Review ArticleClinical Review

Approach to steatotic liver disease in the office

Diagnosis, management, and proposed nomenclature

Andrew Szilagyi and Nir Hilzenrat
Canadian Family Physician April 2025; 71 (4) 249-254; DOI: https://doi.org/10.46747/cfp.7104249

Abstract

Objective To provide an update on the most recent developments regarding diagnosis and outcomes of steatotic liver disease (SLD), review new nomenclature applied to SLD, and provide an approach to the diagnosis and management of SLD.

Sources of information Individual articles published mainly in the past 2 years, found using PubMed and Google Scholar.

Main message Steatotic liver disease is one of the most common diseases encountered in general practice. This condition is an important biological marker for metabolic syndrome. Diagnosis relies on noninvasive tests. Known complications of metabolic syndrome and advanced liver disease are often present at the time of diagnosis. Courses of action should include assessment of cardiometabolic risk factors and progressive liver dysfunction. Subtle differences are present among patients diagnosed with SLD. Practitioners should be aware of a flux in terminology of SLD. Management of SLD can be guided using a simple algorithm.

Conclusion There is a need for evaluation of the SLD epidemic and its systemic nature, along with associated independent risk factors of cardiovascular disease as well as metabolic conditions such as dyslipidemia, hypertension, and type 2 diabetes.

At present, 3 interrelated pandemics are occurring: These are obesity,1 type 2 diabetes (T2D),2 and steatotic liver disease (SLD).3 Steatotic liver disease occurs in 32% to 39% of the world’s population4,5 and many cases will be seen first by family physicians. As SLD can occur with or without metabolic syndrome or obesity, this has led to a reappraisal of clinical evaluation and management of the spectrum of SLD.

Sources of information

This review is based on literature searches in PubMed and Google Scholar, and on individual relevant articles (many from the past year; individual articles believed to be relevant and quoted in recent articles were evaluated). In this review we present 3 cases with different courses of management based on new definitions of SLD and SLD’s systemic nature. Specific therapeutic management as well as pediatric SLD will not be discussed.

Cases

Case 1. A 44-year-old man presents for evaluation, complaining of some right upper abdominal and epigastric discomfort for the past 6 to 8 months. On examination, his blood pressure is 154/92 mm Hg, he is 170 cm tall, and his weight is 89 kg. His body mass index (BMI) is 31 kg/m2. Findings of an abdominal examination are normal, but the abdomen is protuberant. He consumes 3 to 4 alcoholic drinks during the week and a few more on the weekend. He smokes 5 to 10 cigarettes a week. Findings of an abdominal ultrasound scan show moderate SLD. Blood test results show increased triglyceride levels of 3.5 mmol/L (normal level <1.7 mmol/L), a fasting blood glucose level of 5.4 mmol/L (normal level <5.6 mmol/L), and a hemoglobin A1c level of 5.5% (normal level <5.7%). His alanine aminotransferase (ALT) level is 41 U/L (normal <35 U/L), aspartate aminotransferase (AST) level is 36 U/L (normal range 8 to 33 U/L), Embedded Image-glutamyl transpeptidase (GGT) level is 75 U/L (normal <40 U/L), and platelet count is 246×109/L (normal range 150×109/L to 450×109/L).

Case 2. A 50-year-old woman presents for an annual health evaluation. She complains of fatigue but is otherwise well. She denies alcohol consumption. Her height is 167 cm and weight is 77 kg. Her BMI is 27 kg/m2. Blood test results show an increased triglyceride level of 3.6 mmol/L, her high-density lipoprotein level is normal, and her fasting blood glucose level is 16 mmol/L. Her ALT level is 47 U/L, AST level is 39 U/L, GGT level is 39 U/L, and platelet count is 217×109/L. The presence of elevated liver enzyme levels prompts an abdominal ultrasound scan. This reveals a normal biliary tree with moderate SLD.

Case 3. A 34-year-old Asian man presents with dyspepsia. He denies substantial alcohol intake or smoking. Medical evaluation includes normal physical examination findings with a BMI of 22.9 kg/m2. Blood test results show a normal blood glucose level and hemoglobin A1c level, and a triglyceride level of 1.7 mmol/L but otherwise no dyslipidemia. His ALT level is 38 U/L, AST level is 20 U/L, and GGT level is 43 U/L. Viral serology results for hepatitis B and C viruses are negative. Other markers of liver disease are normal. An abdominal ultrasound scan shows moderate SLD. Findings of an upper gastrointestinal barium study are normal.

Main message

Changing nomenclature for SLD. A development in SLD is the change in nomenclature. The first proposed change was by Eslam et al to include metabolic causes for more accurate terminology; therefore, nonalcoholic fatty liver disease was renamed metabolic dysfunction–associated fatty liver disease.6 However, since the term fatty liver may lead to stigmatization, other new names have been considered. A group of expert participants using the Delphi method outlined the most recent proposal for nomenclature.7 The name steatotic liver disease was selected to replace fatty liver disease. Metabolic dysfunction–associated fatty liver disease was changed to metabolic dysfunction–associated steatotic liver disease (MASLD), which is defined as the presence of hepatic steatosis in conjunction with 1 cardiometabolic risk factor and no other discernible cause. The concept of steatohepatitis was retained and when it is related to MASLD it is called metabolic dysfunction–associated steatohepatitis (MASH). The consumption of substantial amounts of alcohol (>140 g to 340 g per week for women and >210 g to 420 g per week for men) associated with metabolic syndrome has been termed metabolic-associated alcoholic liver disease (MetALD), which is the overlap of the above 2 conditions. High consumption of alcohol (quantities exceeding 340 g per week for women and 420 g per week for men) irrespective of its association with metabolic dysfunction is still termed alcoholic liver disease (ALD). The third category of SLD is defined when a specific pathogenesis leads to steatosis. The absence of metabolic or other causes is defined as cryptogenic SLD. The final category of SLD is SLD with a specific pathogenesis such as infection, medication, monogenic disease, or other cause. These terms are compared in Table 1,7-10 and Box 1 outlines definitions of cardiometabolic risk factors.7

View this table:
Table 1.

Three sets of terms used in the literature to refer to SLD

Box 1.

Definitions of cardiometabolic risk factors as described in the proposed new nomenclature for SLD

If a patient has at least 1 of 5 of the following risk factors, they meet the criteria for MASLD in adults based on the multisociety Delphi consensus statement.7

  • BMI ≥25 kg/m2 (≥23 kg/m2 in Asia); WC >94 cm in men or >80 cm in women; or ethnicity-adjusted equivalent

  • Fasting serum glucose level ≥5.6 mmol/L; 2-h postload glucose level of ≥7.8 mmol/L; hemoglobin A1c ≥5.7%; T2D; or prescribed treatment for T2D

  • Blood pressure of 130/85 mm Hg or a prescribed specific antihypertensive drug treatment

  • Plasma triglyceride level ≥1.70 mmol/L or prescribed lipid-lowering treatment

  • Plasma HDL-C level ≤1.3 mmol/L or prescribed lipid-lowering treatment

BMI—body mass index, HDL-C—high-density lipoprotein cholesterol, MASLD—metabolic dysfunction–associated steatotic liver disease, SLD—steatotic liver disease, T2D—type 2 diabetes, WC—waist circumference.

Diagnosis of SLD and further evaluations of disease course. There are several causes of SLD outlined in Box 2.7,11 The criterion standard for diagnosis of SLD is liver biopsy findings of more than 5% fat, but biopsy is done only when the diagnosis or extent of disease is not clear.12 It is safer and more practical to evaluate SLD with noninvasive tests such as biomarker tests and imaging.13,14 While computed tomography scanning and magnetic resonance imaging can detect fat, the most practical imaging test is abdominal ultrasound scanning, but the liver needs to be at least 20% fat for it to be recognized.15

Box 2.

Common secondary causes of metabolic dysfunction–associated steatotic liver disease

  • Obesity and other metabolic conditions (dyslipidemia, type 2 diabetes)

  • Extensive weight loss from gastric bypass or jejunoileal bypass

  • Total parenteral nutrition

  • Celiac disease (especially when treated with a gluten-free diet)

  • Genetic causes (glycogen storage disease, abetalipoproteinemia, etc)

  • Alcohol consumption

  • Medications such as amiodarone, diltiazem, steroids, tamoxifen, or antiretroviral treatment

  • Hepatitis C virus infection

Data from Rinella et al7 and Hilzenrat et al.11

The stage of liver fibrosis can be determined with vibration-controlled transient elastography (VCTE) or ultrasound-dependent shear-wave elastography. Liver stiffness measurement (LSM), irrespective of the technique used, provides prognostic information for compensated advanced chronic liver disease (cACLD). The fibrosis index score can be helpful when LSM is measured at baseline and at follow-up. For example, a VCTE measurement of less than 10 kPa rules out cACLD; however, values greater than 15 kPa are highly suggestive of cACLD.16,17 The controlled attenuation parameter (CAP) is a noninvasive measurement that can be measured at the same time VCTE or shear-wave elastography is performed to quantify liver fat (the level must be at least 10%). Results are closely correlated with biopsy findings.8,18 Therefore, the CAP is helpful for assessment, grading, and monitoring the effects of an intervention for liver steatosis.

In addition, a number of noninvasive biomarker tests have been developed to provide follow-up information on the effectiveness of interventions. The ultrasound-dependent fatty liver index and nonalcoholic steatohepatitis index are mentioned in the literature, but are too complex for daily office use.14,19 The most practical validated estimation tool for determining the extent of liver disease is the Fibrosis-4 (FIB-4) score.20 This formula estimates fibrosis based on age, platelet count, and AST and ALT levels (the calculator can be found at https://www.hepatitisc.uw.edu/page/clinical-calculators/fib-4). It should be noted that about half of patients with SLD can have normal liver enzyme levels.21

The FIB-4 score indicates whether liver stiffness should be further evaluated. The cutoff FIB-4 score should be 1.3 (ie, a score <1.3 indicates advanced fibrosis) for patients between the ages of 35 and 65 years.22 Above age 65 a cutoff of 2 was found to be more accurate due to declining AST levels with age.23

A FIB-4 score of less than 1.3 has a 99% negative predictive value in the absence of T2D. In patients with T2D there may be an 11% to 14.5% false-negative rate.24 Its positive predictive value, however, is only 17% for advanced fibrosis (defined as more than stage 2 fibrosis on histopathology19). Therefore, patients with low scores can be followed in the office, with repetition of liver enzyme level tests after 1 year. The FIB-4 score frequently overestimates the risk of fibrosis in patients with higher BMI, older age, and T2D, all factors that are associated with higher liver stiffness on elastography.25,26 Obesity may predict a worse long-term prognosis in those with MASLD.27 A FIB-4 score above 2.67 is strongly correlated with advanced fibrosis and requires hepatology consultation.

In cases where the patient’s FIB-4 score is between 1.3 and 2.67, measuring liver stiffness is important for proceeding with management, since most pharmacologic interventions are based on patients with advanced liver disease.28 Although this calculated score can be used to determine the course of treatment, elastography is somewhat more sensitive and specific for advanced fibrosis.9

The spectrum of SLD. The most common types of SLD are MASLD, MetALD, and ALD. Steatotic liver disease is now recognized as the hepatic manifestation of metabolic syndrome. Similarly, isolated SLD eventually leads to metabolic syndrome. Thus, MASLD may precede or follow complications such as T2D, hypertension, and cardiovascular and nonhepatic neoplasms.10,29 Additionally it poses a risk of progressive liver disease.30

Most cases of MASLD are associated with obesity or overweight status. Initial work suggested that in Asia SLD may occur without obesity or overweight status,31 but more recently it has been reported that about 40% of patients globally are not obese and 20% are lean.4,32 Presence of the patatin-like phospholipase domain–containing protein 3 gene, which promotes cirrhosis and hepatocellular carcinoma, may be found more often in patients without obesity and SLD.33 This and other genes have been found that may help explain why certain ethnic groups (eg, Hispanic populations) have a higher incidence of SLD.34,35 Of note, cryptogenic SLD may not be caused by these genetic markers.7

In a recent study from the United States in 7367 participants, 34.2% were estimated to have SLD based on LSM. Most were men (almost 60%) and about 63% were non-Hispanic white. Of the SLD group 31.3% had MASLD and 2% and 0.7% had MetALD and ALD, respectively.36

The full spectrum of liver disease can be seen in MASLD. The natural history of MASLD encompasses progression from simple steatosis to MASH and progressive fibrosis and cirrhosis. In MASLD the amount of alcohol consumed is not enough to cause disease (<30 g alcohol [3 drinks/day] for men and <20 g [2 drinks/day] for women).7 However, even moderate alcohol consumption may increase risk of disease progression.37 A Swedish study suggested that at least 17% of patients with MASLD consume substantial amounts of alcohol, which dramatically increases risk of decompensation.38 This appears to be much higher than in the previously mentioned study from the United States and may be due to variation in definitions of substantial alcohol consumption.36 The 20% to 30% of patients with MASH can have their disease progress to cirrhosis and its complications, including hepatocellular carcinoma, even without cirrhosis. End-stage MASLD is becoming the most common reason for liver transplant in Western societies.39

Importance of SLD as a systemic disease. As part of the metabolic syndrome it is not surprising that MASLD is associated with comorbidities that may be dependent on or independent of liver disease. In a longitudinal US study of white participants followed for 30 years, MASLD was independently associated with increased all-cause mortality, as were obesity, hypertension, and sedentary lifestyle. However, SLD was also associated with increased cardiovascular events and cancer deaths.40

Patients with obesity (BMI ≥30 kg/m2) and SLD as well as 2 features of metabolic syndrome or T2D were considered to have different risk patterns from patients with obesity only (ie, no T2D and only 1 feature of metabolic syndrome).41 Such “healthy” MASLD patients made up about 7% of a study group41; their mortality rate, cardiovascular disease prevalence, and cancer risks were similar to those in the non-MASLD group. However, these participants were more often male, younger, and had statistically lower BMIs than “unhealthy” patients (with ≥2 features of metabolic syndrome) with obesity. Their status could deteriorate with time, leading to metabolic syndrome.41

A recent meta-analysis by Chan et al evaluated the systemic nature of MASLD.42 The analysis found that MASLD was associated with outcomes such as cardiovascular disease, coronary artery disease, stroke, and heart failure, but not myocardial infarction. Similarly, higher rates of hypertension; chronic kidney disease; gallstones; and colorectal, esophageal, stomach, and thyroid cancers, but not breast and pancreatic cancers, were related to MASLD. Diabetes was positively correlated with increasing fibrosis.

Guide to diagnosis and courses of action to follow. The cases in this review are typical of patients presenting to an office. Statistically SLD is likely to be associated with metabolic dysfunction43 but other causes need to be ruled out in every case. In practice, alcohol use as a cause should be ruled out using a number of available instruments.44,45 However, as noted, the combination of metabolic cause and alcohol intake still indicates the patient is at risk of both diseases. In case 1 there is a reasonable likelihood that alcohol consumption is contributing to liver abnormalities and the pain may well be related to excess fat in the liver (SLD). In case 2, overweight status with dyslipidemia could be playing a role. The patient’s FIB-4 score is 1.31, which is borderline for possible advanced disease. Case 3 represents a patient who is relatively lean even by Asian standards (an overweight BMI is ≥25 kg/m2). However, this scenario may not be uncommon.

In all 3 cases full workup of liver enzyme levels, including alkaline phosphatase, bilirubin, GGT, ALT, AST, and albumin, should be obtained. Viral studies for hepatitis B and C infection, antinuclear antibody levels, ferritin level, and ceruloplasmin level should be obtained. Dyslipidemia and T2D should be ruled out and a hemoglobin A1c level should be obtained. A biomarker for heavy alcohol consumption has been described (ie, phosphatidylethanol): At a cutoff level of 20 ng/mL, this marker identifies moderate or heavy consumption in the past 3 to 4 weeks.46 While the first 2 cases have potential cardiac and nonhepatic cancer risks, all the cases have a risk of hepatic disease progression that needs to be addressed. Furthermore, advancing age or presence of T2D (note the FIB-4 score is less reliable for predicting fibrosis stage) with chronic SLD increases both hepatic and some nonhepatic disease risks.47 The FIB-4 score is useful for classifying risk in all 3 cases.

A 2-stage fibrosis risk-stratification model using FIB-4 has been proposed. This course of action for liver follow-up is outlined by Shaheen et al48 and a very good algorithm is provided by Alberta Health Services.49 A simplified version of this algorithm starting with established SLD is provided in Figure 1.49,50

Figure 1.
Figure 1.

Algorithm for management of SLD: This simplified outline suggests a course of action based on a diagnosis made by abdominal ultrasound scan, beginning with the recognition of a fatty liver. It should be noted that SLD and liver disease advancement may occur without increased liver enzyme levels. Liver enzyme levels, age, and platelet count are used to calculate the FIB-4 score. In Quebec, referral for VCTE or SWE requires consultation with a gastroenterologist or hepatologist.

Conclusion

While SLD is now usually associated with metabolic syndrome, a considerable number of cases are associated with alcohol consumption. Family physicians need to understand that MASLD is associated with substantial comorbidities that may be independent of liver disease but may advance liver disease complications. When in doubt, refer to a hepatologist.

Notes

Editor’s key points

  • ▸ Steatotic liver disease (SLD) occurs in 32% to 39% of the world’s population, reflecting an epidemic associated with obesity.

  • ▸ Diagnosis of SLD is based on imaging, of which ultrasound is the most readily available and practical. Findings of SLD should alert physicians to the likely presence of cardiometabolic risk factors including dyslipidemia, hypertension, obesity, pre- or overt diabetes, and possibly high alcohol consumption. In addition hepatic and nonhepatic neoplasms occur more often in patients with SLD.

  • ▸ In this approach to the diagnosis and follow-up management of SLD and metabolic dysfunction–associated SLD, new terminology is discussed, which is important for use in therapeutic trials as well as in diagnosis.

  • ▸ The simple Fibrosis-4 score should be used to guide further hepatic management.

Footnotes

  • Contributors

    Dr Andrew Szilagyi was responsible for conceptualizing the review, carrying out a literature search, and writing the manuscript. Dr Nir Hilzenrat contributed to the literature review and to writing the manuscript. Both authors reviewed the manuscript and approved the final version.

  • Competing interests

    None declared

  • This article is eligible for Mainpro+ certified Self-Learning credits. To earn credits, go to https://www.cfp.ca and click on the Mainpro+ link.

  • This article has been peer reviewed.

  • La traduction en français de cet article se trouve à https://www.cfp.ca dans la table des matières du numéro d’avril 2025 à la page e56.

References

  1. 1.↵
    1. Popkin BM,
    2. Adair LS,
    3. Ng SW.
    Global nutrition transition and the pandemic of obesity in developing countries. Nutr Rev 2012;70(1):3-21.
    OpenUrlCrossRefPubMed
  2. 2.↵
    1. Hossain P,
    2. Kawar B,
    3. El Nahas M.
    Obesity and diabetes in the developing world—a growing challenge. N Engl J Med 2007;356(3):213-5. Erratum in: N Engl J Med 2007;356(9):973.
    OpenUrlCrossRefPubMed
  3. 3.↵
    1. Jung UJ,
    2. Choi MS.
    Obesity and its metabolic complications: the role of adipokines and the relationship between obesity, inflammation, insulin resistance, dyslipidemia and nonalcoholic fatty liver disease. Int J Mol Sci 2014;15(4):6184-223.
    OpenUrlCrossRefPubMed
  4. 4.↵
    1. Riazi K,
    2. Azhari H,
    3. Charette JH,
    4. Underwood FE,
    5. King JA,
    6. Afshar EE, et al
    . The prevalence and incidence of NAFLD worldwide: a systematic review and metaanalysis. Lancet Gastroenterol Hepatol 2022;7(9):851-61. Epub 2022 Jul 5.
    OpenUrlCrossRefPubMed
  5. 5.↵
    1. Chan KE,
    2. Koh TJL,
    3. Tang ASP,
    4. Quek J,
    5. Yong JN,
    6. Tay P, et al
    . Global prevalence and clinical characteristics of metabolic-associated fatty liver disease: a meta-analysis and systematic review of 10,739,607 individuals. J Clin Endocrinol Metab 2022;107(9):2691-700.
    OpenUrlPubMed
  6. 6.↵
    1. Eslam M,
    2. Sanyal AJ,
    3. George J; International Consensus Panel
    . MAFLD: a consensus-driven proposed nomenclature for metabolic associated fatty liver disease. Gastroenterology 2020;158(7):1999-2014.e1. Epub 2020 Feb 8.
    OpenUrlCrossRefPubMed
  7. 7.↵
    1. Rinella ME,
    2. Lazarus JV,
    3. Ratziu V,
    4. Francque SM,
    5. Sanyal AJ,
    6. Kanwal F, et al
    . A multisociety Delphi consensus statement on new fatty liver disease nomenclature. J Hepatol 2023;79(6):1542-56. Epub 2023 Jun 24.
    OpenUrlCrossRefPubMed
  8. 8.↵
    1. Rinella ME,
    2. Neuschwander-Tetri BA,
    3. Siddiqui MS,
    4. Abdelmalek MF,
    5. Caldwell S,
    6. Barb D, et al
    . AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology 2023;77(5):1797-835. Epub 2023 Mar 17.
    OpenUrlCrossRefPubMed
  9. 9.↵
    1. Damjanovska S,
    2. Karb DB,
    3. Tripathi A,
    4. Asirwatham J,
    5. Delozier S,
    6. Perez JA, et al
    . Accuracy of ultrasound elastography and Fibrosis-4 Index (FIB-4) in ruling out cirrhosis in obese non-alcoholic fatty liver disease (NAFLD) patients. Cureus 2022;14(9):e29445.
    OpenUrl
  10. 10.↵
    1. Marchesini G,
    2. Brizi M,
    3. Bianchi G,
    4. Tomassetti S,
    5. Bugianesi E,
    6. Lenzi M, et al
    . Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. Diabetes 2001;50(8):1844-50.
    OpenUrlAbstract/FREE Full Text
  11. 11.↵
    1. Hilzenrat N,
    2. Lamoureux E,
    3. Szilagyi A.
    Fatty liver disease. In: Thomson ABR, Shaffer EA, editors. First principles of gastroenterology and hepatology. The basis of disease and an approach to management. CAPstone Academic Publishers; 2012. p. 413-24.
  12. 12.↵
    1. Muthiah MD,
    2. Han NC,
    3. Sanyal AJ.
    A clinical overview of non-alcoholic fatty liver disease: a guide to diagnosis, the clinical features, and complications—what the non-specialist needs to know. Diabetes Obes Metab 2022;24(Suppl 2):3-14.
    OpenUrl
  13. 13.↵
    1. Wieckowska A,
    2. Feldstein AE.
    Diagnosis of nonalcoholic fatty liver disease: invasive versus noninvasive. Semin Liver Dis 2008;28(4):386-95. Epub 2008 Oct 27.
    OpenUrlCrossRefPubMed
  14. 14.↵
    1. Wong VWS,
    2. Adams LA,
    3. de Lédinghen V,
    4. Wong GLH,
    5. Sookoian S.
    Noninvasive biomarkers in NAFLD and NASH – current progress and future promise. Nat Rev Gastroenterol Hepatol 2018;15(8):461-78.
    OpenUrlCrossRefPubMed
  15. 15.↵
    1. Gao X,
    2. Fan JG.
    Diagnosis and management of non-alcoholic fatty liver disease and related metabolic disorders: consensus statement from the Study Group of Liver and Metabolism, Chinese Society of Endocrinology. J Diabetes 2013;5(4):406-15. Epub 2013 Jun 4.
    OpenUrlPubMed
  16. 16.↵
    1. De Franchis R,
    2. Bosch J,
    3. Garcia-Tsao G,
    4. Reiberger T,
    5. Ripoll C; Baveno VII Faculty
    . Baveno VII – renewing consensus in portal hypertension. J Hepatol 2022;76(4):959-74. Epub 2021 Dec 30. Erratum in: J Hepatol 2022;77(1):271. Epub 2022 Apr 14.
    OpenUrlCrossRefPubMed
  17. 17.↵
    1. Sasso M,
    2. Beaugrand M,
    3. de Ledinghen V,
    4. Douvin C,
    5. Marcellin P,
    6. Poupon R, et al
    . Controlled attenuation parameter (CAP): a novel VCTE™ guided ultrasonic attenuation measurement for the evaluation of hepatic steatosis: preliminary study and validation in a cohort of patients with chronic liver disease from various causes. Ultrasound Med Biol 2010;36(11):1825-35. Epub 2010 Sep 27.
    OpenUrlCrossRefPubMed
  18. 18.↵
    1. Eddowes P,
    2. Sasso M,
    3. Allison M,
    4. Tsochatzis E,
    5. Anstee QM,
    6. Sheridan D, et al
    . Accuracy of FibroScan controlled attenuation parameter and liver stiffness measurement in assessing steatosis and fibrosis in patients with nonalcoholic fatty liver disease. Gastroenterology 2019;156(6):1717-30. Epub 2019 Jan 25.
    OpenUrlCrossRefPubMed
  19. 19.↵
    1. Sanyal AJ,
    2. Castera L,
    3. Wong VWS.
    Noninvasive assessment of liver fibrosis in NAFLD. Clin Gastroenterol Hepatol 2023;21(8):2026-39. Epub 2023 Apr 14. Erratum in: Clin Gastroenterol Hepatol 2024;22(3):676. Epub 2023 Dec 27.
    OpenUrlPubMed
  20. 20.↵
    1. Sterling RK,
    2. Lissen E,
    3. Clumeck N,
    4. Sola R,
    5. Correa MC,
    6. Montaner J, et al
    . Development of a simple noninvasive index to predict significant fibrosis patients with HIV/HCV coinfection. Hepatology 2006;43(6):1317-25.
    OpenUrlCrossRefPubMed
  21. 21.↵
    1. Noureddin M,
    2. Loomba R.
    Nonalcoholic fatty liver disease: indications for liver biopsy and noninvasive biomarkers. Clin Liver Dis (Hoboken) 2012;1(4):104-7.
    OpenUrlCrossRef
  22. 22.↵
    1. Davyduke T,
    2. Tandon P,
    3. Al-Karaghouli M,
    4. Abraldes JG,
    5. Ma MM.
    Impact of implementing a “FIB-4 First” strategy on a pathway for patients with NAFLD referred from primary care. Hepatol Commun 2019;3(10):1322-33.
    OpenUrlPubMed
  23. 23.↵
    1. McPherson S,
    2. Hardy T,
    3. Dufour JF,
    4. Petta S,
    5. Romero-Gomez M,
    6. Allison M, et al
    . Age as a confounding factor for the accurate non-invasive diagnosis of advanced NAFLD fibrosis. Am J Gastroenterol 2017;112(5):740-51. Epub 2016 Oct 11.
    OpenUrlCrossRefPubMed
  24. 24.↵
    1. Arai T,
    2. Takahashi H,
    3. Seko Y,
    4. Toyoda H,
    5. Hayashi H,
    6. Yamaguchi K, et al
    . Accuracy of the enhanced liver fibrosis test in patients with type 2 diabetes mellitus and its clinical implications. Clin Gastroenterol Hepatol 2024;22(4):789-97.e8. Epub 2023 Dec 2.
    OpenUrlPubMed
  25. 25.↵
    1. Chang M,
    2. Chang D,
    3. Kodali S,
    4. Harrison SA,
    5. Ghobrial M,
    6. Alkhouri N, et al
    . Degree of discordance between FIB-4 and transient elastography: an application of current guidelines on general population cohort. Clin Gastroenterol Hepatol 2024;22(7):1453-61.e2. Epub 2024 Feb 29.
    OpenUrlPubMed
  26. 26.↵
    1. Graupera I,
    2. Thiele M,
    3. Serra-Burriel M,
    4. Caballeria L,
    5. Roulot D,
    6. Wong GLH, et al
    . Low accuracy of FIB-4 and NAFLD fibrosis scores for screening for liver fibrosis in the population. Clin Gastroenterol Hepatol 2022;20(11):2567-76.e6. Epub 2021 Dec 29.
    OpenUrlPubMed
  27. 27.↵
    1. Lu FB,
    2. Hu ED,
    3. Xu LM,
    4. Chen L,
    5. Wu JL,
    6. Li H, et al
    . The relationship between obesity and the severity of non-alcoholic fatty liver disease: systematic review and metaanalysis. Expert Rev Gastroenterol Hepatol 2018;12(5):491-502. Epub 2018 Apr 2.
    OpenUrlPubMed
  28. 28.↵
    1. Harrison SA,
    2. Loomba R,
    3. Dubourg J,
    4. Ratziu V,
    5. Noureddin M.
    Clinical trial landscape in NASH. Clin Gastroenterol Hepatol 2023;21(8):2001-14. Epub 2023 Apr 12.
    OpenUrlPubMed
  29. 29.↵
    1. Lonardo A,
    2. Ballestri S,
    3. Marchesini G,
    4. Angulo P,
    5. Loria P.
    Nonalcoholic fatty liver disease: a precursor of the metabolic syndrome. Dig Liver Dis 2015;47(3):181-90. Epub 2014 Nov 18.
    OpenUrlCrossRefPubMed
  30. 30.↵
    1. Sanyal AJ,
    2. Van Natta ML,
    3. Clark J,
    4. Neuschwander-Tetri BA,
    5. Diehl A,
    6. Dasarathy S, et al
    . Prospective study of outcomes in adults with nonalcoholic fatty liver disease. N Engl J Med 2021;385(17):1559-69.
    OpenUrlCrossRefPubMed
  31. 31.↵
    1. Mitra S,
    2. De A,
    3. Chowdhury A.
    Epidemiology of non-alcoholic and alcoholic fatty liver diseases. Transl Gastroenterol Hepatol 2020;5:16.
    OpenUrlPubMed
  32. 32.↵
    1. Ye Q,
    2. Zou B,
    3. Yeo YH,
    4. Li J,
    5. Huang DQ,
    6. Wu Y, et al
    . Global prevalence, incidence, and outcomes of non-obese or lean non-alcoholic fatty liver disease: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol 2020;5(8):739-52. Epub 2020 May 12.
    OpenUrlPubMed
  33. 33.↵
    1. Lin H,
    2. Wong GLH,
    3. Whatling C,
    4. Chan AWH,
    5. Leung HHW,
    6. Tse CH, et al
    . Association of genetic variations with NAFLD in lean individuals. Liver Int 2022;42(1):149-60. Epub 2021 Oct 12.
    OpenUrlPubMed
  34. 34.↵
    1. Yip TCF,
    2. Vilar-Gomez E,
    3. Petta S,
    4. Yilmaz Y,
    5. Wong GLH,
    6. Adams LA, et al
    . Geographical similarity and differences in the burden and genetic predisposition of NAFLD. Hepatology 2023;77(4):1404-27. Epub 2022 Oct 11.
    OpenUrlCrossRefPubMed
  35. 35.↵
    1. Romeo S,
    2. Kozlitina J,
    3. Xing C,
    4. Pertsemlidis A,
    5. Cox D,
    6. Pennacchio LA, et al
    . Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease. Nat Genet 2008;40(12):1461-5. Epub 2008 Sep 25.
    OpenUrlCrossRefPubMed
  36. 36.↵
    1. Lee BP,
    2. Dodge JL,
    3. Terrault NA.
    National prevalence estimates for steatotic liver disease and subclassifications using consensus nomenclature. Hepatology 2024;79(3):666-73. Epub 2023 Sep 20.
    OpenUrlCrossRefPubMed
  37. 37.↵
    1. Rice BA,
    2. Naimi TS,
    3. Long MT.
    Nonheavy alcohol use associates with liver fibrosis and nonalcoholic steatohepatitis in the Framingham Heart Study. Clin Gastroenterol Hepatol 2023;21(11):2854-63.e2. Epub 2022 Dec 8.
    OpenUrlPubMed
  38. 38.↵
    1. Nasr P,
    2. Wester A,
    3. Ekstedt M,
    4. Strandberg R,
    5. Kechagias S,
    6. Shang Y, et al
    . Misclassified alcohol-related liver disease is common in presumed metabolic dysfunction-associated steatotic liver disease and highly increases risk for future cirrhosis. Clin Gastroenterol Hepatol 2024;22(5):1048-57.e2. Epub 2024 Jan 17.
    OpenUrlPubMed
  39. 39.↵
    1. Vinaixa C,
    2. Selzner N,
    3. Berenguer M.
    Fat and liver transplantation: clinical implications. Transpl Int 2018;31(8):828-37.
    OpenUrlPubMed
  40. 40.↵
    1. De Avila L,
    2. Henry L,
    3. Paik JM,
    4. Ijaz N,
    5. Weinstein AA,
    6. Younossi ZM.
    Nonalcoholic fatty liver disease is independently associated with higher all-cause and cause-specific mortality. Clin Gastroenterol Hepatol 2023;21(10):2588-96.e3. Epub 2023 Jan 13.
    OpenUrlPubMed
  41. 41.↵
    1. Chan KE,
    2. Ng CH,
    3. Fu CE,
    4. Quek J,
    5. Kong G,
    6. Goh YJ, et al
    . The spectrum and impact of metabolic dysfunction in MAFLD: a longitudinal cohort analysis of 32,683 overweight and obese individuals. Clin Gastroenterol Hepatol 2023;21(10):2560-9.e15. Epub 2022 Oct 3.
    OpenUrlPubMed
  42. 42.↵
    1. Chan KE,
    2. Ong EYH,
    3. Chung CH,
    4. Ong CEY,
    5. Koh B,
    6. Tan DJH, et al
    . Longitudinal outcomes associated with metabolic dysfunction-associated steatotic liver disease: a meta-analysis of 129 studies. Clin Gastroenterol Hepatol 2024;22(3):488-98.e14. Epub 2023 Sep 28.
    OpenUrlCrossRefPubMed
  43. 43.↵
    1. Loomba R,
    2. Wong VWS.
    Implications of the new nomenclature of steatotic liver disease and definition of metabolic dysfunction-associated steatotic liver disease. Aliment Pharmacol Ther 2024;59(2):150-6.
    OpenUrlCrossRefPubMed
  44. 44.↵
    1. Hernandez-Tejero M,
    2. Clemente-Sanchez A,
    3. Bataller R.
    Spectrum, screening, and diagnosis of alcohol-related liver disease. J Clin Exp Hepatol 2023;13(1):75-87. Epub 2022 Oct 13.
    OpenUrlPubMed
  45. 45.↵
    1. Harris SK,
    2. Louis-Jacques J,
    3. Knight JR.
    Screening and brief intervention for alcohol and other abuse. Adolesc Med State Art Rev 2014;25(1):126-56.
    OpenUrlPubMed
  46. 46.↵
    1. Hahn JA,
    2. Fatch R,
    3. Barnett NP,
    4. Marcus GM.
    Phosphatidylethanol vs transdermal alcohol monitoring for detecting alcohol consumption among adults. JAMA Netw Open 2023;6(9):e2333182.
    OpenUrlPubMed
  47. 47.↵
    1. Huang DQ,
    2. Wilson LA,
    3. Behling C,
    4. Kleiner DE,
    5. Kowdley KV,
    6. Dasarathy S, et al
    . Fibrosis progression rate in biopsy-proven nonalcoholic fatty liver disease among people with diabetes versus people without diabetes: a multicenter study. Gastroenterology 2023;165(2):463-72.e5. Epub 2023 Apr 29.
    OpenUrlPubMed
  48. 48.↵
    1. Shaheen AA,
    2. Riazi K,
    3. Medellin A,
    4. Bhayana D,
    5. Kaplan GG,
    6. Jiang J, et al
    . Risk stratification of patients with nonalcoholic fatty liver disease using a case identification pathway in primary care: a cross-sectional study. CMAJ Open 2020;8(2):E370-6.
    OpenUrlAbstract/FREE Full Text
  49. 49.↵
    Non-alcoholic fatty liver disease (NAFLD) primary care pathway. Edmonton, AB: Alberta Health Services; 2021. Available from: https://www.albertahealthservices.ca/assets/about/scn/ahs-scn-dh-pathway-nafld.pdf. Accessed 2025 Feb 26.
  50. 50.↵
    Attribution NonCommercial ShareAlike 4.0 International. Version 4.0. Mountain View, CA: Creative Commons. Available from: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode.en. Accessed 2025 Feb 26.
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Approach to steatotic liver disease in the office
Andrew Szilagyi, Nir Hilzenrat
Canadian Family Physician Apr 2025, 71 (4) 249-254; DOI: 10.46747/cfp.7104249
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