MASLD and MASH: Steatotic liver disease joins the deadly quartet

  • Cleveland Clinic Journal of Medicine
  • September 2026,
  • 93
  • (9)
  • 551-559;
  • DOI: https://doi.org/10.3949/ccjm.93a.25117

ABSTRACT

Metabolic dysfunction–associated steatotic liver disease (MASLD) is linked to insulin resistance and cardiometabolic disorders. This review synthesizes current information on the epidemiology, pathophysiology, and treatment of MASLD and its progressive form, metabolic dysfunction– associated steatohepatitis (MASH), underscoring how to integrate established metabolic care with emerging treatments to address the growing MASLD burden.

KEY POINTS

  • MASLD is the most prevalent chronic liver disease in the world and has strong ties to cardiometabolic risk factors and a growing burden of cirrhosis and liver-related mortality.

  • Lifestyle modification remains key, and losing at least 10% of body weight offers the greatest benefit.

  • The US Food and Drug Administration has approved resmetirom and semaglutide for treating patients with MASH and stage 2 or 3 fibrosis, on the basis of reducing steatohepatitis and fibrosis in clinical trials.

  • Agents such as glucagon-like peptide 1 receptor agonists other than semaglutide, sodium-glucose cotransporter 2 inhibitors, pioglitazone, and statins show promise in improving liver outcomes and cardiometabolic health, though guideline recommendations vary regarding their off-label use.

  • Noninvasive assessments of liver disease are essential for determining whether a patient needs treatment.

Obesity. Dyslipidemia. High blood pressure. Type 2 diabetes mellitus. And now, to this deadly quartet of metabolic diseases that primary care physicians manage every day, add fatty liver—or, to use the latest nomenclature, metabolic dysfunction–associated steatotic liver disease (MASLD).

Like the other 4, with which it is linked, MASLD is ubiquitous. Although it often leads to cirrhosis and liver cancer, awareness of it is low, even among physicians. But now we have 2 approved drugs for it and guidelines from specialist societies on how to treat it.

Here, we review the science and the guidelines (Table 1) and propose an algorithm to assist outpatient physicians in screening for, diagnosing, and treating MASLD and its severe form, metabolic-associated steatohepatitis (MASH) (Figure 1).1–8

View this table:
TABLE 1

Criteria for diagnosing metabolic–associated steatotic liver disease

Proposed algorithm for outpatient management of metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic dysfunction–associated steatohepatitis (MASH). aFibrosis-4 index = (age [years] × AST level [U/L]) / (platelet count [× 109/L] × √ALT level [U/L]) bA fibrosis-4 score higher than 2.67 indicates highest risk of advanced fibrosis, and these patients should be referred directly to hepatology. Based on information from references 1–8.
Figure 1

Proposed algorithm for outpatient management of metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic dysfunction–associated steatohepatitis (MASH).

aFibrosis-4 index = (age [years] × AST level [U/L]) / (platelet count [× 109/L] × √ALT level [U/L])

bA fibrosis-4 score higher than 2.67 indicates highest risk of advanced fibrosis, and these patients should be referred directly to hepatology. Based on information from references 1–8.

NEW NAMES FOR A GROWING PROBLEM

Until 2023, MASLD was known as nonalcoholic fatty liver disease (NAFLD), and MASH was called nonalcoholic steatohepatitis (NASH).9 The name changes were driven by a desire to represent more accurately the disease’s pathophysiology and its strong association with insulin resistance and cardiometabolic disorders, which are now understood to be primary underlying drivers.2,9 Furthermore, the term “nonalcoholic” carried a stigma and contributed to a lack of public and governmental recognition, impeding research.9,10

Patients who meet the criteria for MASLD and also consume a moderate amount of alcohol (140–350 g/week for women; 210–420 g/week for men) are now specifically classified as having metabolic dysfunction and alcohol-associated liver disease.

Clinically, this nomenclature change does not significantly affect how we look at previous data, as the NAFLD and MASLD populations almost completely overlap in their clinical characteristics.2,8,11

In the past, without any approved medications, treatment focused predominantly on lifestyle modifications for weight loss and off-label use of medications such as metformin, pioglitazone, glucagon-like peptide (GLP) 1 receptor agonists, vitamin E, and statins.12 However, research has led to updated guidelines and the recent approval of resmetirom and semaglutide specifically indicated for MASH.

THE NUMBER ONE CAUSE OF CHRONIC LIVER DISEASE

MASLD has become the number one cause of chronic liver disease in the United States and the world. In a 2023 meta-analysis, Younossi et al13 estimated its global prevalence at 30.05% and rising, affecting 1.66 billion people. In the United States, it is estimated to be the cause of 52% of cases of chronic liver disease,14 and to affect as many as 65% of people with type 2 diabetes mellitus.7

Globally, MASLD is the most rapidly increasing contributor to complications of chronic liver disease, including cirrhosis and hepatocellular carcinoma,15 and in the United States it is the second most frequent indication for liver transplantation, after alcohol-associated liver disease.16

MASLD is closely associated with metabolic disorders such as obesity, insulin resistance, type 2 diabetes mellitus, hypertension, and atherogenic dyslipidemia. It is defined by excessive hepatic triglyceride storage (> 5% in hepatocytes) without an identified alternative cause of steatosis (eg, medications, starvation) with limited alcohol use (< 20 g/day for women, < 30 g/day for men), plus at least 1 cardiometabolic risk factor (Table 1).2,9

A SPECTRUM OF CONDITIONS

MASLD is a spectrum of conditions, including isolated liver steatosis (MASL), MASH, fibrosis, and cirrhosis.

MASH is the most severe form, characterized by histologic features of hepatocellular ballooning (tissue injury) and lobular inflammation, in addition to steatosis.5 Compared with simple steatosis (MASL), MASH progresses faster to high-level fibrosis, at a rate of 1 stage per 7.1 years vs 1 stage per 14.3 years.17

DRIVEN BY GENETICS AND DIET

The pathogenesis of MASLD is complex, highly heterogeneous, and incompletely elucidated. MASLD progresses to MASH through a multistep process driven by interactions between genetics and factors such as diet, insulin resistance, and gut dysbiosis.18

A proposed primary mechanism begins with excessive dietary intake of glucose and fructose, which contributes to production of fatty acid in the liver. Toxic lipid intermediates disrupt cellular signaling, causing insulin resistance, compensatory hyperinsulinemia, and hyperglycemia, in a cycle that further amplifies hepatic de novo lipogenesis. When combined with a high intake of saturated fatty acids, this overfeeding leads to subclinical inflammation in adipose tissue, the liver, and skeletal muscles.

Elevated saturated fatty acids and hyperglycemia overwhelm the mitochondria’s capacity to metabolize free fatty acids, leading to mitochondrial dysfunction, oxidative stress, and excessive production of reactive oxygen species and hepatocyte injury. The resulting cellular stress activates resident immune cells, which then stimulate hepatic stellate cells, driving the fibrogenic response and leading to cirrhosis.11,18

Genetic variants increase risk

Genetic variants play an important role in how MASLD develops and progresses, influencing core molecular pathways such as lipolysis, triglyceride export, and energy metabolism.11,19 Genome-wide association studies have identified key variants that disrupt normal liver function:

  • PNPLA3 rs738409, which impairs the break-down and mobilization of triglycerides from liver cells, leading to fat accumulation, and also leads to increased inflammatory activation of hepatic stellate cells in fibrosis19

  • TM6SF2 rs58542926, which hinders fat transport out of the liver

  • MBOAT7 rs641738, which alters lipid remodeling and contributes to inflammation.11,19

Adiposity significantly amplifies the harmful effects of these genetic risk alleles, accelerating progression. However, the potency of the PNPLA3 rs738409 variant highlights the disease’s heterogeneity, as even people with normal weight who carry this allele can have increased liver fat content, underscoring that MASLD is not solely a consequence of obesity.11

SCREENING AND DIAGNOSIS

The primary goal of screening is to identify patients with clinically significant liver fibrosis (stage F2 or higher on a scale that ranges from F0 [normal] to F4 [cirrhosis]). Liver fibrosis is the most critical determinant of both liver-related and nonliver outcomes in MASLD, with the risk of future clinical events increasing significantly starting at stage F2.6,7 Patients with stage F2 fibrosis or higher were the key population targeted in all phase 3 MASH clinical trials and are the primary candidates for drug therapy.7

Which patients should be screened?

Guidelines from the American Gastroenterological Association (AGA)6,7 recommend screening patients at high risk for whom timely diagnosis may prevent disease progression, ie, those with the following:

  • Type 2 diabetes mellitus

  • Overweight or obesity plus 1 additional metabolic risk factor, including increased waist circumference, elevated serum triglycerides or treatment for it, low high-density lipoprotein cholesterol or treatment for it, hypertension, prediabetes, or insulin resistance

  • An incidental finding of hepatic steatosis on imaging or elevated aminotransferase levels.

These patients should initially be screened for alcohol use using a standardized test such as the Alcohol Use Disorders Identification Test-Consumption (AUDIT-C), where a score of 3 or higher for women or 4 or higher for men is positive, or the National Institute on Alcohol Abuse and Alcoholism screening question (“How many times in the past year have you had 4 or more drinks [for women] or 5 or more drinks [for men] in a day?”), to which any answer greater than 0 should prompt follow-up questions to quantify weekly alcohol intake.

They should also have a complete blood cell count and a comprehensive metabolic panel; the former will give you the platelet count and the latter will give you the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, which you need to calculate the fibrosis-4 index (see next section below).20 Beyond calculating the fibrosis-4 index, these routine panels offer critical diagnostic clues. On a complete blood cell count, thrombocytopenia (platelet count < 150 × 109/L) is a red flag for portal hypertension and cirrhosis. On a comprehensive metabolic panel, clinicians should evaluate serum albumin and total bilirubin, as hypoalbuminemia and hyperbilirubinemia signal worsening hepatic synthetic function and advanced liver disease.

Stratify risk by fibrosis-4 index

Risk should then be stratified using simple, nonproprietary scores; the fibrosis-4 index is preferred because it has a high negative predictive value for advanced fibrosis.6 It is calculated as follows: Formula

Note that in patients with type 2 diabetes mellitus, who have a high prevalence of advanced fibrosis, it is reasonable to proceed directly to imaging-based noninvasive liver disease assessments if these tests are readily available (see below).7

If the fibrosis-4 score is less than 1.3, or less than 2.0 for patients age 65 years or older, the patient probably doesn’t have advanced fibrosis, as the negative predictive value is at least 90%. You can follow up and reevaluate the score with these patients in 1 to 2 years.1,5–7

Measure liver stiffness

However, if the fibrosis-4 score is 1.3 or higher, or 2.0 or higher for patients 65 years or older, the patient should undergo liver stiffness measurement using vibration-controlled transient elastography (VCTE, also called FibroScan), or if this is not available, blood testing for the Enhanced Liver Fibrosis (ELF) score.3,7 Results are categorized as follows:

Low risk. A VCTE measurement less than 8.0 Kpa or ELF score less than 9.2 is consistent with stage F0 or F1 fibrosis and reliably excludes advanced fibrosis (negative predictive value 98%–99%).7 Manage with lifestyle intervention and optimization of metabolic comorbidities, and repeat surveillance every 3 years.7

At risk. A VCTE measurement of 8.0 to 19.9 kPa or ELF score of 9.2 to 11.2 suggests moderate to advanced fibrosis (stage F2 or F3). These patients are prime candidates for drug treatment (eg, with a GLP-1 receptor agonist or resmetirom). Referral to gastroenterology-hepatology is recommended for management and consideration of additional confirmatory tests such as magnetic resonance elastography (MRE) if the diagnosis is uncertain.7

High risk. A VCTE measurement of 20.0 kPa or higher or an ELF score of 11.3 or higher strongly suggests compensated cirrhosis (stage F4). Alternative criteria for high risk or cirrhosis include an MRE measurement of 5.0 kPa or higher. Promptly refer to a gastroenterology-hepatology service for specialized cirrhosis care, including hepatocellular carcinoma surveillance and screening for gastroesophageal varices due to portal hypertension.

Although biopsy remains the gold standard for diagnosing fibrosis and cirrhosis, most liver specialists consider doing one only in patients with discordant findings on noninvasive assessments or when an alternative diagnosis is being considered. Patients at risk (with a VCTE measurement 8.0–19.9 kPa) generally do not need a biopsy to initiate therapy with resmetirom or semaglutide, as noninvasive tests are now recognized as sufficient for identifying treatment candidates in routine clinical practice.3,4,7

LIFESTYLE CHANGES ARE STILL KEY

Lifestyle changes remain the cornerstone of treatment1,8,21:

  • Losing weight by consuming fewer calories

  • Adopting a Mediterranean-style diet

  • Engaging in at least 150 minutes of moderate-intensity physical activity per week.

While a 5% or more reduction in body weight offers clinical benefits, losing 10% or more provides the most significant improvements in hepatic steatosis and fibrosis and cardiometabolic health.8 However, very few patients can achieve and sustain a weight loss of more than 10% through lifestyle alone; most also need pharmacotherapy or bariatric surgery. Lassailly et al,22 in a prospective study, found that bariatric surgery was highly effective not only for weight loss but also for resolving steatohepatitis and halting the progression of advanced disease.

RESMETIROM, THE FIRST FDA-APPROVED THERAPY

Resmetirom is a liver-directed selective agonist of thyroid hormone receptor beta that promotes lipophagy, mitochondrial biogenesis, and mitophagy, stimulating increased hepatic fatty acid beta oxidation, thereby decreasing the burden of lipotoxic lipids while promoting low-density lipoprotein uptake and favorable effects on lipid profiles.23

In the phase 3 MAESTRO-NASH trial,24 MASH resolved without worsening fibrosis in 29.9% of patients receiving resmetirom 100 mg daily, compared with 9.7% in the placebo group. Fibrosis improved by at least 1 stage in 25.9% of patients receiving this dose, vs 14.2% in the placebo group.

In March 2024, the US Food and Drug Administration (FDA) granted resmetirom accelerated approval for adults with at-risk MASH with moderate to advanced liver fibrosis (stages F2 or F3), in conjunction with diet and exercise. Although the trials of this drug required a liver biopsy for enrollment, the FDA approval does not mandate one to confirm the diagnosis in clinical practice, recognizing the limitations of liver biopsy in practice settings.3 Physicians can identify eligible patients using noninvasive liver disease assessments such as the fibrosis-4 score followed by VCTE combined with blood-based biomarkers.3

While resmetirom represents a significant advance, it is estimated to cost private payers approximately $43,951 per patient per year.25,26

SEMAGLUTIDE, THE SECOND APPROVED THERAPY

GLP-1 receptor agonists such as semaglutide and liraglutide are cornerstone treatments for type 2 diabetes mellitus and obesity, as they produce robust weight loss and improve glycemic control and are associated with positive cardiometabolic outcomes.

A phase 2 trial demonstrated steatohepatitis resolution in 59% of patients receiving semaglutide 0.4 mg daily, vs 17% with placebo, along with significant weight loss.27

The phase 3 ESSENCE (Effect of Semaglutide in Subjects With Noncirrhotic Nonalcoholic Steatohepatitis) trial28 found that steatohepatitis resolved without worsening fibrosis in 62.9% of patients receiving semaglutide 2.4 mg once weekly, compared with 34.3% with placebo, with at least a 1-stage reduction in fibrosis in 36.8% of the treated group vs 22.4% in the placebo group.

Based on these results, in August 2025 the FDA approved semaglutide (specifically the Wegovy formulation from Novo Nordisk) for treating noncirrhotic MASH with moderate to advanced liver fibrosis (stages F2 or F3).

Semaglutide is also expensive, but not as expensive as resmetirom—about $1,350 per month.

CHOOSING BETWEEN RESMETIROM AND SEMAGLUTIDE

For patients with MASH who have concomitant severe obesity or type 2 diabetes mellitus, semaglutide is generally preferred because of its profound cardiometabolic and weight-loss benefits. Resmetirom may be favored in patients with “lean MASH” (ie, who have MASH but not obesity), those who cannot tolerate GLP-1 receptor agonists, or those who require targeted liver-directed therapy independent of weight loss.29

MONITORING DURING TREATMENT

During treatment with resmetirom or semaglutide, the American Association for the Study of Liver Diseases (AASLD) recommends frequent monitoring for common adverse events and for therapeutic response.3,4

Resmetirom can induce transient ALT and AST elevations during the first months of therapy, particularly in patients taking statins. Aminotransferases should be monitored at baseline and at 3, 6, and 12 months. Additionally, due to cytochrome P450 2C8 interactions, statin doses must be reduced (eg, rosuvastatin and simvastatin to 20 mg/day or less; pravastatin and atorvastatin to 40 mg/day or less) and pioglitazone must be limited to 15 mg daily. Baseline thyroid function should also be checked.

Semaglutide. Nongastroenterology-hepatology specialists should monitor closely and adjust concurrent antihypertensive and antihyperglycemic medications during the initial titration and weight-loss phase. Renal function must be monitored in patients with preexisting renal impairment who experience significant gastrointestinal side effects, which can lead to dehydration.

Response to therapy should be assessed using imaging-based noninvasive liver disease assessments (eg, VCTE or MRE) and aminotransferases based on the specific agent’s clinical trial timeline. For resmetirom, assess at approximately 12 months (52 weeks); at least a 25% improvement in liver stiffness by VCTE or at least a 20% improvement by MRE is considered a significant surrogate for histologic improvement.3 For semaglutide, assess at about 72 weeks; a VCTE improvement of 30% or greater, an MRE improvement of 20% or greater, or an ALT reduction of 17 U/L or greater (or ≥ 20%) likely reflects a beneficial response.4 However, changes in liver stiffness should be interpreted cautiously, as massive weight loss itself can confound elastography readings.

Noninvasive assessments should be done after 52 weeks of treatment with resmetirom and after 72 weeks with semaglutide; if these show that liver disease has not improved or has gotten worse, clinicians should consider stopping the medication, switching therapies, or exploring combination therapy to prevent financial toxicity and unnecessary drug exposure.

OFF-LABEL AND ADJUNCT THERAPIES

Many of the drugs that patients with MASLD receive for type 2 diabetes mellitus, dyslipidemia, or obesity also may have a “two-for-one” benefit in the liver.

Liraglutide, like semaglutide, is a GLP-1 receptor agonist. In the LEAN (Liraglutide Efficacy and Action in Nonalcoholic Steatohepatitis) trial,30 NASH resolved in 9 (39%) of 23 patients receiving liraglutide 1.8 mg daily compared with 9% with placebo.

Tirzepatide, a dual glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 receptor agonist approved for type 2 diabetes mellitus and obesity, has shown highly promising off-label efficacy for liver disease.

A phase 3 trial found that patients without diabetes who had obesity lost nearly 50% more weight with tirzepatide than with semaglutide, and the drug showed potential for fibrosis regression.7 Phase 2 trials demonstrated potent reductions in liver fat content and high rates of MASH resolution, making tirzepatide a powerful tool for weight and metabolic management; we look forward to results from phase 3 trials in patients with MASH.31

The American Association of Clinical Endocrinology (AACE) originally gave a grade A recommendation for GLP-1 receptor agonists in patients with type 2 diabetes mellitus with MASH, and then extended it to patients without diabetes who have biopsy-proven MASH as well.1,10

Pioglitazone, a thiazolidinedione, is a potent PPAR (peroxisome proliferator–activated receptor) gamma activator that improves insulin sensitivity, lowers free fatty acid levels, and reduces hepatic lipid accumulation. Clinical studies showed it significantly reduced hepatic steatosis, inflammation, and hepatocellular ballooning.32,33

In the PIVENS (Pioglitazone Versus Vitamin E Versus Placebo for the Treatment of Nondiabetic Patients With Nonalcoholic Steatohepatitis) trial,34 MASH resolved in 47% of patients without diabetes receiving pioglitazone after 96 weeks. An 18-month study in patients with obesity and prediabetes or type 2 diabetes mellitus demonstrated MASH resolution in 51%.33 Meta-analyses consistently show that pioglitazone is significantly more effective than placebo in achieving MASH resolution and at least a 1-stage improvement in liver fibrosis regardless of diabetes status.35

Side effects include dose-dependent weight gain, heart failure, fluid retention, bone fracture, and a potential association with bladder cancer.8,33

The AACE gives a grade A recommendation to use pioglitazone in patients with type 2 diabetes mellitus and biopsy-proven MASH,1 and the AASLD recommends considering it for patients with MASH who have type 2 diabetes mellitus.5 European guidelines give it a weak recommendation in adults with noncirrhotic MASH regardless of diabetes status; while acknowledging its safety, they do not endorse it as primary MASH-targeted therapy because we lack robust data from phase 3 clinical trials.8

Sodium-glucose cotransporter (SGLT) 2 inhibitors reduce glucose reabsorption, lowering blood glucose and insulin, which contributes to reduced hepatic de novo lipogenesis and weight loss. The recent phase 3 DEAN (Dapagliflozin Efficacy and Action in NASH) trial36 reported that 53% of patients receiving dapagliflozin showed MASH improvement without worsening of fibrosis, vs 30% with placebo, and 45% showed fibrosis improvement without MASH worsening, vs 20% with placebo.

Currently, AACE and AASLD guidelines recommend considering SGLT-2 inhibitors in patients with type 2 diabetes mellitus and MASLD for their cardiometabolic benefits, but not specifically for treating MASH.1,5 The European guidelines concur, stating that they are safe and beneficial in patients with MASLD with type 2 diabetes mellitus, heart failure, or chronic kidney disease, but are not MASH-targeted therapies.8 However, with the promising results from the DEAN trial,36 updates to these recommendations may be anticipated from national and international organizations.

Vitamin E (d-alpha-tocopherol) is a potent lipidsoluble antioxidant with anti-inflammatory properties. The PIVENS trial34 showed that vitamin E (800 IU/day) significantly improved key histologic features of MASH in adults without diabetes (steatosis, lobular inflammation, and hepatocellular ballooning). It did not, however, show a statistically significant improvement in liver fibrosis stage. Long-term observational studies show that vitamin E use is associated with lower rates of hepatic decompensation and higher transplant-free survival in patients with advanced fibrosis.37

The AASLD and AACE guidelines give grade B recommendations for vitamin E for adults without diabetes who have biopsy-confirmed MASH, based on evidence of histologic improvement.1,5 It is not recommended for individuals with diabetes, MASLD without MASH, or MASH-related cirrhosis. The European guidelines do not recommend it as a targeted therapy for MASH.8

Statins are cornerstone therapies for reducing cardiovascular events. Current guidelines affirm that statins are safe across the MASLD spectrum, including in patients with compensated cirrhosis.5 They not only reduce cardiovascular morbidity and mortality rates but may also confer hepatic benefits. Observational data suggest a protective association between statin use and progression of liver fibrosis, hepatocellular carcinoma, and cirrhotic complications.38,39 Statins are contraindicated only in cases of decompensated cirrhosis and acute liver failure.

Metformin, a biguanide that enhances insulin sensitivity, has been extensively studied as an off-label agent. Mechanistically, it activates adenosine monophosphate–activated protein kinase, which reduces fatty acid synthesis and improves metabolic homeostasis.

While a systematic review of 78 trials found that metformin alone did not significantly improve liver histology compared with placebo, combining it with an SGLT-2 inhibitor or a thiazolidinedione has been associated with MASLD regression in patients with type 2 diabetes.39,40 Furthermore, observational data suggest metformin may improve transplant-free survival and reduce the risk of primary liver and extrahepatic cancers in patients with type 2 diabetes mellitus and MASLD-related advanced fibrosis and cirrhosis. Therefore, metformin should generally be continued in these patients unless contraindicated.

Investigational drugs in late-stage clinical development show promise in both improving fibrosis and resolving disease. These include fibroblast growth factor 21 analogs (pegozafermin and efruxifermin, in phase 3 trials) and lanifibranor, a pan-PPAR agonist, with phase 3 results expected in late 2026.

CHALLENGES IN MANAGEMENT

Public and clinical awareness of MASLD is alarmingly low, with fewer than 5% of individuals with MASLD aware of their condition.10 This low awareness extends to clinicians, leading to underestimation of prevalence and underutilization of effective interventions. Particular problems compound this:

  • MASLD is often asymptomatic or associated with vague symptoms, leading to delayed or missed diagnoses.

  • Distinguishing MASH and assessing fibrosis severity still rely heavily on liver biopsy—the current gold standard. The reliance on invasive liver biopsies as primary end points in clinical trials contributes to high costs and patient burden.

  • The exact mechanisms of development and progression of MASLD and MASH remain unsettled. In particular, development and progression at later stages are not fully elucidated.

  • There is no FDA-approved noninvasive test for MASH fibrosis or for monitoring the response to pharmacotherapy, which makes drug development and application to true disease nonstandard.3

DISCLOSURES

The authors report no relevant financial relationships which, in the context of their contributions, could be perceived as a potential conflict of interest.

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Cleveland Clinic Journal of Medicine

Cleveland Clinic Journal of Medicine

Vol. 93, Issue 9

1 Sep 2026

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    MASLD and MASH: Steatotic liver disease joins the deadly quartet
    • Cleveland Clinic Journal of Medicine
    • September 2026,
    • 93
    • (9)
    • 551-559;
    • DOI: 10.3949/ccjm.93a.25117

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    MASLD and MASH: Steatotic liver disease joins the deadly quartet
    • Cleveland Clinic Journal of Medicine
    • September 2026,
    • 93
    • (9)
    • 551-559;
    • DOI: 10.3949/ccjm.93a.25117

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