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Summary: Background: Economic hardship associated with chronic liver disease (CLD) may delay timely access to healthcare. Aim: To estimate the national burden of financial hardship across the spectrum of CLD in the United States (US) during the coronavirus disease 2019 (COVID‐19) pandemic. Methods: A cross‐sectional analysis was performed using the 2020–2021 US National Health Interview Survey database. The questionnaire defined financial hardship from medical bills and cost‐related nonadherence to medications in patients with CLD. We used weighted survey analysis to obtain the national estimates. Results: While 6.9% (95% confidence interval [CI]: 6.7%–7.2%) out of 60,689 US adults (weighted sample: 251 million) reported financial hardship and inability to pay medical bills; 10.6% (95% CI: 8.3%–13.4%), 18.2% (95% CI: 14.5%–22.6%), 22.6% (95% CI: 11.0%–41.0%) with hepatitis, CLD/cirrhosis, and liver cancer experienced an inability to pay their medical bills due to financial hardship, respectively. 19.8% (95% CI: 15.9%–24.5%) and 23.3% (95% CI: 12.5%–39.3%) with CLD/cirrhosis and liver cancer, respectively experienced cost‐related nonadherence to medications, compared to a tenth of US adults (10.7%, 95% CI: 10.3%–11.2%). CLD/cirrhosis demonstrated an independent association with financial hardship from medical bills and cost‐related nonadherence to medications. Overall, these disparities were more pronounced in individuals aged <65 years old. In addition, over 40% of individuals with CLD/cirrhosis reported difficulties accessing medical care during the COVID‐19 pandemic. CLD/cirrhosis showed an independent association with difficulties accessing medical care due to COVID‐19. Conclusions: Financial hardship from medical bills and cost‐related nonadherence to medication can negatively impact individuals with CLD and need further evaluation. [ABSTRACT FROM AUTHOR]

Summary: Background: Recently, a panel of multi‐society experts proposed steatotic liver disease (SLD) as an alternative terminology for metabolic dysfunction‐associated fatty liver disease (MAFLD) or nonalcoholic fatty liver disease (NAFLD). Aims: We compared the impact of SLD, subtype of SLD, MAFLD and NAFLD on all‐cause and cause‐specific mortality. Methods: A total of 7811 individuals in the third National Health and Nutrition Examination Survey and linked mortality through 2019 were analysed. SLD was defined based on ultrasonographic hepatic steatosis. SLD, subtype of SLD and MAFLD were defined using the proposed definitions. The Cox proportional hazard model assessed all‐cause/cause‐specific mortality. Results: During a median follow‐up of 27.1 years, individuals with SLD and MAFLD experienced approximately 13%–23% higher risk of all‐cause mortality (hazard ratio [HR]: 1.15, 95% confidence interval [CI]: 1.02–1.29 for SLD; HR: 1.23, 95% CI: 1.09–1.38 for MAFLD; HR: 1.13, 95% CI: 1.01–1.27 for metabolic dysfunction‐associated steatotic liver disease [MASLD]). Individuals with MetALD demonstrated a higher risk of all‐cause (HR: 1.68, 95% CI: 1.10–2.57) and cancer‐related mortality (HR: 2.40, 95% CI: 1.23–4.66). MASLD with advanced fibrosis had an increased risk of all‐cause mortality compared to MASLD without advanced fibrosis. Conclusions: SLD, especially MASLD and MetALD, is associated with increased all‐cause mortality among adults in the US. Given this significant association between SLD or subtype of SLD (MASLD and MetALD) and all‐cause mortality, adopting the proposed SLD criteria may help identify a sub‐group of individuals with SLD who are at an increased risk for all‐cause mortality. [ABSTRACT FROM AUTHOR]

Summary: Background and Aims: Patients with pre‐existing cirrhosis and exposure to coronavirus disease‐19 (COVID‐19) may portend a poor prognosis. We evaluated the temporal trends in aetiology‐based hospitalisations and potential predictors of in‐hospital mortality in hospitalisation with cirrhosis before and during the COVID‐19 pandemic. Methods: Based on the US National Inpatient Sample 2019–2020, we determined quarterly trends in aetiology‐based hospitalisations with cirrhosis and decompensated cirrhosis and identified predictors of in‐hospital mortality in hospitalisation with cirrhosis. Results: We analysed 316,418 hospitalisations, representing 1,582,090 hospitalisations with cirrhosis. Hospitalisations for cirrhosis increased at a relatively higher rate during the COVID‐19 era. Hospitalisation rates for alcohol‐related liver disease (ALD)‐related cirrhosis increased significantly (quarterly percentage change [QPC]: 3.6%, 95% CI: 2.2%–5.1%), with a notably higher rate during the COVID‐19 era. In contrast, hospitalisation rates for hepatitis C virus (HCV)‐related cirrhosis decreased steadily with a trend of −1.4% of QPC (95% CI: −2.5% to −0.1%). Quarterly trends in the proportion of ALD‐ (QPC: 1.7%, 95% CI: 0.9%–2.6%) and nonalcoholic fatty liver disease‐related (QPC: 0.7%, 95% CI: 0.1%–1.2%) hospitalisations with cirrhosis increased significantly but declined steadily for viral hepatitis. The COVID‐19 era and COVID‐19 infection were independent predictors of in‐hospital mortality during hospitalisation with cirrhosis and decompensated cirrhosis. Compared with HCV‐related cirrhosis, ALD‐related cirrhosis was associated with a 40% higher risk of in‐hospital mortality. Conclusion: In‐hospital mortality in cirrhosis was higher in the COVID‐19 era than in the pre‐COVID‐19 era. ALD is the leading aetiology‐specific cause of in‐hospital mortality in cirrhosis with an independent detrimental impact of the COVID‐19 infection. [ABSTRACT FROM AUTHOR]

Summary: Background: Non‐alcoholic fatty liver disease (NAFLD) affects obese and non‐obese individuals. However, mechanisms underlying non‐obese non‐alcoholic steatohepatitis (NASH) remain unclear. Aims: To attempt to identify metabolic perturbations associated with non‐obese and obese NAFLD using a lipidomics approach. Methods: A cross‐sectional analysis of 361 subjects with biopsy‐proven NAFLD (157 NAFL and 138 NASH) and healthy controls (n = 66) was performed. Individuals were categorised as obese or non‐obese based on the Asian cut‐off for body mass index. Circulating lipidomic profiling of sera was performed based on the histological severity of NAFLD. Circulating lipidomic alterations were validated with an independent validation set (154 NAFLD subjects [93 NAFL and 61 NASH] and 21 healthy controls). Results: Saturated sphingomyelin (SM) species were significantly associated with visceral adiposity in non‐obese NAFLD (SM d38:0; P < 0.001) but not in obese NAFLD. Additionally, SM levels were significantly associated with systemic and adipose tissue insulin resistance (SM d38:0; P = 0.002 and <0.001, respectively). Five potential lipid metabolites for non‐obese subjects and seven potential lipids for obese subjects were selected to predict NAFLD and NASH. These lipid combinations showed good diagnostic performance for non‐obese (area under the curve [AUC] for NAFLD/NASH = 0.916/0.813) and obese (AUC for NAFLD/NASH = 0.967/0.812) subjects. Moreover, distinctly altered patterns of diacylglycerol (DAG), triacylglycerol (TAG) and SM levels were confirmed in the validation set depending on the histological severity of NAFLD. Conclusion: Non‐obese and obese NAFLD subjects exhibit unique circulating lipidomic signatures, including DAGs, TAGs and SMs. These lipid combinations may be useful biomarkers for non‐obese and obese NAFLD patients. [ABSTRACT FROM AUTHOR]

Summary: Background: Currently, the relationship between depression and non‐alcoholic fatty liver disease (NAFLD) is not clearly defined. Aim: To determine whether depression is associated with NAFLD and NAFLD‐related advanced fibrosis in a large population sample. Methods: We performed a cross‐sectional analysis using the 2007‐2016 National Health and Nutrition Examination Survey database among adults (20 years or older) in the United States (US). Depression and functional impairment due to depression were assessed with the Patient Health Questionnaire (PHQ‐9). NAFLD was defined by utilising the US fatty liver index (USFLI), hepatic steatosis index (HSI) and the fatty liver index (FLI) in the absence of other causes of chronic liver disease. The presence and absence of advanced fibrosis in NAFLD were defined by Fibrosis‐4 score. Results: Of the 10 484 subjects (mean age 47.0 years; 48.8% men), the prevalence of depression and functional impairment due to depression was higher in subjects with NAFLD than in those without. Compared to subjects without depression, those with depression were 1.6‐2.2‐fold more likely to have NAFLD. In our multivariate analyses, depression_med was associated with increased risk of NAFLD using USFLI (odds ratio [OR] 1.48 95% confidence interval [CI] 1.17‐1.87), HSI (OR 1.51 95% CI 1.04‐2.19) and FLI (OR 2.01 95% CI 1.65‐2.48), respectively. The addition of diabetes, obesity and lipid profile to the model reduced the ORs for depression, but the significance persisted. Depression was not associated with NAFLD‐related advanced fibrosis. Conclusions: In a nationally representative sample of US adults, depression was independently associated with NAFLD. [ABSTRACT FROM AUTHOR]

Summary: Background: Long term renal safety of antiviral agents against hepatitis B virus (HBV) has been debated. Aim: To compare longitudinal trends of renal function among HBV mono‐infected patients receiving entecavir (ETV), tenofovir disoproxil fumarate (TDF), and adefovir (ADV) in comparison to untreated subjects. Methods: A retrospective cohort consisting of 815 patients with chronic HBV infection was constructed. Serial estimated glomerular filtration rate (eGFR) was compared to the expected rate of age‐dependent decline in eGFR, derived from the National Health and Nutrition Examination Survey (NHANES) data. Generalised estimating equations and linear mixed‐effects models were used to compare trends in eGFR (in mL/min/1.73m2 as a "unit"). Results: In NHANES data (n = 23 051), each year of age was associated with a 0.86 unit decrease in eGFR in subjects without hypertension and 0.96 units with hypertension. The Stanford cohort consisted of patients who received ETV (n = 207), TDF (n = 191), ADV (n = 46) or no therapy (n = 371). After a median follow‐up 4.0 (interquartile range: 1.9‐6.5) years, there was no significant difference in the expected and observed rates of eGFR decline in untreated HBV patients. Patients receiving antiviral treatment experienced steeper reduction in renal function than expected. In the multivariable model, ETV was associated with eGFR loss at 1.81 units per year (P = 0.06, compared to untreated patients). TDF‐ and ADV‐treated patients experienced significantly higher rate of eGFR loss at 2.21 and 2.63 units per year, respectively (both P < 0.01). Conclusion: In this longitudinal cohort study, HBV patients receiving antiviral therapy, particularly TDF and ADV, experienced more rapid loss in eGFR. [ABSTRACT FROM AUTHOR]