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Purpose: To examine nativity differences of co-occurring liver disease (LD) and heart failure (HF) on 13-year mortality among Mexican American older adults., Methods: Prospective cohort study of 1601 Mexican Americans aged ≥ 75 years from the Hispanic Established Population for the Epidemiologic Study of the Elderly (2004/05-2016). Participants were grouped into four groups: no LD and no HF (n = 1138), LD only (n = 53), HF only (n = 382), and both LD and HF (n = 28). We used Cox proportional hazards regression model to estimate the hazard ratio (HR) and 95% confidence interval (CI) of death over time., Results: The HR of death, as a function of HF only, was 1.32 (95% CI=1.07-1.62) among US-born and 1.36 (95% CI=1.04-1.78) among foreign-born participants, vs. those with no LD and no HF. Among foreign-born participants, the HR of death as a function of LD and HF was 3.39 (95% CI=1.65-6.93) vs. those without either. LD alone was not associated with mortality in either group. Among US-born, co-occurring LD and HF was not associated with mortality., Conclusions: Foreign-born participants with both LD and HF were at higher risk of mortality over 13 years of follow up., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

The Fontan operation is the current standard of care for single-ventricle congenital heart disease. Individuals with a Fontan circulation (FC) exhibit central venous hypertension and face life-threatening complications of hepatic fibrosis, known as Fontan-associated liver disease (FALD). The fundamental biology and mechanisms of FALD are little understood. Here, we generated a transcriptomic and epigenomic atlas of human FALD at single-cell resolution using multiomic snRNA-ATAC-seq. We found profound cell type-specific transcriptomic and epigenomic changes in FC livers. Central hepatocytes (cHep) exhibited the most substantial changes, featuring profound metabolic reprogramming. These cHep changes preceded substantial activation of hepatic stellate cells and liver fibrosis, suggesting cHep as a potential first "responder" in the pathogenesis of FALD. We also identified a network of ligand-receptor pairs that transmit signals from cHep to hepatic stellate cells, which may promote their activation and liver fibrosis. We further experimentally demonstrated that activins A and B promote fibrotic activation in vitro and identified mechanisms of activin A's transcriptional activation in FALD. Together, our single-cell transcriptomic and epigenomic atlas revealed mechanistic insights into the pathogenesis of FALD and may aid identification of potential therapeutic targets.

Studies that examine racial disparities in health outcomes often include analyses that account or adjust for baseline differences in co-morbid conditions. Often, these conditions are defined as dichotomous (Yes/No) variables, and few analyses include clinical and/or laboratory data that could allow for more nuanced estimates of disease severity. However, disease severity - not just prevalence - can differ substantially by race and is an underappreciated mechanism for health disparities. Thus, relying on dichotomous disease indicators may not fully describe health disparities. This study explores the effect of substituting continuous clinical and/or laboratory data for dichotomous disease indicators on racial disparities, using data from the Queen's Medical Center's (QMC) cardiac surgery database (a subset of the national Society of Thoracic Surgeon's cardiothoracic surgery database) as an example case. Two logistic regression models predicting in-hospital mortality were constructed: (I) a baseline model including race and dichotomous (Yes/No) indicators of disease (diabetes, heart failure, liver disease, kidney disease), and (II) a more detailed model with continuous laboratory values in place of the dichotomous indicators (eg, including Hemoglobin A1c level rather than just diabetes yes/no). When only dichotomous disease indicators were used in the model, Native Hawaiian and other Pacific Islander (NHPI) race was significantly associated with in-hospital mortality (OR: 1.57[1.29,2.47], P=.04). Yet when the more specific laboratory values were included, NHPI race was no longer associated with in-hospital mortality (OR: 1.67[0.92,2.28], P=.28). Thus, researchers should be thoughtful in their choice of independent variables and understand the potential impact of how clinical measures are operationalized in their research., Competing Interests: None of the authors identify a conflict of interest., (©Copyright 2023 by University Health Partners of Hawai‘i (UHP Hawai‘i).)

There are well-described racial and ethnic disparities in the burden of chronic liver diseases. Hispanic persons are at highest risk for developing nonalcoholic fatty liver disease, the fastest growing cause of liver disease. Hepatitis B disproportionately affects persons of Asian or African descent. The highest rates of hepatitis C occur in American Indian and Alaskan Native populations. In addition to disparities in disease burden, there are also marked racial and ethnic disparities in access to treatments, including liver transplantation. Disparities also exist by gender and geography, especially in alcohol-related liver disease. To achieve health equity, we must address the root causes that drive these inequities. Understanding the role that social determinants of health play in the disparate health outcomes that are currently observed is critically important. We must forge and/or strengthen collaborations between patients, community members, other key stakeholders, health care providers, health care institutions, professional societies, and legislative bodies. Herein, we provide a high-level review of current disparities in chronic liver disease and describe actionable strategies that have potential to bridge gaps, improve quality, and promote equity in liver care., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

The COVID-19 pandemic and social justice movement have highlighted the impact of social determinants of health (SDOH) and structural racism in the United States on both access to care and patient outcomes. With the evaluation for liver transplantation being a highly subjective process, there are multiple ways for SDOH to place vulnerable patients at a disadvantage. This policy corner focuses on three different methods to reverse the deleterious effects of SDOH-identify and reduce implicit bias, expand and optimize telemedicine, and improve community outreach., (© 2021 by the American Association for the Study of Liver Diseases.)