Clin Mol Hepatol > Volume 31(2); 2025 > Article
Park and Yu: Revealing the importance of a multidisciplinary approach to reducing the global burden of SLD through the COVID-19 pandemic: Editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”
As the obesity crisis worsens worldwide, the global prevalence of steatotic liver disease (SLD) is rapidly increasing, which leads to a significant rise in liver-related complications such as liver cirrhosis and hepatocellular carcinoma [1-3]. As part of efforts to address this issue, the American and European liver associations have introduced a new nomenclature for SLD and its subclassifications, including metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related SLD (MetALD), and alcohol-related liver disease (ALD) [4]. It facilitates the estimation of disease burden prevalence, the risk stratification of patients based on variations in pathogenesis, drug development, and risk-based precision management for each individual [5,6].
In this issue, Kim et al. [5] investigated the contemporary prevalence of SLD, MASLD, MetALD, and ALD in the United States using data from the National Health and Nutrition Examination Survey (NHANES), specifically comparing the prevalence between the pre-pandemic period (from 2017 until March 2020) and the COVID-19 pandemic period (from August 2021 to August 2023). In addition, they assessed the presence of significant fibrosis, advanced fibrosis, and liver cirrhosis using transient elastography, comparing MASLD, MetALD, ALD, and SLD-related fibrosis and cirrhosis between the two periods. In the United States, among individuals aged over 18 years, the weighted age-adjusted prevalence of SLD (cut-off: 285 dB/m) was 35.0% (95% confidence interval [CI] 33.4–36.7). Within this category, the prevalence was 31.9% (95% CI 30.4–33.4) for MASLD, 2.2% (95% CI 1.8–2.6) for MetALD, and 0.8% (95% CI 0.6–1.1) for ALD. SLD prevalence was higher among men and Hispanics. When broken down by subclassification, MASLD was most prevalent among Hispanics followed by non-Hispanic Asians, while MetALD and ALD were more common among non-Hispanic Whites and Hispanics, respectively. Between the pre-pandemic and COVID-19 pandemic periods, there was no significant difference in prevalence of SLD; however, there was a significant increase in the proportion of significant fibrosis and advanced fibrosis in SLD patients during the COVID-19 pandemic compared to the pre-pandemic period. Although not statistically significant, during the COVID-19 pandemic period, an increase in alcohol consumption was associated with an increase in the prevalence of ALD, while the prevalence of MASLD relatively decreased.
A concerning finding from Kim et al.’s research is that nearly one-third of US adults have MASLD. Additionally, MASLD is predicted to become the most rapidly growing contributor to the disease burden associated with adverse liver outcomes, including liver cirrhosis and HCC, in the future [7]. Recently, resmetirom was approved as a treatment for NASH patients with liver fibrosis, but its application remains very limited [8]. Therefore, lifestyle modification is still recognized as the most important treatment to date.
In the United States, a diverse range of ethnicities coexists, and Kim et al. [5] investigated the prevalence of SLD and its subclasses among different racial groups. Particularly, non-Hispanic Asians showed a relatively high prevalence of MASLD, while non-Hispanic Whites and Hispanics had higher proportions of MetALD and ALD. In non-Hispanic Blacks, the prevalence of SLD, as well as its subclasses MASLD, MetALD, and ALD, was consistently low. Several factors can be considered to explain the differences in prevalence among racial groups. Firstly, variations in the PNPLA3 gene contribute to ancestry-related and individual differences in hepatic fat content and susceptibility to nonalcoholic fatty liver disease (NAFLD) [9]. A variant of PNPLA3 (rs738409[G], encoding I148M) was strongly associated with increased hepatic fat levels and hepatic inflammation, increasing susceptibility to NAFLD. This allele was most commonly found in Hispanics and Asians, but less frequently in Africans [10]. Conversely, another variant of PNPLA3 (rs6006460[T], encoding S453I) was associated with lower hepatic fat content in African Americans, the group with the lowest risk of NAFLD [9]. This may explain why African Americans, despite having similar prevalence rates of obesity and insulin resistance, tend to show significantly lower prevalence rates of SLD [10]. Secondly, in American society, non-Hispanic Asians and Blacks often include populations that are underserved in terms of health-related screenings, which may lead to an underestimation of prevalence [11]. This suggests a need for further research into these racial groups.
The COVID-19 pandemic disrupted regular routines and involuntarily led to irregular and unhealthy lifestyle habits. As described by Kim et al. [5], during this period in the United States, people were confined to their homes, leading to a significant reduction in physical activity and an increase in alcohol consumption. In addition, due to the healthcare system’s focus on COVID-19, high-risk patients did not receive adequate monitoring or appropriate treatment. Consequently, there was a significant increase in the occurrence of fibrosis associated with SLD progression. This not only underscored the critical importance of lifestyle modifications in the management of SLD but also highlighted the necessity of a multidisciplinary approach, including appropriate healthcare system interventions and the establishment of relevant legislation. Historically, pandemics have occurred repeatedly. Given this, it seems prudent to establish strategies in advance for effectively managing SLD patients during future pandemics, taking lessons from the COVID-19 pandemic.

FOOTNOTES

Authors’ contribution
The corresponding author SJY have full access to all study data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: JP and SJY. Data analysis and interpretation: JP and SJY. Manuscript writing: JP and SJY.
Conflicts of Interest
Jeayeon Park: Nothing to declare. Su Jong Yu: Research Funding - Yuhan Pharmaceuticals and Daewoong Pharmaceuticals.

Abbreviations

ALD
alcohol-related liver disease
CI
confidence interval
MASLD
metabolic dysfunction-associated steatotic liver disease
MetALD
metabolic dysfunction and alcohol-related SLD
NAFLD
nonalcoholic fatty liver disease
SLD
steatotic liver disease

REFERENCES

1. Jeong S, Oh YH, Ahn JC, Choi S, Park SJ, Kim HJ, et al. Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: a nationwide cohort study. Clin Mol Hepatol 2024;30:487-499.
crossref pmid pmc pdf
2. Moon AM, Singal AG, Tapper EB. Contemporary epidemiology of chronic liver disease and cirrhosis. Clin Gastroenterol Hepatol 2020;18:2650-2666.
crossref pmid pmc
3. Teng ML, Ng CH, Huang DQ, Chan KE, Tan DJ, Lim WH, et al. Global incidence and prevalence of nonalcoholic fatty liver disease. Clin Mol Hepatol 2023;29(Suppl):S32-S42.
crossref pmid pmc pdf
4. Rinella ME, Lazarus JV, Ratziu V, Francque SM, Sanyal AJ, Kanwal F, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology 2023;78:1966-1986.
pmid
5. Kim D, Danpanichkul P, Wijarnpreecha K, Cholankeril G, Loomba R, Ahmed A. Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023. Clin Mol Hepatol 2025;31:382-393.
crossref pmid pdf
6. Loomba R, Wong VW. Implications of the new nomenclature of steatotic liver disease and definition of metabolic dysfunction-associated steatotic liver disease. Aliment Pharmacol Ther 2024;59:150-156.
crossref pmid pmc
7. Miao L, Targher G, Byrne CD, Cao YY, Zheng MH. Current status and future trends of the global burden of MASLD. Trends Endocrinol Metab 2024;35:697-707.
crossref pmid
8. Harrison SA, Bedossa P, Guy CD, Schattenberg JM, Loomba R, Taub R, et al. A phase 3, randomized, controlled trial of resmetirom in NASH with liver fibrosis. N Engl J Med 2024;390:497-509.
pmid
9. Romeo S, Kozlitina J, Xing C, Pertsemlidis A, Cox D, Pennacchio LA, et al. Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet 2008;40:1461-1465.
crossref pmid pmc pdf
10. Kozlitina J, Sookoian S. Global epidemiological impact of PNPLA3 I148M on liver disease. Liver Int 2025;45:e16123.
pmid
11. Fiscella K, Sanders MR. Racial and ethnic disparities in the quality of health care. Annu Rev Public Health 2016;37:375-394.
crossref pmid

Editorial Office
The Korean Association for the Study of the Liver
Room A1210, 53 Mapo-daero(MapoTrapalace, Dowha-dong), Mapo-gu, Seoul, 04158, Korea
TEL: +82-2-703-0051   FAX: +82-2-703-0071    E-mail: cmh_journal@ijpnc.com
Copyright © The Korean Association for the Study of the Liver.         
COUNTER
TODAY : 689
TOTAL : 2631688
Close layer