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AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease
Open accessAbstract
PREAMBLE The study of NAFLD has intensified significantly, with more than 1400 publications since 2018, when the last American Association for the Study of Liver Diseases (AASLD) Guidance document was published.1 This new AASLD Guidance document reflects many advances in the field pertinent to any practitioner caring for patients with NAFLD and emphasizes advances in noninvasive risk stratification and therapeutics. A separate guideline focused on the management of patients with NAFLD in the context of diabetes has been written jointly by the American Association of Clinical Endocrinology and AASLD.2 Given the significant growth in pediatric NAFLD, it will not be covered here to allow for a more robust discussion of the diagnosis and management of pediatric NAFLD in the upcoming AASLD Pediatric NAFLD Guidance. A “Guidance” differs from a “Guideline” in that it is not bound by the Grading of Recommendations, Assessment Development and Evaluation system. Thus, actionable statements rather than formal recommendations are provided herein. The highest available level of evidence was used to develop these statements, and, where high-level evidence was not available, expert opinion was used to develop guidance statements to inform clinical practice. Key points highlight important concepts relevant to understanding the disease and its management. The most profound advances in NAFLD relevant to clinical practice are in biomarkers and therapeutics. Biomarkers and noninvasive tests (NITs) can be used clinically to either exclude advanced diseases or identify those with a high probability of cirrhosis.3,4 NIT “cut points” vary with the populations studied, underlying disease severity, and clinical setting. Those proposed in this guidance are meant to aid decision-making in the clinic and are not meant to be interpreted in isolation. Identifying patients with “at-risk” NASH (biopsy-proven NASH with stage 2 or higher fibrosis) is a more recent area of interest. Although the definitive diagnosis and staging of NASH remain linked to histology, noninvasive tools can now be used to assess the likelihood of significant fibrosis, predict risk of disease progression and decompensation, make management decisions, and, to some degree, assess response to treatment. There is an ongoing debate over the nomenclature of fatty liver disease, which had not been finalized at the time this guidance was published. At the culmination of a rigorous consensus process, it is intended that any formal change in nomenclature will advance the field without a negative impact on disease awareness, clinical trial endpoints, or the drug development/approval process. Furthermore, it should allow for the emergence of newly recognized disease subtypes to address the impact of disease heterogeneity, including the role of alcohol, on disease progression and response to therapy. Input from patients has been central to all stages of the consensus process to ensure the minimization of nomenclature-related stigma. DEFINITIONS NAFLD is an overarching term that includes all disease grades and stages and refers to a population in which ≥5% of hepatocytes display macrovesicular steatosis in the absence of a readily identified alternative cause of steatosis (eg, medications, starvation, monogenic disorders) in individuals who drink little or no alcohol (defined as < 20 g/d for women and <30 g/d for men). The spectrum of disease includes NAFL, characterized by macrovesicular hepatic steatosis that may be accompanied by mild inflammation, and NASH, which is additionally characterized by the presence of inflammation and cellular injury (ballooning), with or without fibrosis, and finally cirrhosis, which is characterized by bands of fibrous septa leading to the formation of cirrhotic nodules, in which the earlier features of NASH may no longer be fully appreciated on a liver biopsy. UPDATE ON EPIDEMIOLOGY AND NATURAL HISTORY The prevalence of NAFLD and NASH is rising worldwide in parallel with increases in the prevalence of obesity and metabolic comorbid disease (insulin resistance, dyslipidemia, central obesity, and hypertension).5,6 The prevalence of NAFLD in adults is estimated to be 25%–30% in the general population7–9 and varies with the clinical setting, race/ethnicity, and geographic region studied but often remains undiagnosed.10–14 The associated economic burden attributable to NASH is substantial.15–17 The prevalence of NASH in the general population is challenging to determine with certainty; however, NASH was identified in 14% of asymptomatic patients undergoing colon cancer screening.14 This study also highlights that since the publication of a prior prospective prevalence study,18 the prevalence of clinically significant fibrosis (stage 2 or higher fibrosis) has increased >2-fold. This is supported by the projected rise in NAFLD prevalence by 2030, when patients with advanced hepatic fibrosis, defined as bridging fibrosis (F3) or compensated will the proj
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“Based on this, it seems reasonable to conclude that should patients continue to complete guideline-based amounts of aerobic exercise over a longer duration, fibrosis improvement may follow [35, 36].”
From Aerobic Exercise Training Leads to MASH Resolution as Defined by the MASH Resolution Index (2026) · cites this paper as [35]
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“Moreover, interventions in diet and physical activity are considered to be the cornerstone of management in the whole MASLD spectrum [7, 10].”
From Effects of Mediterranean diet, exercise, and their combination on body composition and liver outcomes in metabolic dysfunction-associated steatotic liver disease: a systematic review and meta-analysis of randomized controlled trials (2025) · cites this paper as [7]
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“Although there is no consensus on the optimal diet for treating MASLD, the EASL-EASD-EASO guidelines recently recommended the MD as the preferred option [7, 10].”
From Effects of Mediterranean diet, exercise, and their combination on body composition and liver outcomes in metabolic dysfunction-associated steatotic liver disease: a systematic review and meta-analysis of randomized controlled trials (2025) · cites this paper as [7]
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“Current guidelines recommend weight loss through dietary modifications, increased physical activity, or both combined in MASLD patients [7, 11, 12].”
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“Various scienti fi c societies have recommended clinical care pathways with an emphasis on the use of non-invasive tests (NITs) and the liaison between primary care/non-hepatology and hepatology settings.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [126]
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“GLP-1RA-based drugs have been proven beneficial to some extent in dedicated trials and should be considered in patients with obesity and/or T2D and metabolic dysfunction-associated steatohepatitis (MASH)90.”
From Incretin-based therapies for the treatment of obesity-related diseases (2024) · cites this paper as [90]
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InfluentialSelf-citationNatural history and progression of metabolic dysfunction-associated steatotic liver disease
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“Therefore, counselling and appropriate interventions should be considered to help people who smoke stop smoking and for those who consume alcohol to decrease or stop their alcohol consumption, especially in the presence of fibrosis 11,54–56 (Table 4).”
BackgroundMetabolic dysfunction-associated steatotic liver disease and risk of cardiovascular disease
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“Alcohol intake can be broadly classified as mild (up to 20 g (women) and 30 g (men) per day), moderate (21–39 g (women) and 31–59 g (men) per day), or heavy (≥40 g (women) and ≥60 g (men) per day) 9 .”
BackgroundInfluentialFeng, G., Valenti, L. V. C., Wong, V. W., Fouad, Y. M., Yilmaz, Y. N., Kim, W. K., Sebastiani, G., Younossi, Z. M., Hernández–Gea, V., & Zheng, M. (2023) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-023-00846-4 · Cited by 212
“However, we need to be aware that decompensated cirrhosis should be considered an absolute contraindication for bariatric surgery owing to increased risk and unproven liver-related benefits, unless performed in conjunction with liver transplantation at specialist centres 103 .”
Abdelhameed, F., Kite, C., Lagojda, L., Dallaway, A., Chatha, K. K., Chaggar, S. S., Dalamaga, Μ., Kassi, E. N., Kyrou, I., & Randeva, H. S. (2024) · Current Obesity Reports · doi:10.1007/s13679-024-00574-z · Cited by 193
“…fibrosis (ELF) Fig.3 A suggested simplified algorithm for the use of non-invasive serum biomarker scores for the assessment of patients across the three diagnostic entities of steatotic liver disease (NAFLD/MAFLD/ MASLD) [6, 91] test which combines hyaluronic acid, PIIINP and TMP1 with age [99].”
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“As noted, it is widely recommended that cardiometabolic risk factors be evaluated, according to their respective cardiometabolic guidelines, 15,16,20,21 regardless of availability of MASH-speci fi c treatment.”
Huang, D. Q., Wilson, L. A., Behling, C., Kleiner, D. E., Kowdley, K. V., Dasarathy, S., Amangurbanova, M., Terrault, N. A., Diehl, A. M., Chalasani, N., et al. (2023) · Gastroenterology · doi:10.1053/j.gastro.2023.04.025 · Cited by 190
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Chew, N., Mehta, A., Goh, R. S. J., Zhang, A. A. Y., Chen, Y., Chong, B., Chew, H. S. J., Shabbir, A., Brown, A. C., Dimitriadis, G. K., et al. (2024) · Circulation · doi:10.1161/circulationaha.124.070535 · Cited by 191
“37 As cardiovascular complications often determine the clinical outcomes of MASLD, current guidelines emphasize the screening for CVD using standard ASCVD Three main mechanistic pathways underlie the development of CVD in MASLD: (1) MASLD is a chronic inflammatory state, associated with increased release of cytokines…”
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“A person living with MAFLD plays a vital role in their disease management as the cornerstone of treatment is adherence to a healthy diet and being physically active [24, 156, 251].”
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Self-citationObesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease?
Huttasch, M., Roden, M., & Kahl, S. (2024) · Metabolism · doi:10.1016/j.metabol.2024.155937 · Cited by 169
Steatotic liver disease, MASLD and risk of chronic kidney disease
Bilson, J., Mantovani, A., Byrne, C. D., & Targher, G. (2023) · Diabetes & Metabolism · doi:10.1016/j.diabet.2023.101506 · Cited by 179
Sterling, R. K., Patel, K., Duarte‐Rojo, A., Asrani, S. K., Alsawas, M., Dranoff, J. A., Fiel, M. I., Murad, M. H., Leung, D. H., Levine, D., et al. (2024) · Hepatology · doi:10.1097/hep.0000000000000845 · Cited by 188
Tincopa, M. A., & Loomba, R. S. (2023) · The Lancet. Gastroenterology & hepatology · doi:10.1016/s2468-1253(23)00066-3 · Cited by 163
Self-citationElSayed, N. A., Aleppo, G., Bannuru, R. R., Bruemmer, D., Collins, B. S., Cusi, K. J., Ekhlaspour, L., Fleming, T. K., Hilliard, M. E., Johnson, E. L., et al. (2023) · Diabetes Care · doi:10.2337/dc24-s004 · Cited by 173
EASL Clinical Practice Guidelines on the management of autoimmune hepatitis
Dalekos, G., Gatselis, N., Drenth, J. P. H., Heneghan, M., Jørgensen, M., Lohse, A. W., Londoño, M., Muratori, L., Papp, M., Samyn, M., et al. (2025) · Journal of Hepatology · doi:10.1016/j.jhep.2025.03.017 · Cited by 175
Newsome, P. N., Sanyal, A. J., Engebretsen, K. A., Kliers, I., Østergaard, L., Vanni, D. S., Bugianesi, E., Rinella, M. E., Roden, M., & Ratziu, V. (2024) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.18331 · Cited by 155
Self-citationNadolsky, K., Garvey, W. T., Agarwal, M., Bonnecaze, A., Burguera, B., Chaplin, M. D., Griebeler, M. L., Harris, S. R., Schellinger, J. N., Simonetti, J., et al. (2025) · Endocrine Practice · doi:10.1016/j.eprac.2025.07.017 · Cited by 141
The bidirectional immune crosstalk in metabolic dysfunction-associated steatotic liver disease
Sawada, K., Chung, H., Softic, S., Moreno-Fernandez, M. E., & Divanovic, S. (2023) · Cell Metabolism · doi:10.1016/j.cmet.2023.10.009 · Cited by 139
Ferraioli, G., Barr, R. G., Berzigotti, A., Sporea, I., Wong, V. W., Reiberger, T., Karlas, T., Thiele, M. S., Cardoso, A. C., Ayonrinde, O. T., et al. (2024) · Ultrasound in Medicine & Biology · doi:10.1016/j.ultrasmedbio.2024.03.014 · Cited by 140
Efruxifermin in Compensated Liver Cirrhosis Caused by MASH
Noureddin, M., Rinella, M. E., Chalasani, N., Neff, G. W., Lucas, K. J., Rodriguez, M. E., Rudraraju, M., Patil, R., Behling, C. A., Burch, M., et al. (2025) · New England Journal of Medicine · doi:10.1056/nejmoa2502242 · Cited by 144
Self-citationSanyal, A. J., Ratziu, V., Loomba, R., Anstee, Q. M., Kowdley, K. V., Rinella, M. E., Sheikh, M. Y., Trotter, J. F., Knapple, W., Lawitz, E. J., et al. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.07.014 · Cited by 137
Self-citationAnstee, Q. M., Berentzen, T. L., Nitze, L. M., Jara, M., Jensen, A. B., Kjær, M. S., Mangla, K. K., Tarp, J. M., & Khunti, K. (2023) · The Lancet Regional Health - Europe · doi:10.1016/j.lanepe.2023.100780 · Cited by 137
“3,14,17 Our study demonstrates that a 12-month increase/decrease in FIB-4 is associated with higher/lower risk of liver events across the FIB-4 baseline groups.”
BackgroundResultInfluentialMASLD and the Development of HCC: Pathogenesis and Therapeutic Challenges
Phoolchund, A. G. S., & Khakoo, S. I. (2024) · Cancers · doi:10.3390/cancers16020259 · Cited by 137
“The term metabolic-dys-function-associated steatotic liver disease (MASLD) has now replaced NAFLD [1,2].”
BackgroundMethodKim, G., Moon, J. H., & Kim, W. K. (2023) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2023.0277 · Cited by 128
“In contrast, the new nomenclature SLD applies the five CMRFs to all patients for classifying its subcategories, including MASLD, MetALD, cryptogenic SLD, and other specific etiology SLD. NAFLD and MASLD differ because SLD adopts a positive criterion and incorporates metabolic risk factors while striving to retain the…”
InfluentialBansal, M. B., Patton, H. M., Morgan, T. R. M., Carr, R. M., Dranoff, J. A., & Allen, A. M. (2025) · Hepatology · doi:10.1097/hep.0000000000001608 · Cited by 139
Nogueira, J. P., & Cusi, K. J. (2024) · Diabetes Spectrum · doi:10.2337/dsi23-0013 · Cited by 132
“Nonalcoholic steatohepatitis (NASH) is a histological diagnosis de fi ned as having, in addition to steatosis, active hepatocyte injury (ballooning) and lobular in fl ammation, often with liver fi brosis (5).”
BackgroundMethodInfluentialSchnabl, B., Damman, C. J., & Carr, R. M. (2025) · Journal of Clinical Investigation · doi:10.1172/jci186423 · Cited by 133
Noninvasive Assessment of Liver Fibrosis
Castéra, L., Rinella, M. E., & Tsochatzis, E. A. (2025) · New England Journal of Medicine · doi:10.1056/nejmra2403308 · Cited by 120
Self-citationConfirmatory biomarker diagnostic studies are not needed when transitioning from NAFLD to MASLD
Ratziu, V., Boursier, J., de Lédinghen, V., Anty, R., Costentin, C. E., & Bureau, C. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.07.017 · Cited by 111
Non-invasive testing and risk-stratification in patients with MASLD
Zoncapè, M., Liguori, A., & Tsochatzis, E. A. (2024) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2024.01.013 · Cited by 112
Qi, X., Li, J., Caussy, C., Teng, G., & Loomba, R. (2024) · Hepatology · doi:10.1097/hep.0000000000000913 · Cited by 113
“Guidelines/guidance Recommendations for screening 2023 AASLD Practice Guidance [3] Patients with NAFLD should be screened for the presence of T2DM.”
InfluentialSelf-citationMellemkjær, A., Kjær, M. B., Haldrup, D., Grønbæk, H., & Thomsen, K. L. (2023) · European Journal of Internal Medicine · doi:10.1016/j.ejim.2023.11.012 · Cited by 110
Harrison, S. A., Frías, J. P., Lucas, K. J., Reiss, G. M., Neff, G. W., Bollepalli, S., Su, Y., Chan, D. C., Tillman, E. J., Moulton, A. W., et al. (2024) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2024.02.022 · Cited by 117
de Souza, M. H. G., Al‐Sharif, L., Antunes, V., Huang, D. Q., & Loomba, R. (2025) · Hepatology · doi:10.1097/hep.0000000000001254 · Cited by 114
“…least 1 established or potentially beneficial therapy for MASH based on the American Association for the Study of Liver Diseases (AASLD) guidelines [18] to each other or placebo; (iv) follow-up ≥ 6 months; and (v) reported at least 1 endpoint of interest: ≥ 1 stage improvement in fibrosis without…”
Self-citationGlobal burden of MAFLD, MAFLD related cirrhosis and MASH related liver cancer from 1990 to 2021
Guo, Z., Wu, D., Mao, R., Yao, Z., Wu, Q., & Lv, W. (2025) · Scientific Reports · doi:10.1038/s41598-025-91312-5 · Cited by 100
“…(NAFLD) is a chronic progressive liver disease caused by over nutrition and insulin resistance (IR) in genetically susceptible individuals, with a spectrum of diseases including non-alcoholic fatty liver (NAFL), non-alcoholic steatohepatitis (NASH) and its associated fibrosis and cirrhosis 1,2 .”
Byrne, C. D., Armandi, A., Pellegrinelli, V., Vidal‐Puig, A., & Bugianesi, E. (2025) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-025-01045-z · Cited by 113
Is ChatGPT an Effective Tool for Providing Dietary Advice?
Ponzo, V., Goitre, I., Favaro, E., Merlo, F. D., Mancino, M. V., Riso, S., & Bo, S. (2024) · Nutrients · doi:10.3390/nu16040469 · Cited by 100
Gawrieh, S., Vilar-Gomez, E., Wilson, L. A., Pike, F., Kleiner, D. E., Neuschwander-Tetri, B. A., Diehl, A. M., Dasarathy, S., Kowdley, K. V., Hameed, B., et al. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.05.008 · Cited by 94
Self-citationAspirin for Metabolic Dysfunction–Associated Steatotic Liver Disease Without Cirrhosis
Simon, T. G., Wilechansky, R. M., Stoyanova, S., Grossman, A., Dichtel, L. E., Lauer, G. M., Miller, K. K., Hoshida, Y., Corey, K. E., Loomba, R. S., et al. (2024) · JAMA · doi:10.1001/jama.2024.1215 · Cited by 96
Self-citationRinella, M. E., Lieu, H. D., Kowdley, K. V., Goodman, Z. D., Alkhouri, N., Lawitz, E., Ratziu, V., Abdelmalek, M. F., Wong, V. W., Younes, Z. H., et al. (2023) · Hepatology · doi:10.1097/hep.0000000000000607 · Cited by 99
“[15,16] 17 – 19] Aldafermin exhibits biased FGFR4-KLB receptor signaling through modification within the amino terminus to eliminate tumorigenicity while retaining potent activity to suppress CYP7A1, which encodes the first and rate-limiting enzyme of bile acid synthesis.”
Self-citationAbushamat, L. A., Shah, P. A., Eckel, R. H., Harrison, S. A., & Barb, D. (2024) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2024.01.032 · Cited by 103
Self-citationHarrison, S. A., Ratziu, V., Anstee, Q. M., Noureddin, M., Sanyal, A. J., Schattenberg, J. M., Bédossa, P., Bashir, M. R., Schneider, D., Taub, R. A., et al. (2023) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.17734 · Cited by 94
“1,2,6 As shown in recent studies and in the MAESTRO-NASH screening paradigm, 23,35– 37 NASH may be more accurately diagnosed using more advanced imaging”
BackgroundSelf-citationA global action agenda for turning the tide on fatty liver disease
Lazarus, J. V., Mark, H. E., Allen, A. M., Arab, J. P., Carrieri, P., Noureddin, M., Alazawi, W., Alkhouri, N., Alqahtani, S. A., Anstee, Q. M., et al. (2023) · Hepatology · doi:10.1097/hep.0000000000000545 · Cited by 98
Self-citationLe, M. H., Le, D. M., Baez, T. C., Dang, H., Nguyen, V. H., Lee, K., Stave, C. D., Ito, T., Wu, Y., Yeo, Y. H., et al. (2024) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2023.0485 · Cited by 92
Barb, D., Kalavalapalli, S., Leiva, E. G., Bril, F., Huot-Marchand, P., Dzen, L., Rosenberg, J. T., Junien, J., Broqua, P., Rocha, A. O., et al. (2025) · Journal of Hepatology · doi:10.1016/j.jhep.2024.12.045 · Cited by 101
Self-citationXuan, Y., Wu, D., Zhang, Q., Yu, Z., Yu, J., & Zhou, D. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1457598 · Cited by 90
Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction
Choi, W., Woo, G. H., Kwon, T., & Jeon, J. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26199715 · Cited by 120
“Obesity-driven MASLD is now recognized by recent guidelines and reviews as a disease state propelled by a self-reinforcing loop between hepatic mitochondrial dysfunction and innate–adaptive immune inflammation [235,236].”
Noureddin, M., Truong, E., Mayo, R., Martínez‐Arranz, I., Mincholé, I., Bañales, J. M., Arrese, M. A., Cusi, K. J., Arias, M., Brůha, R., et al. (2023) · Hepatology · doi:10.1097/hep.0000000000000542 · Cited by 89
“[11] 12 – 14] These recommendations for sequential testing are based on how (1) FIB-4 has at least 30% of the patients failing to be classified and therefore falling into an indeterminate zone for diagnosis and (2) sequential testing has been shown to narrow this indeterminate zone.”
MethodChoe, H. J., Moon, J. H., Kim, W. K., Koo, B. K., & Cho, N. H. (2024) · Metabolism · doi:10.1016/j.metabol.2024.155800 · Cited by 89
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Rao, G., Peng, X., Li, X., An, K., He, H., Fu, X., Li, S., & An, Z. (2023) · Frontiers in Medicine · doi:10.3389/fmed.2023.1294267 · Cited by 93
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Diabetes and cirrhosis: Current concepts on diagnosis and management
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NASH drug treatment development: challenges and lessons
Tilg, H., Byrne, C. D., & Targher, G. (2023) · The Lancet Gastroenterology & Hepatology · doi:10.1016/s2468-1253(23)00159-0 · Cited by 81
Genetics of Metabolic Dysfunction-associated Steatotic Liver Disease: The State of the Art Update
Sookoian, S. C., Rotman, Y., & Valenti, L. V. C. (2024) · Clinical Gastroenterology and Hepatology · doi:10.1016/j.cgh.2024.05.052 · Cited by 88
Xanthakos, S. A., Ibrahim, S. H., Adams, K. H., Kohli, R., Sathya, P., Sundaram, S. S., Vos, M. B., Dhawan, A., Caprio, S., Behling, C. A., et al. (2025) · Hepatology · doi:10.1097/hep.0000000000001368 · Cited by 88
Saeed, H., Díaz, L. A., Gil‐Gómez, A., Burton, J. P., Bajaj, J. S., Romero‐Gómez, M., Arrese, M. A., Arab, J. P., & Khan, M. Q. (2024) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2024.0811 · Cited by 84
“MASLD encompasses a broad spectrum of clinical phenotypes ranging from isolated steatosis, different degrees of inflammation and fibrosis, to cirrhosis 7 .”
Metadata
- Authors
- Rinella, M. E., Neuschwander-Tetri, B. A., Siddiqui, M. S., Abdelmalek, M. F., Caldwell, S., Barb, D., Kleiner, D. E., & Loomba, R.
- Affiliations
- University of Chicago (US)
- Saint Louis University School of Medicine, Saint Louis, Missouri, USA
- Virginia Commonwealth University (US)
- Mayo Clinic (US)
- University of Virginia (US)
- University of Florida Health (US)
- National Institutes of Health (US)
- University of California San Diego (US)
- Corresponding author
- Rinella, Mary E.
- ORCID
- Venue
- Hepatology
- Published
- 2023-03-17
- Volume
- 77
- Issue
- 5
- Pages
- 1797-1835
- ISSN
- 0270-9139 (ISSN-L)
- PMC
- PMC10735173
- OpenAlex
- W4318923555
- Cited by
- 2,667
- References
- 502
- Citations by year
- 2026: 849 · 2025: 845 · 2024: 691 · 2023: 281
- FWCI
- 532.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Bristol-Myers Squibb
- American Association for the Study of Liver Diseases
- NGM Biopharmaceuticals
- Novo Nordisk
- National Institutes of Health
- Allergan
- National Cancer Institute (ZICBC010685)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
- Keywords
- non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, non-invasive risk stratification, non-invasive tests, fibrosis staging, liver cirrhosis
- MeSH terms
- Humans, Liver, Liver Cirrhosis, Disease Progression, Non-alcoholic Fatty Liver Disease
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