Liver Disease Mortality Research Articles

Incidence, prevalence and mortality of chronic liver diseases in Sweden between 2005 and 2019

BackgroundUpdated data on the incidence, prevalence, and regional differences of chronic liver disease are missing from many countries. In this study, we aimed to describe time trends, incidence, prevalence, and mortality of a wide range of chronic liver diseases in Sweden.MethodsIn this register-based, nationwide observational study, patients with a register-based diagnosis of chronic liver disease, during 2005–2019, were retrieved from the Swedish National Board of Health and Welfare. Annual age-standardized incidence and mortality rates, and prevalence per 100,000 inhabitants was calculated and stratified on age, sex, and geographical region.ResultsThe incidence of alcohol-related cirrhosis increased by 47% (2.6% annually), reaching an incidence rate of 13.1/100,000 inhabitants. The incidence rate of non-alcoholic fatty liver disease and unspecified liver cirrhosis increased by 217% and 87% (8.0 and 4.3% annually), respectively, reaching an incidence rate of 15.2 and 18.7/100,000 inhabitants, and a prevalence of 24.7 and 44.8/100,000 inhabitants. Furthermore, incidence rates of chronic hepatitis C declined steeply, but liver malignancies have become more common. The most common causes of liver-related mortality were alcohol-related liver disease and unspecified liver disease.ConclusionThe incidence rates of diagnosed non-alcoholic fatty liver disease, alcohol-related cirrhosis, unspecified liver cirrhosis, and liver malignancies have increased during the last 15 years. Worryingly, mortality in several liver diseases increased, likely reflecting increasing incidences of cirrhosis in spite of a decreasing rate of hepatitis C. Significant disparities exist across sex and geographical regions, which need to be considered when allocating healthcare resources.

Serological Evidence of Hepatitis B Virus among Secondary School Students in a Community in Plateau State, Nigeria

Hepatitis B virus is among the common viral infectious agents of global public health concern because it increases the risk of hepatocellular cancer, liver fibrosis, and mortality from liver disease. The study's objectives were to detect hepatitis B surface antigen (HBsAg) in the blood samples of students of Government Secondary School, Bet, Pankshin, Plateau State. A cross-sectional analytical study was conducted between October and November 2018. Blood samples were collected from 168 participants which were analysed for HBsAg using a One-step Rapid Strip (Royal Care) and HBeAg by Combo Test Device (Skytech USA). Data were analyzed using SPSS version 21.0 (USA). P-values < 0.05 were considered significant. An overall 7.1% of the 168 samples analysed were seropositive for HBsAg and 6.7% for HBeAg. Males had a seropositivity of 11.6%, whereas females had a seropositivity of 4.0% (p = 0.061). The distribution of HBsAg in relation to age group was higher in the age group 13-19 years with 7.3% and the lowest in the age group 6-12 years with 6.7%. Those with history of sexual exposures had a seropositivity of 14.3% (p = 0.174; OR = 0.371, those with history of exposure to sharp objects had 7.3% (p = 0.869; OR = 0.876), those with the history of blood transfusion had none (p = 0.319; OR = 1.00), participants without history of ever screened for the virus had a seropositivity of 7.4% (p = 0.529; OR = 1.00) while the alcoholics had 13.6% (p = 0.205; OR = 0.416. It is imperative to act quickly to prevent liver disease morbidity and mortality given the seropositivity of 7.1% of HBV, which is of considerable public health concern. There is need to intensify campaign awareness and vaccination against HBV among all unvaccinated age groups.

Association of dietary insulinemic and inflammatory potential with risk of liver cancer and chronic liver disease mortality in postmenopausal women: a prospective cohort study

BackgroundLow diet quality, diabetes, and chronic inflammation are risk factors of liver cancer and chronic liver disease (CLD), but the extent to which insulinemic and inflammatory diets are independently associated with risk of liver cancer and CLD mortality is unknown. MethodsWe conducted a prospective cohort analysis among 78,356 postmenopausal women in the Women’s Health Initiative Observational Study. Two validated dietary indices, the empirical dietary index for hyperinsulinemia (EDIH) and the empirical dietary inflammation pattern (EDIP), were estimated from a food-frequency questionnaire. Incident cases of liver cancer and CLD mortality were adjudicated via review of medical records and linkage to National Death Index. Multivariable hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using Cox proportional hazards models, adjusted for age, diabetes, body mass index, and other covariates. ResultsDuring a median 22.1 y of follow-up, we documented 176 primary liver cancer cases and 156 CLD mortality cases. EDIH was positively associated with incident liver cancer (HRQuartile 4 vs. Quartile 1 = 1.68; 95% CI: 1.00, 2.83; P-trend = 0.05) and CLD mortality (HRQ4 vs. Q1 = 2.28; 95% CI: 1.25, 4.15; P-trend = 0.02) in the multivariable model. EDIP was also positively associated with liver cancer (HRQ4 vs. Q1 = 1.88; 95% CI: 1.17, 3.03; P-trend = 0.009) and CLD mortality (HRQ4 vs. Q1 = 1.85; 95% CI: 1.09, 3.15; P-trend = 0.007). Estimates remained significant and robust in sensitivity analyses. Further analyses indicated positive associations for refined grains, processed meat, sugary beverages, and eggs, and inverse associations for coffee/tea and poultry. ConclusionsDietary insulinemic and inflammatory potentials were independently associated with higher risk of liver cancer and CLD mortality in U.S. postmenopausal women. These findings suggest a potential role for diet modification to reduce risk of liver cancer and CLD.

AutoFibroNet: A deep learning and multi-photon microscopy-derived automated network for liver fibrosis quantification in MAFLD.

Liver fibrosis is the strongest histological risk factor for liver-related complications and mortality in metabolic dysfunction-associated fatty liver disease (MAFLD). Second harmonic generation/two-photon excitation fluorescence (SHG/TPEF) is a powerful tool for label-free two-dimensional and three-dimensional tissue visualisation that shows promise in liver fibrosis assessment. To investigate combining multi-photon microscopy (MPM) and deep learning techniques to develop and validate a new automated quantitative histological classification tool, named AutoFibroNet (Automated Liver Fibrosis Grading Network), for accurately staging liver fibrosis in MAFLD. AutoFibroNet was developed in a training cohort that consisted of 203 Chinese adults with biopsy-confirmed MAFLD. Three deep learning models (VGG16, ResNet34, and MobileNet V3) were used to train pre-processed images and test data sets. Multi-layer perceptrons were used to fuse data (deep learning features, clinical features, and manual features) to build a joint model. This model was then validated in two further independent cohorts. AutoFibroNet showed good discrimination in the training set. For F0, F1, F2 and F3-4 fibrosis stages, the area under the receiver operating characteristic curves (AUROC) of AutoFibroNet were 1.00, 0.99, 0.98 and 0.98. The AUROCs of F0, F1, F2 and F3-4 fibrosis stages for AutoFibroNet in the two validation cohorts were 0.99, 0.83, 0.80 and 0.90 and 1.00, 0.83, 0.80 and 0.94, respectively, showing a good discriminatory ability in different cohorts. AutoFibroNet is an automated quantitative tool that accurately identifies histological stages of liver fibrosis in Chinese individuals with MAFLD.

Pregnane X Receptor Gene Variation and Total Mortality in Nonalcoholic Fatty Liver Disease

The pregnane X receptor (PXR) is a nuclear receptor that plays a role in regulating the metabolism and clearance of drugs and xenobiotics in the liver. Variations in the PXR gene, including the rs7643645 variant, have been associated with altered PXR activity and potential implications for various liver-related conditions, including nonalcoholic fatty liver disease (NAFLD). It is known that the more progressive the NAFLD, the higher the hepatic and extra-hepatic mortality and morbidity. Käräjämäki et al investigated the total mortality in Finnish middle-aged ultrasonographically verified NAFLD patients with PXR rs7643645 variants. In up to 30 years of follow-up, PXR rs7643645 GG subjects were at an increased risk of total mortality compared with AA/AG subjects. The statistically significant difference prevailed after multiple adjustments for potentially confounding factors, RR, 2.024 (1.191-3.440), P = 0.009. In the subjects without NAFLD, the mortality risk was not associated with rs7643645 variants, 1.051 (0.708-1.560; P = 0.804). As the rs7643645 G variant disrupts a putative hepatocyte nuclear factor 4α binding site located in the PXR gene promoter and is associated with lower hepatic expression of PXR and its target genes, their result suggests that genetic disruption of xenobiotic metabolism increases mortality in subjects with NAFLD. Pharmacogenet Genomics. 2023 Feb 1;33(2):35-39. doi: 10.1097/FPC.0000000000000489.

Association of Statin Use With Risk of Liver Disease, Hepatocellular Carcinoma, and Liver-Related Mortality

Given the burden of chronic liver disease on the health care system, more information on the hepatoprotective association of statins in the general population is needed. To examine whether regular statin use is associated with a reduction in liver disease, particularly hepatocellular carcinoma (HCC) and liver-related deaths, in the general population. This cohort study used data from the UK Biobank (UKB) (individuals aged 37-73 years) collected from baseline (2006-2010) to the end of follow-up in May 2021, from the TriNetX cohort (individuals aged 18-90 years) enrolled from baseline (2011-2020) until end of follow-up in September 2022, and from the Penn Medicine Biobank (PMBB) (individuals aged 18-102 years) with ongoing enrollment starting in 2013 to the end of follow-up in December 2020. Individuals were matched using propensity score matching according to the following criteria: age, sex, body mass index, ethnicity, diabetes with or without insulin or biguanide use, hypertension, ischemic heart disease, dyslipidemia, aspirin use, and number of medications taken (UKB only). Data analysis was performed from April 2021 to April 2023. Regular statin use. Primary outcomes were liver disease and HCC development as well as liver-associated death. A total of 1 785 491 individuals were evaluated after matching (aged 55 to 61 years on average, up to 56% men, and up to 49% women). A total of 581 cases of liver-associated death, 472 cases of incident HCC, and 98 497 new liver diseases were registered during the follow-up period. Individuals were aged 55-61 years on average, with a slightly higher proportion of men (up to 56%). In UKB individuals (n = 205 057) without previously diagnosed liver disease, statin users (n = 56 109) had a 15% lower hazard ratio (HR) for the association of developing a new liver disease (HR, 0.85; 95% CI, 0.78-0.92; P < .001). In addition, statin users demonstrated a 28% lower HR for the association with liver-related death (HR, 0.72; 95% CI, 0.59-0.88; P = .001) and a 42% lower HR for the development of HCC (HR, 0.58; 95% CI, 0.35-0.96; P = .04). In TriNetX individuals (n = 1 568 794), the HR for the association of HCC was reduced even further for statin users (HR, 0.26; 95% CI, 0.22-0.31; P = .003). The hepatoprotective association of statins was time and dose dependent, with a significant association in PMBB individuals (n = 11 640) for incident liver diseases after 1 year of statin use (HR, 0.76; 95% CI, 0.59-0.98; P = .03). Taking statins was particularly beneficial in men, individuals with diabetes, and individuals with a high Fibrosis-4 index at baseline. Carriers of the heterozygous minor allele of PNPLA3 rs738409 benefited from statin use and had a 69% lower HR for the association with HCC (UKB HR, 0.31; 95% CI, 0.11-0.85; P = .02). This cohort study indicates substantial preventive associations of statins against liver disease, with an association with duration and dose of intake.

Trends in alcohol-related liver disease mortality in Australia: An age-period-cohort perspective.

There have been few systematic attempts to examine how alcohol-related mortality has changed in Australia, and no studies that have explored cohort effects in alcohol-related mortality. This study uses more than 50 years of data to measure age, period and cohort trends in alcohol-related liver disease (ALD) mortality. This was a retrospective age-period-cohort analysis of total Australian ALD mortality data from 1968 to 2020 in Australia. There was a total of 35 822 deaths-27 208 men (76%) and 8614 women (24%). Deaths from ALD were grouped into 5-year age groups and periods (e.g. deaths for 20-24-year-olds between 1968 and 1972 were combined). ALD mortality peaked in the late 1970s and early 1980s for both men and women. In age-period-cohort models, mortality was highest for cohorts born 1915-30. For example, men born between 1923 and 1927 had a relative risk of 1.58 [95% confidence interval (CI) = 1.52, 1.64] compared with men born between 1948 and 1952. For women, there was an increase in risk for cohorts born in the 1960s [e.g. the 1963-67 cohort had a relative risk (RR) of 1.16 (95% CI = 1.07, 1.25) compared with women born in 1948-52]. For men, there was a broad decline in mortality over time [e.g. in 2020, the RR was 0.87 (95% CI = 0.82, 0.92) compared with the reference year of 2000]. For women, mortality declined until 2000 and has been stable since. Alcohol-related liver disease mortality has declined across the Australian population since the 1970s and 1980s partly due to cohort-specific shifts as the highest-risk birth cohorts age. For women, this decline had stalled by the year 2000, and cohorts of women born during the 1960s were at higher risk than earlier cohorts, suggesting the need for thoughtful interventions as this population enters its highest-risk years for ALD mortality.

Cost-effectiveness of treating all hepatitis B-positive individuals in the United States.

Chronic hepatitis B virus (HBV) infection is a leading cause of liver disease and related mortality globally. However, most of the infected individuals in the United States remain undiagnosed and untreated. There is a need to understand more completely the economic and disease burden impact of removing treatment restrictions and increasing diagnosis and treatment. The PRoGReSs model, a dynamic HBV model that tracks the infected population by year, disease stage, and gender, was used to quantify the disease and economic burden of chronic HBV infection in the United States from 2020 to 2050 based on four scenarios: a status quo (base) scenario and three treat-all scenarios, in which screening, diagnosis, and treatment were maximized at different annual treatment price levels of $5382, $2000 and $750. Compared to the base scenario, the treat-all scenarios would avert 71,100 acute and 11,100 chronic incident cases of HBV, and 169,000 liver-related deaths from 2020 to 2050. At an annual treatment cost of $2000, treating all HBV infections would be highly cost-effective, and at $750 would be cost saving and would achieve a positive return on investment before 2050. Maximizing the diagnosed and treated HBV population in the United States would avert a significant number of cases of advanced liver disease and related mortality. Such interventions can also be cost-effective compared to the status quo strategy, and cost saving at a treatment price threshold of $750 annually, above the current lowest annual treatment cost of $362.

THU-430 - Prevalence and mortality of non-alcoholic fatty liver disease (NAFLD) in non-diabetics, pre-diabetics, and diabetics in the United States

THU-430 - Prevalence and mortality of non-alcoholic fatty liver disease (NAFLD) in non-diabetics, pre-diabetics, and diabetics in the United States

FRI-422 - Diabetes increases risk of mortality in alcohol-related liver disease

FRI-422 - Diabetes increases risk of mortality in alcohol-related liver disease

Low vitamin A levels are associated with liver-related mortality: a nationally representative cohort study.

Vitamin A, a fat-soluble vitamin that includes retinol and carotenoids, is implicated in liver fibrosis, whereas its deficiency has been associated with various liver diseases and higher overall mortality. This study aims to determine the relationship between levels of vitamin A species and liver fibrosis, as well as liver-related mortality in the population of the US. A total of 12,299 participants from the National Health and Nutrition Examination Survey III (NHANES III) were analyzed to provide nationally representative estimates of the relationship between the levels of vitamin A species and liver fibrosis measured by Fibrosis-4 (FIB-4) index and liver-related mortality. A low blood level of retinol, but not other retinoid derivatives, was associated with significant liver fibrosis after adjustment for demographics, anthropometric measurements, medical history, retinol, and carotene intakes. Compared with vitamin D and E, retinol deficiency demonstrated much stronger associations with a high FIB-4 score. Individuals with known risks of chronic liver disease (CLD) and the lowest pentile of retinol levels had ORs of 3.12 (95% CI, 1.64-5.91) for possible fibrosis and 19.7 (95% CI, 5.71-67.7) for likely fibrosis, and an HR of 7.76 (95% CI, 1.19-50.5) for liver-related mortality compared with those in the highest retinol-level pentile. These relationships were more pronounced among individuals with known risks of chronic liver disease than without. A low circulating retinol level is associated with liver fibrosis and liver-related mortality in chronic liver disease. This relationship is potentially driven by a mechanistic link rather than the malabsorption of fat-soluble vitamins and may be leveraged for disease prognostication and have therapeutic implications.

Feasibility and acceptability of a primary care liver fibrosis testing pathway centred on the diabetes annual review: PRELUDE1 prospective cohort study protocol

IntroductionNon-alcoholic fatty liver disease is the most common chronic liver disease worldwide affecting 20%–25% in the USA and Europe with a 60%–80% lifetime prevalence for people with type 2 diabetes...

Alcohol-Associated Liver Disease Mortality Rates by Race Before and During the COVID-19 Pandemic in the US

This cross-sectional study examines the national- and state-level age-adjusted mortality rates for alcohol-associated liver disease in 4 racial groups, with a focus on the American Indian or Alaska Native population.

Left ventricular remodeling in end-stage liver disease and post-transplant mortality assessed using end-diastolic pressure-volume relation analysis: Observational retrospective study

Diastolic dysfunction is regarded as an important predictor of outcome after liver transplantation (LT). We investigated the influence of liver disease severity on left ventricular diastolic properties using end-diastolic pressure-volume relationship (EDPVR) analysis in patients with end-stage liver disease (ESLD). Association between alterations of the EDPVR and mortality after LT was evaluated. In this observational retrospective cohort study, 3,211 patients who underwent LT for ESLD were included in analysis. Variables derived from single-beat EDPVR (diastolic stiffness-coefficient [β] and end-diastolic volume at an end-diastolic pressure of 20 mmHg [EDVI20] indicating ventricular capacitance) were estimated using preoperative echocardiographic data. Alterations in EDPVR with increased stiffness (β > 6.16) were categorized into 3 groups; leftward-shifted (EDVI20 <51 mL/m2), rightward-shifted (EDVI20 > 69.7 mL/m2), and intermediate (EDVI20 51-69.7 mL/m2). As the model for ESLD score increases, both EDVI20 and β gradually increased, which indicated ventricular remodeling with larger capacitance and higher diastolic stiffness. Among patients with increased stiffness (β > 6.16, n=1,090), survival rates after LT were lower in leftward-shifted EDPVR than in rightward-shifted EDPVR (73.7% vs 82.9%; log-rank P=0.002). In the adjusted Cox proportional hazard model, risk of cumulative all-cause mortality at 11 years was the highest in leftward-shifted EDPVR (hazard ratio [HR]: 1.93; 95% confidence interval [CI]: 1.27-2.92), followed by intermediate EDPVR (HR: 1.55; 95% CI: 1.12-2.26), compared with rightward-shifted EDPVR. The SHapley Additive exPlanation model revealed that the variables associated with leftward-shifted EDPVR were diabetes, female sex, old age, and hypertension. As ESLD advances, diastolic ventricular properties are characterized by increased EDVI20 and β on rightward-shifted EDPVR, indicating larger capacitance and higher stiffness. However, leftward-shifted EDPVR with left ventricle remodeling failure is associated with poor post-LT survival.

Abstract 6456: Association of dietary inflammatory and insulinemic potential with risk of liver cancer and chronic liver disease mortality

Abstract Background: Increasing burdens of liver cancer and chronic liver disease (CLD) urge investigation of modifiable risk factors for primary prevention. Despite strong experimental evidence showing the role of chronic insulin resistance/hyperinsulinemia and inflammation in liver cancer and CLD, whether the insulinemic and inflammatory potential of diet are independently associated with higher risk of these outcomes requires further investigation. Methods: We conducted a prospective cohort study among 78,356 postmenopausal women in the Women’s Health Initiative Observational Study. Two validated dietary indices that predict circulating C-peptide or biomarkers of inflammation, namely, the empirical dietary index for hyperinsulinemia (EDIH) and the empirical dietary inflammation pattern (EDIP), were estimated from a food frequency questionnaire. Incident cases of liver cancer and CLD mortality were ascertained via review of medical records and linkage to national registries. Multivariable hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using Cox proportional hazard models, adjusted for age, diabetes, body mass index (BMI), and other covariates. Results: During a median 22.1 years of follow-up, we documented 176 primary liver cancer cases and 156 CLD mortality cases. The EDIH was positively associated with incident liver cancer risk (HRQuartile4 vs. Quartile1 = 1.70; 95% CI: 1.03, 2.81; p-trend = 0.03) and CLD mortality risk (HRQ4 vs. Q1 = 2.75; 95% CI: 1.54, 4.93; p-trend = 0.01) in the multivariable adjusted model, including diabetes and BMI as covariates. The EDIP was also positively associated with liver cancer (HRQ4 vs. Q1 = 1.93; 95% CI: 1.21, 3.09; p-trend &amp;lt;0.001) and CLD mortality risk (HRQ4 vs. Q1 = 2.09; 95% CI: 1.24, 3.52; p-trend &amp;lt;0.001) in the multivariable adjusted model. The estimates remained significant and robust in sensitivity analyses, after exclusion of cases in the first 2 years of follow-up or with liver disease history. There was no additive effect between the two dietary indices. Further analyses of individual food groups and liver outcomes indicated positive associations with refined grains, processed meat, butter, and eggs, and inverse associations with coffee, poultry, green leafy vegetables, and dark yellow vegetables. Conclusions: Dietary insulinemic and inflammatory potential were independently associated with higher risk of liver cancer and CLD mortality in US postmenopausal women. Monitoring dietary patterns to reduce chronic hyperinsulinemia and inflammation may contribute to the primary prevention of liver cancer and CLD mortality. Citation Format: Xinyuan Zhang, Longgang Zhao, Cami Christopher, Fred K. Tabung, Wei Bao, David O. Garcia, Marian L. Neuhouser, Aladdin H. Shadyab, Nazmus Saquib, Lesley Tinker, Xuehong Zhang. Association of dietary inflammatory and insulinemic potential with risk of liver cancer and chronic liver disease mortality. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6456.

72 Establishing a histologically defined NAFLD cohort in the Million Veteran Program for further genetic analyses

OBJECTIVES/GOALS: Research in Non Alcoholic Fatty Liver Disease Genetics is ongoing. In this project, we aim to: 1.Identify and describe a histological NAFLD Cohort in the MVP Biobank by extracting liver biopsy proven NAFLD patients using natural language processing (NLP) 2.Confirm previously defined NALFD genetic loci (via look up-GWAS) in the histological NLP cohort METHODS/STUDY POPULATION: We will utilize the Million Veteran Program Biobank where a total of 10,959 subjects have been identified using liver biopsy reports in the EMR via CPT codes. Cases will be based on i) steatosis, steatohepatitis, inflammation or fibrosis in liver biopsy reports with ii) exclusion of other causes of liver disease. Controls will be comprised of the general VA population. In collaboration with the Applied NLP and Precision Medicine groups at the VA Informatics and Computing Infrastructure(VINCI); we will attempt to create and validate a histological cohort of NAFLD in the MVP database by: 1)Annotation of biopsy reports for the NLP algorithm 2)Automation/training of the NLP algorithm We will then perform a multi-ancestry genetic lookup of previously established genetic loci among the cases identified. RESULTS/ANTICIPATED RESULTS: Recently published data: the MVP NAFLD research led by Dr. Chang and Dr. Vujkovic had first validated a proxy NAFLD phenotype based on chronic alanine aminotransferase elevation (cALT). A GWAS was then performed using this phenotype which revealed 77 loci of genome-wide significance including 10 established NAFLD- and 52 ALT-associated SNPs were identified. Replication in external Liver Biopsy and Imaging Cohorts validated 17 SNPs of which 9 were novel. Preliminary data on Liver Biopsy reports: Using CPT codes for Liver Biopsy we estimated a total of 10,959 unique patients and 18,812 notes in the MVP biobank. We anticipate 2,000-3,000 NAFLD cases (based on the prevalence of NAFLD in the general population). Initial review reveals 90% concordance between analysts for the purposes of developing an NLP. DISCUSSION/SIGNIFICANCE: NAFLD is a major cause for morbidity and mortality in liver disease. Gold standard for diagnosis is based on biopsy. GWAS studies with biopsy proven phenotypes are limited. The study will aim to isolate a histologically defined NAFLD cohort in MVP to conduct further GWAS that can provide new clinically relevant knowledge for future research.Contemporary Research Challenges

Cardiovascular Disease Risk and Statin Use Among Adults with Metabolic Dysfunction Associated Fatty Liver Disease

BackgroundA leading cause of mortality in fatty liver disease is cardiovascular disease. Metabolic dysfunction-associated fatty liver disease (MAFLD) is new terminology that classifies fatty liver due to metabolic dysfunction attributable to obesity and associated complications. We evaluated atherosclerotic cardiovascular disease (ASCVD) risk and statin use in adults with MAFLD. MethodsThis was a retrospective study of the 2011-2018 National Health and Nutrition Examination Survey. Adults with MAFLD were identified using established criteria: presence of hepatic steatosis (US Fatty Liver Index>30) plus ≥1 of the following: 1) body mass index >25 kg/m2 in non-Asians or >23 kg/m2 in Asians, 2) diabetes mellitus, and 3) ≥2 metabolic risk factors. Cardiovascular disease risk was estimated using the validated 10-year ASCVD risk score. Statin use was assessed in intermediate and high 10-year ASCVD risk groups. ResultsPrevalence of MAFLD was 34.8% (95% confidence interval [CI], 33.9%-35.8%), comprising 54.4% males, 27.9% aged 65 years and older, and 38.2% non-Hispanic white. Among adults with MAFLD, 23.3% and 23.0% had intermediate and high 10-year ASCVD risk, respectively. Compared with females, males were more likely to have high 10-year ASCVD risk (28.7% vs 16.1%, adjusted odds ratio 5.24, 95% CI, 3.87-7.10, P < .01). In intermediate and high ASCVD risk groups, overall statin use was 48.3% (95% CI, 46.1-51.3). ConclusionsOver 46% of adults with MAFLD had intermediate or high 10-year ASCVD risk. Statin use was underutilized at 48.3% in those meeting statin criteria. These findings are alarming given the high cardiovascular disease risk and low statin use in this cohort.

Associations of serum uric acid levels with liver disease-related morbidity and mortality: A prospective cohort study of the UK Biobank.

The association of serum uric acid (SUA) levels with liver-related morbidity and mortality remains undetermined. Therefore, we aimed to explore the association of SUA levels with liver-related morbidity and mortality. The present cohort study included 459,619 adults from the UK Biobank. Multivariable Cox proportional hazards models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of SUA levels with morbidity and mortality of overall liver disease. Mendelian randomization (MR) analyses were conducted to explore the underlying causality. A polygenic risk score was generated to assess whether there was a gene-exposure interaction. During a median follow-up of 12.6 years, 14,302 nonfatal and 609 fatal cases of overall liver disease were identified. Compared to individuals in the lowest quartile, the HRs (95% CI) of incident overall liver disease were 1.08 (1.02-1.14), 1.13 (1.07-1.20), and 1.44 (1.36-1.53) for individuals with SUA levels in quartiles 2, 3, and 4, respectively. Similarly, the HRs (95% CI) of liver disease-associated mortality were 1.09 (0.78-1.52), 1.55 (1.14-2.13), and 1.96 (1.42-2.69) for individuals with SUA levels in quartiles 2, 3, and 4, respectively. The MR results did not support the causal association of SUA levels with liver disease. In addition, there was a significant modification effect of the polygenic risk score on the association of SUA levels with incident overall liver disease (Pinteraction = 0.003). Higher SUA levels were significantly associated with an increased risk of overall liver disease morbidity and mortality.

Characterization of social determinants of health of a liver transplant referral population.

Disparities exist in referral and access to the liver transplant (LT) waitlist, and social determinants of health (SDOH) are increasingly recognized as important factors driving health inequities, including in LT. The SDOH of potential transplant candidates is therefore important to characterize when designing targeted interventions to promote equity in access to LT. Yet, it is uncertain how a transplant center should approach this issue, characterize SDOH, identify disparities, and use these data to inform interventions. We performed a retrospective study of referrals for first-time, single-organ LT to our center from 2016 to 2020. Addresses were geoprocessed and mapped to the corresponding county, census tract, and census block group to assess their geospatial distribution, identify potential disparities in referrals, and characterize their communities across multiple domains of SDOH to identify potential barriers to evaluation and selection. We identified variability in referral patterns and areas with disproportionately low referrals, including counties in the highest quartile of liver disease mortality (9%) and neighborhoods in the highest quintile of socioeconomic deprivation (17%) and quartile of poverty (21%). Black individuals were also under-represented compared with expected state demographics (12% vs. 18%). Among the referral population, several potential barriers to evaluation and selection for LT were identified, including poverty, educational attainment, access to healthy food, and access to technology. This approach to the characterization of a transplant center's referral population by geographic location and associated SDOH demonstrates a model for identifying disparities in a referral population and potential barriers to evaluation that can be used to inform targeted interventions for disparities in LT access.

Seroprevalence and Sociodemographic Characteristics for Hepatitis C Infection in North Central Nigeria

Hepatitis C virus infection is a concern for global health because it increases the risk of hepatocellular cancer, liver fibrosis, and mortality from liver disease. No safeguarding vaccination is yet accessible. The study's objectives were to identify the sociodemographic characteristics and the seroprevalence of the hepatitis C virus in the study area. A cross-sectional study was conducted by collecting blood samples from 1511 participants which were analysed for anti-HCV using a third-generation ELISA Kit. Data were analysed using SPSS version 23.0. p-values &lt; 0.05 were considered significant. An overall 5.2% of the 1511 samples analysed were seropositive. Males had a seroprevalence of 7.1%, whereas females had a seroprevalence of 3.9% (p=0.01). The lowest seroprevalence was among the divorced and widowed, who had no detectable anti-HCV (p=0.007). Singles had the highest seroprevalence at 7.1%. Seroprevalence was highest (5.9%) among those with tertiary education and lowest (2.7%; p=0.461) among those with primary education. The highest seroprevalence was 6.9% among unemployed people, whereas the lowest was 3.4% among farmers (p=0.414). The highest seroprevalence was seen in monogamists (6.1%), with polygamists having none (p = 0.05). The seroprevalence was highest in non-alcoholics at 5.5% and lowest in alcoholics at 4.1% (p=0.407). Smokers had the lowest seroprevalence, at 3.2%, whereas non-smokers had the highest, at 5.3% (p=0.462). It is imperative to act quickly to prevent liver disease morbidity and mortality given the seroprevalence of 5.2% of HCV, which is of considerable public health concern.