Background Chronic liver disease (CLD) represents a major global health burden. We undertook this study to identify the factors associated with adverse outcomes in patients with CLD who acquire the novel coronavirus-2019 (COVID-19). Methods We conducted a multi-center, observational cohort study across 21 institutions in the United States (US) of adult patients with CLD and laboratory-confirmed diagnosis of COVID-19 between March 1, 2020 and May 30, 2020. We performed survival analysis to identify independent predictors of all-cause mortality and COVID-19 related mortality, and multivariate logistic regression to determine the risk of severe COVID-19 in patients with CLD. Results Of the 978 patients in our cohort, 867 patients (mean age 56.9±14.5 years, 55% male) met inclusion criteria. The overall all-cause mortality was 14.0% (n = 121), and 61.7% (n = 535) had severe COVID-19. Patients presenting with diarrhea or nausea/vomiting were more likely to have severe COVID-19. The liver-specific factors associated with independent risk of higher overall mortality were alcohol-related liver disease (ALD) (hazard ratio [HR] 2.42, 95% confidence interval [CI] 1.29-4.55), decompensated cirrhosis (HR 2.91 [1.70-5.00]) and hepatocellular carcinoma (HCC) (HR 3.31 [1.53-7.16]). Other factors were increasing age, diabetes, hypertension, chronic obstructive pulmonary disease and current smoker. Hispanic ethnicity (odds ratio [OR] 2.33 [1.47-3.70]) and decompensated cirrhosis (OR 2.50 [1.20-5.21]) were independently associated with risk for severe COVID-19. Conclusions The risk factors which predict higher overall mortality among patients with CLD and COVID-19 are ALD, decompensated cirrhosis and HCC. Hispanic ethnicity and decompensated cirrhosis are associated with severe COVID-19. Our results will enable risk stratification and personalization of the management of patients with CLD and COVID-19.

Background Coronavirus disease 2019 (COVID-19) is associated with liver injury, but the prevalence and patterns of liver injury in liver transplant (LT) recipients with COVID-19 is not defined. Approach and Results We conducted a multicenter study in the US of 112 adult LT recipients with COVID-19. The median age was 61 years (IQR 20), 54.5% (n=61) were male, and 39.3% (n=44) Hispanic. The mortality rate was 22.3% (n=25); 72.3% (n=81) were hospitalized and 26.8% (n=30) admitted to the ICU. Analysis of peak values of alanine aminotransferase (ALT) during COVID-19 showed moderate liver injury (ALT 2-5x ULN) in 22.2% (n= 18) and severe liver injury (ALT > 5x ULN) in 12.3% (n= 10). Compared to age and gender matched non-transplant patients with CLD and COVID-19 (n=375), the incidence of acute liver injury was lower in LT recipients (47.5% vs. 34.6%; p=0.037). Variables associated with liver injury in LT recipients were younger age (p= 0.009, odds ratio (OR) 2.06 [1.20-3.54]), Hispanic ethnicity (p= 0.011; OR 6.01 [1.51-23.9]), metabolic syndrome (p= 0.016; OR 5.87 [1.38-24.99]), vasopressor use (p= 0.018; OR 7.34 [1.39-38.52]) and antibiotic use (p= 0.046; OR 6.93 [1.04-46.26]). Reduction in immunosuppression (49.4%) was not associated with liver injury (p= 0.156) or mortality (p= 0.084). Liver injury during COVID-19 was significantly associated with mortality (p= 0.007; OR 6.91 [95% CI: 1.68-28.48]) and ICU admission (p=0.007; OR 7.93[1.75-35.69]) in LT recipients. Conclusion Liver injury is associated with higher mortality and ICU admission in LT recipients with COVID-19. Hence, monitoring liver enzymes closely can help in early identification of patients at risk for adverse outcomes. Reduction of immunosuppression during COVID-19 did not increase risk for mortality or graft failure.

GME leadership curricula are heterogeneous and limited in effectiveness. Small group teaching, project-based learning, mentoring, and coaching were more frequently used in higher-quality studies.

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Background and study aims: Current diagnostic testing is inadequate to determine the malignant potential of pancreatic cysts, resulting in overcautious patient management. Integrated molecular pathology (IMP) testing combines molecular analysis with first-line test results (cytology, imaging, and fluid chemistry) to assess the malignant potential of pancreatic cysts. This multicenter study aimed to determine the diagnostic accuracy of IMP for pancreatic adenocarcinoma, and the utility of IMP testing under current guideline recommendations for managing pancreatic cysts. Patients and methods: Patients who had undergone previous IMP testing as prescribed by their physician and for whom clinical outcomes were available from retrospective record review were included (n?=?492). Performance was determined by correlation between clinical outcome and previous IMP diagnosis (?benign?/?statistically indolent? vs. ?statistically higher risk [SHR]?/ ?aggressive?) or an International Consensus Guideline (Sendai 2012) criteria model for ?surveillance? vs. ?surgery.? The Cox proportional hazards model determined hazard ratios for malignancy. Results: Benign and statistically indolent IMP diagnoses had a 97?% probability of benign follow-up for up to 7 years and 8 months from initial IMP testing. SHR and aggressive diagnoses had relative hazard ratios for malignancy of 30.8 and 76.3, respectively (both P??93?% probability of benign follow-up, with relative hazard ratios for SHR and aggressive IMP diagnoses of 16.1 and 50.2, respectively (both P?

Wilson's disease (WD) is a rare liver disease characterized by copper accumulation. Interestingly, iron overload has been observed in patients with WD without a diagnosis of primary hemochromatosis. This association has been recognized in the literature for almost two decades. 1-3 Of the chronic liver diseases known to cause secondary hemochromatosis, WD is classically not listed among them. The prevalence of secondary hemochromatosis in patients with WD is unknown. Despite the rarity of this disease, this knowledge is important because it yields therapeutic and monitoring implications in patients with WD. This article will begin with a review of the etiology and pathophysiology of WD, as well as the iron overload syndromes, followed by an explanation of the mechanism of secondary hemochromatosis in patients with WD. Finally, the authors will discuss the clinical implications of this knowledge with a focus on therapeutics. HePaTiC MeTal sTOraGe DisOrDers: COPPer anD irOn The mechanisms of hepatic transport of copper and iron are intimately related. 1 This relatedness can be observed in pathological states. 1 WD is a disorder of copper metabolism that is caused by mutations in the ATP7B gene, which codes for a copper transport protein in the liver. 4-6 The absent or compromised ATP7B protein not only causes copper accumulation in the liver and other organs but also reduces the amount of circulating ceruloplasmin. 4-6 Normally, the ATP7B protein loads copper onto ceruloplasmin, the primary means of copper transport throughout the body (Fig. 1). 1,7 In WD, the inability of the ATP7B protein to transport copper and thus facilitate its secretion through the biliary system leads to copper accumulation in the liver. 8,9 Copper accumulation and toxicity lead to hepatic, neurological, and psychiatric dysfunction, and

http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/video/17-4-reading-duong a video presentation of this article

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