with a high short‐term mortality rate in the absence of liver transplantation. The role of therapeutic plasma exchange (TPE) in improving the outcomes of ACLF and acute decompensation (AD) is unclear. In this retrospective analysis, we aimed to determine the impact of TPE on mortality in patients with ACLF. Methods ACLF patients receiving TPE with standard medical treatment (SMT) were propensity score matched (PSM) with those receiving SMT alone (1:1) for sex, grades of ACLF, CLIF C ACLF scores, and the presence of hepatic encephalopathy. The primary outcomes assessed were mortality at 30 and 90 days. Survival analysis was performed using Kaplan Meier survival curves. Results A total of 1151 patients (ACLF n = 864 [75%], AD [without organ failure] n = 287 [25%]) were included. Of the patients with ACLF (n = 864), grade 1, 2, and 3 ACLF was present in 167 (19.3%), 325 (37.6%), and 372 (43.0%) patients, respectively. Thirty‐nine patients received TPE and SMT, and 1112 patients received only SMT. On PSM analysis, there were 38 patients in each group (SMT plus TPE vs SMT alone). In the matched cohort, the 30‐days mortality was lower in the TPE arm compared to SMT (21% vs 50%, P = .008), however, the 90‐day mortality was not significantly different between the two groups (36.8% vs 52.6%, P = .166); HR, 0.82 (0.44‐1.52), P = .549. Conclusion TPE improves short‐term survival in patients with ACLF, but has no significant impact on long‐term outcomes. Randomized control trials are needed to obtain a robust conclusion in this regard.

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