Metabolically dysregulated steatotic liver disease (MASLD) affects approximately one-third of the global adult population. This narrative review presents the clinical profile of the contemporary patient with MASLD, focusing on the systemic nature of the disease and risk stratification. MASLD is a systemic metabolic disorder in which hepatic steatosis serves as a marker of insulin resistance, systemic inflammation, and atherogenic dyslipidemia. The leading cause of death in MASLD patients is cardiovascular events, with a two-fold increase in cardiovascular mortality that persists across all fibrosis stages. Disease trajectory is determined by fibrosis stage, comorbid profile (type 2 diabetes, hypertension, dyslipidemia), and phenotype. Three main phenotypes have been identified: classical metabolic (60-70%, dominant cardiovascular risk), lean (15-20%, higher PNPLA3 I148M carriage, faster fibrosis progression, underdiagnosis), and mixed Met-ALD (10–15%, synergistic liver damage from alcohol and metabolic disturbances). Non-invasive fibrosis assessment using FIB-4 followed by elastography is the first step after diagnosis. Patients with fibrosis F3–F4 require aggressive monitoring, including hepatocellular carcinoma screening every 6 months, while patients with F0–F2 require mandatory cardiovascular risk control in primary care. Management priorities differ by phenotype: cardiometabolic control for classical metabolic, fibrosis screening and genetic counseling for lean, and complete alcohol cessation for Met-ALD. Lifestyle modification (weight loss of 5–10%, Mediterranean diet, 150 minutes of physical activity per week) has stronger evidence than any experimental drug. The proposed risk stratification algorithm can be implemented both in primary care and in specialized hepatology centers.
Introduction
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic condition defined by the accumulation of triglycerides in hepatocytes exceeding 5% of liver weight, in the absence of hepatotoxic alcohol consumption (less than 30 g of ethanol per day for men and less than 20 g for women) (Eslam et al., 2020; Lazarus et al., 2024). MASLD is not a single disease but a spectrum of pathological states ranging from reversible steatosis (fat accumulation without inflammation) to non-alcoholic steatohepatitis (NASH), where inflammation and hepatocyte ballooning appear, and further to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) (Younossi et al., 2016). For a long time, clinicians considered MASLD a benign condition that did not require active intervention, but this view has now been revised (Younossi et al., 2018).
According to a 2022 global meta-analysis including over 10 million people from 22 countries, the prevalence of MASLD among adults is 32.4% (Riazi et al., 2022). The highest rates are in the Middle East (38%) and South America (35%), while the lowest rates are in Africa (17%) (Riazi et al., 2022). Recent Russian research has focused on emerging pharmacotherapeutic targets for NAFLD, including novel agents targeting insulin resistance, lipotoxicity, and inflammation (Prikhodko et al., 2022). Over the past 20 years, the incidence of MASLD has more than doubled, and if current trends continue, the number of patients with MASLD-related cirrhosis will increase by 168% by 2030 (Estes et al., 2018). In the Russian Federation, the prevalence of MASLD is estimated at 28–37%, comparable to European data, and MASLD is the most common chronic liver disease in Russia, surpassing viral hepatitis and alcoholic liver disease (Maevskaya et al., 2022). The condition is also affecting younger people: the prevalence of MASLD among children in developed countries reaches 7–8%, and among children with obesity, it reaches 34% (Nobili et al., 2019; Maevskaya et al., 2022).
MASLD is a systemic pathology (Targher et al., 2024). First, the disease has a long asymptomatic course. Early stages show no jaundice, no pain, and no pruritus. The most common complaints are non-specific fatigue and right upper quadrant discomfort, which have no diagnostic value (Amangurbanova et al., 2023). By the time overt clinical signs appear (ascites, variceal bleeding, hepatic encephalopathy), patients typically already have decompensated cirrhosis (Sanyal et al., 2021). Second, the leading cause of death in MASLD patients is not liver complications but cardiovascular events. Prospective cohort studies show that MASLD is associated with a two-fold increase in cardiovascular mortality, a risk that persists across all stages of fibrosis (Zheng et al., 2025). The pathophysiological basis includes insulin resistance, systemic inflammation, and atherogenic dyslipidemia, for which fatty liver serves as a marker (Targher et al., 2024). Third, 20–30% of patients with NASH develop cirrhosis within 10–15 years, and among patients with MASLD-related cirrhosis, the annual risk of HCC is 2–4% (Le et al., 2024). In developed countries, MASLD has become the third leading cause of HCC (Le et al., 2024).
The key clinical challenge is the heterogeneity of patients with MASLD (Younossi et al., 2018). Disease trajectory differs significantly between individuals and is determined by multiple factors: fibrosis stage, comorbid conditions (type 2 diabetes, hypertension, dyslipidemia), genetic polymorphisms (notably PNPLA3 I148M), and alcohol consumption patterns (Eslam et al., 2020; Zheng et al., 2025). Thus, MASLD represents a spectrum of pathological states with different prognoses and management approaches. Figure 1 shows disease progression from reversible steatosis to irreversible stages of fibrosis, cirrhosis, and HCC (Le et al., 2024). The main therapeutic window is in the early stages (steatosis and steatohepatitis without advanced fibrosis), whereas at stages F3–F4, intervention options are substantially limited.
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Figure 1. Progression of MASLD (from steatosis to hepatocellular carcinoma). |
The figure shows disease stages from steatosis to hepatocellular carcinoma (HCC), including the proportion of patients transitioning to each subsequent stage and the time intervals for progression. Solid arrows indicate disease progression, while dashed arrows indicate possible stabilization or regression. Green (steatosis) and yellow (NASH) mark stages with high potential for reversal through lifestyle modification. Orange and red mark stages where regression is unlikely and therapeutic options are largely limited to slowing progression. Dark red (HCC) marks the terminal stage with the poorest prognosis. The time intervals shown are average data from cohorts of patients with NASH and may vary significantly depending on risk factors such as type 2 diabetes, genetic polymorphisms, and alcohol consumption. F1–F4 indicate fibrosis stages according to the Kleiner (METAVIR) scale.
Goal of this work: Based on an analysis of current data, including the new MASLD nomenclature (Metabolic Dysfunction-Associated Steatotic Liver Disease), this work aims to present the clinical profile of the contemporary patient with steatotic liver disease associated with metabolic dysfunction (Abdulrahman et al., 2023; Zigmantavičius et al., 2023; Chakraborty & Rajasekar, 2024; Son & Lee, 2024). The main focus is on the systemic nature of the disease and on patient risk stratification.
Demographic Profile of the Patient and the New Nomenclature
The classic demographic profile of patients with NAFLD, established by population-based studies over the past decade, is now being refined with the introduction of new nomenclature (Guo et al., 2025). The average patient profile is as follows. Age is over 40 years, although patients aged 30–35 years with confirmed steatosis are increasingly seen in clinical practice; the peak incidence occurs in the 50–65 year age group (Younossi et al., 2023). Gender differences are ambiguous: NAFLD is slightly more common in men, but under MASLD criteria, the proportion of women may increase due to metabolic disturbances associated with the postmenopausal period (Shaheen et al., 2021). Body mass index (BMI) typically exceeds 25 kg/m², indicating overweight or obesity. Waist circumference (greater than 94 cm in men and greater than 80 cm in women) indicates abdominal fat distribution, which is most closely associated with insulin resistance (Ross et al., 2020).
A key clinical feature is the existence of the "lean" phenotype. Up to 22% of patients with confirmed steatotic liver disease have a normal BMI (<25 kg/m²) (Danpanichkul et al., 2025). These patients have no visible signs of obesity, but instrumental imaging reveals excessive visceral obesity (Seko et al., 2025). Some data suggest that the risk of fibrosis progression in this patient group is higher than in patients with overt obesity (Ampuero et al., 2024). This is likely explained by a higher frequency of pathogenic genetic variants, most notably PNPLA3 I148M (Boeckmans et al., 2023).
At the end of 2023, the American Association for the Study of Liver Diseases (AASLD) and the European Association for the Study of the Liver (EASL) proposed replacing the term NAFLD with MASLD (Metabolic Dysfunction-Associated Steatotic Liver Disease) (Rinella et al., 2023). This change reflects a shift in diagnostic logic: from a "diagnosis of exclusion" to a "diagnosis of inclusion." MASLD requires the presence of hepatic steatosis plus at least one cardiometabolic risk factor (Kanwal et al., 2024). The alcohol criterion is preserved. For patients with metabolic dysfunction and alcohol consumption above the MASLD threshold (more than 20 g/day for women and 30 g/day for men) but below the threshold for isolated alcoholic liver disease, the category Met-ALD (metabolic dysfunction-associated alcoholic liver disease) has been introduced. This category reflects the synergistic damaging effect of alcohol and metabolic disturbances (Kido et al., 2025). The diagnostic criteria for MASLD are presented in Table 1 (Rinella et al., 2023).
Table 1. Diagnostic criteria for MASLD (Rinella et al., 2023)
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Parameter |
Criterion |
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Mandatory condition |
Presence of hepatic steatosis (confirmed by imaging, biopsy, or biomarkers) |
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Plus, at least one of the five cardiometabolic risk factors |
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1. Anthropometric measures |
BMI ≥25 kg/m² or waist circumference >94 cm (men) / >80 cm (women) |
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2. Glucose metabolism |
Fasting glucose ≥5.6 mmol/L or postprandial glucose ≥7.8 mmol/L or HbA1c ≥5.7% or established type 2 diabetes |
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3. Blood pressure |
≥130/85 mmHg or use of antihypertensive drugs |
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4. Triglycerides |
≥1.7 mmol/L or use of lipid-lowering drugs |
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5. HDL cholesterol |
≤1.0 mmol/L (men) / ≤1.3 mmol/L (women) or use of lipid-lowering drugs |
The shift to MASLD nomenclature has several practical consequences (Kanwal et al., 2024). First, it is no longer necessary to exclude other liver diseases. Combined diagnoses are now possible (e.g., MASLD + chronic hepatitis B). Second, the focus shifts from the liver as an isolated organ to systemic metabolic disturbances. Third, the term “steatotic” is considered less stigmatizing than “fatty” (Rinella et al., 2023).
Criticisms of the new nomenclature exist. One concern is the difficulty of interpreting clinical studies conducted under the old NAFLD label. Another is the possible invalidity of cardiometabolic risk factor thresholds across different racial and ethnic groups (Teng et al., 2023). Nevertheless, the scientific literature of 2024–2025 predominantly uses the term MASLD (Younossi et al., 2025).
Thus, analyzing the profile of the contemporary patient requires abandoning the concept of the “NAFLD patient” as an isolated hepatological case. Instead, we must adopt a model of a patient with metabolic dysfunction, for whom the liver is one of several target organs—and often not the most important one for prognosis (Kanwal et al., 2024).
Comorbid Profile: Associated Diseases as Key to Prognosis
The leading cause of death in patients with MASLD is not liver complications but cardiovascular disease (Zheng et al., 2024; Lim et al., 2025). According to prospective cohort studies and meta-analyses, myocardial infarction and ischemic stroke rank first in the mortality structure of this patient group. Liver cirrhosis and its complications rank second, and hepatocellular carcinoma ranks third (Wong et al., 2023). The gap between cardiovascular and liver mortality persists across all stages of fibrosis, except in decompensated cirrhosis, where liver causes become predominant (Carrieri et al., 2022). This observation has two implications. First, managing a MASLD patient based solely on liver tests and fibrosis stage ignores the main threat to life. Second, comorbid diseases (arterial hypertension, dyslipidemia, type 2 diabetes mellitus (T2DM), and obesity) are key drivers of both liver damage and overall mortality (Grander et al., 2023; Nysather et al., 2023).
The link between MASLD and cardiovascular disease has independent pathophysiological mechanisms beyond shared risk factors (Gao et al., 2025). The fatty liver secretes pro-inflammatory cytokines (C-reactive protein, tumor necrosis factor-alpha, interleukin-6), coagulation factors (plasminogen activator inhibitor-1), and atherogenic lipoproteins (Miller et al., 2025). The resulting systemic inflammatory and procoagulant state damages the vascular endothelium, promotes atherosclerosis, and increases the risk of thrombosis (Byrne & Targher, 2022). In addition, MASLD serves as a marker of severe insulin resistance, which underlies most cardiometabolic disturbances (Hagström et al., 2024). Patients with MASLD have significantly higher rates of coronary artery calcification, increased carotid intima-media thickness, and ventricular arrhythmias (Lee et al., 2024). Importantly, the elevated cardiovascular risk persists after adjusting for traditional risk factors, allowing MASLD to be considered an independent predictor of cardiovascular events (Zhou et al., 2025).
Type 2 diabetes mellitus occupies a special place in the comorbid profile. The prevalence of T2DM among MASLD patients reaches 30–40%, compared to 9–10% in the general population (Ferguson & Finck, 2021). The combination of MASLD and T2DM is associated with a 2.5- to 3-fold higher risk of developing advanced fibrosis (stages F3–F4) compared to patients without diabetes (Genua et al., 2023). Chronic hyperglycemia and insulin resistance enhance lipotoxicity, oxidative stress, and hepatocyte apoptosis, accelerating the transition from steatosis to steatohepatitis and fibrosis (Lee et al., 2022). Conversely, MASLD in a patient with T2DM increases the risk of microvascular (nephropathy, retinopathy) and macrovascular complications. Thus, T2DM and MASLD form a mutually reinforcing combination (Cho et al., 2023).
Arterial hypertension and dyslipidemia are found in 60–80% of patients with MASLD, often in forms resistant to standard therapy (Zisis et al., 2025). The characteristic dyslipidemia profile includes elevated triglycerides, decreased HDL cholesterol, and an increased proportion of small, dense LDL particles—the most atherogenic fraction (Stefan et al., 2025). Statins, often unjustifiably avoided in patients with “liver disease,” are safe in most MASLD patients and may provide additional hepatoprotective effects through anti-inflammatory action (Bharali et al., 2021).
Obstructive sleep apnea (OSA) is a common but underrecognized comorbid condition. In patients with obesity and MASLD, the prevalence of OSA can reach 70% (Bonsignore, 2022). Episodes of nocturnal hypoxia followed by reoxygenation trigger oxidative stress and activate pro-inflammatory pathways in the liver, accelerating fibrosis progression (Ji et al., 2022). Treating OSA with CPAP therapy may slow the progression of liver damage (Parola & Pinzani, 2024).
Chronic kidney disease (CKD) is closely associated with MASLD. Shared pathophysiological mechanisms include endothelial dysfunction, activation of the renin-angiotensin-aldosterone system, and chronic systemic inflammation (Bilson et al., 2024). The risk of developing CKD in MASLD patients is 1.5- to 2-fold higher than in the general population (Yang et al., 2021). In patients with MASLD-related cirrhosis, the rate of estimated glomerular filtration rate decline exceeding 40% reaches 3 events per 100 person-years, necessitating regular monitoring of kidney function (Baratta et al., 2022).
Endocrine comorbidities include hypothyroidism and polycystic ovary syndrome (PCOS). The prevalence of hypothyroidism in MASLD patients is significantly higher than in the general population, especially among women (Mantovani et al., 2024). Hypothyroidism worsens dyslipidemia and slows intrahepatic lipid metabolism. PCOS, characterized by hyperandrogenism and insulin resistance, is associated with a higher prevalence of MASLD in women of reproductive age (Falzarano et al., 2022). Identifying and correcting these conditions is an integral part of managing MASLD patients.
In summary, the comorbid profile of a patient with MASLD is a systemic picture where each accompanying disease is linked to the others (Djeagou et al., 2025). Cardiovascular risks determine overall mortality. T2DM and obesity drive fibrosis progression. OSA, hypothyroidism, and PCOS act as additional modulators requiring special attention. Figure 2 presents the pathogenetic links between MASLD and the main comorbid conditions, illustrating that the fatty liver is an active participant in systemic inflammation and metabolic dysregulation, justifying a multidisciplinary approach.
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Figure 2. Pathogenetic links between MASLD and major comorbid conditions. Abbreviations: CRP, C-reactive protein; IL-6, interleukin-6; TNF-α, tumor necrosis factor-alpha; TG, triglycerides; HDL, high-density lipoprotein; LDL, low-density lipoprotein; T2DM, type 2 diabetes mellitus; HCC, hepatocellular carcinoma. Note: The diagram is not exhaustive and reflects only the most established links. Interactions between individual comorbid conditions (e.g., the effect of T2DM on CKD risk) are not shown to preserve clarity. |
The diagram illustrates the central role of MASLD in generating systemic metabolic and inflammatory disturbances. Solid arrows indicate direct pathophysiological links. Dashed arrows indicate links mediated through intermediate mechanisms. Yellow highlights the central condition (MASLD). Orange highlights key comorbid diseases and pathological processes. Red highlights terminal outcomes.
Prognostic Profile: From Steatosis to Cirrhosis
The disease trajectory of MASLD varies substantially between patients (Lekakis & Papatheodoridis, 2024). In some patients, steatosis does not progress for decades. These individuals are highly likely to die from cardiovascular disease without ever developing clinically significant liver damage (Noureddin & Wong, 2023; Sarkar et al., 2023; Wang, 2024). In other patients, steatosis transforms relatively quickly (within 5–7 years) into non-alcoholic steatohepatitis (NASH), then into fibrosis and cirrhosis (Fang et al., 2024). A third group first comes to attention already at the stage of decompensated cirrhosis (Sanyal et al., 2025). The clinical task is to identify patients at high risk of progression as early as possible.
The most powerful prognostic factor for liver outcomes in MASLD is fibrosis stage (Angulo et al., 2015). It is the degree of replacement of normal liver parenchyma by connective tissue, rather than the severity of steatosis or aminotransferase levels, that determines the risk of liver complications and mortality (Dulai et al., 2017). In a prospective multicenter study by Sanyal et al. (2021) including 1,773 patients with biopsy-proven NAFLD, total mortality was 0.32 per 100 person-years in patients with fibrosis stages F0–F2, with virtually no liver complications (Quek et al., 2023). At stage F3, mortality increased to 0.89 per 100 person-years. At established cirrhosis (stage F4), mortality reached 1.76 per 100 person-years, and the frequency of decompensation and hepatocellular carcinoma (HCC) increased significantly (Quek et al., 2023). Importantly, the rate of cardiovascular events did not differ between fibrosis stages, meaning that elevated cardiovascular risk persists at all stages (Kasper et al., 2021). Figure 3 shows fibrosis stages with corresponding mortality rates and risks of liver complications.
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Figure 3. Stages of liver fibrosis in MASLD and associated risks. Abbreviation: HCC, hepatocellular carcinoma. |
Figure 3 illustrates fibrosis stages according to the METAVIR scale (F0–F4). Each block shows the stage, its characteristics, total mortality (per 100 person-years of follow-up), and the frequency of liver complications. Green highlights stages F0–F2 (low risk of liver complications; mortality is determined primarily by cardiovascular causes). Orange highlights stage F3 (intermediate risk). Red highlights stage F4 (cirrhosis, high risk of decompensation and hepatocellular carcinoma). Arrows indicate the direction of fibrosis progression.
Assessment of fibrosis stage should be the first step after diagnosing MASLD (Pouwels et al., 2022). Liver biopsy, while the reference standard, has limitations for routine screening due to invasiveness, cost, and sampling error (Abdelhameed et al., 2024). Non-invasive methods are used in clinical practice, primarily calculated indices. The FIB-4 index and the NAFLD Fibrosis Score (NFS) have high negative predictive value (Kang et al., 2024). A FIB-4 value below 1.3 reliably excludes advanced fibrosis; such patients can be followed in primary care, with emphasis on controlling cardiometabolic risk factors (Kjaergaard et al., 2023). A FIB-4 value above 2.67 requires elastography or, in doubtful cases, biopsy (Mózes et al., 2022). Vibration-controlled transient elastography (VCTE) and magnetic resonance elastography (MRE) have established optimal cut-off values for diagnosing advanced fibrosis in patients with NAFLD, with high diagnostic accuracy (Chon et al., 2024).
Beyond fibrosis, genetic polymorphisms have prognostic significance (Cherubini et al., 2023). The PNPLA3 I148M variant, carried by up to 40% of European-descent individuals and up to 70% in some Latin American populations, is associated with higher liver fat content, accelerated fibrosis progression, and increased HCC risk (Cherubini et al., 2021). In homozygous carriers, the risk of advanced fibrosis is 2–3 times higher than in wild-type carriers (Hsueh et al., 2022). A young patient with normal BMI and normal liver tests who carries PNPLA3 I148M may have a worse prognosis than an older patient with obesity without this variant (Wang et al., 2026). Genetic testing is not yet routine but may be justified in patients with positive family history or aggressive disease without obvious metabolic risk factors (Cherubini et al., 2023).
Patient age at the time of steatosis diagnosis is also significant (Alqahtani & Schattenberg, 2021). In patients younger than 40–45 years, longer exposure to metabolic disturbances leads to a higher cumulative risk of progression to cirrhosis by age 60–70 years. In patients older than 65 years, newly diagnosed steatosis without aggressive factors (T2DM, high baseline fibrosis) is likely to remain stable. Age influences therapeutic strategy: more aggressive intervention is indicated for younger patients, while older patients require control of cardiometabolic risks (Alqahtani & Schattenberg, 2021).
Fibrosis progression rate is variable (Huang et al., 2023). In patients with NASH, transition by one fibrosis stage takes an average of 7–10 years (Paternostro & Trauner, 2022). However, in patients with T2DM, high histological activity, and genetic predisposition, progression may take 3–5 years, whereas in the absence of these factors, it may take 15–20 years (Huang et al., 2023). This requires individualization of follow-up intervals. Low-risk patients (FIB-4 <1.3, no T2DM, no PNPLA3) should be reassessed every 2–3 years. Intermediate-risk patients (FIB-4 1.3–2.67, T2DM or obesity) should be reassessed annually. High-risk patients (FIB-4 >2.67, confirmed fibrosis F3–F4) should be reassessed every 6 months with mandatory liver ultrasound for HCC screening (Koh et al., 2024).
Although this review focuses on adults, a brief comment on pediatric MASLD is warranted. The prevalence of MASLD among children in developed countries reaches 7–8%, and among children with obesity, it reaches 34% (Nobili et al., 2019). Longitudinal data suggest that pediatric MASLD can progress to advanced fibrosis and cirrhosis by early adulthood, particularly in the presence of type 2 diabetes or PNPLA3 risk alleles (Nobili et al., 2019; Cherubini et al., 2023). However, pharmacotherapy options for children are extremely limited, and lifestyle modification remains the cornerstone of management. Screening strategies for pediatric populations are not yet standardized, representing a critical gap for future research (Nobili et al., 2019).
Synthetic Profile: Patient Phenotypes
Behind the diagnosis of MASLD lies a heterogeneous group of patients (Baratta et al., 2022). However, this heterogeneity can be organized into several recurring phenotypes. Each phenotype has a characteristic disease trajectory, specific risks, and consequently requires different management strategies (Cusi et al., 2025). Identifying phenotypes is a practical tool for patient stratification in the context of limited consultation time (Houttu et al., 2024).
Based on analysis of demographic, comorbid, and genetic data, three main phenotypes have been identified: classical metabolic, lean (genetically driven), and mixed Met-ALD (metabolic dysfunction-associated alcoholic liver disease) (Powell et al., 2021; Israelsen et al., 2024). Their comparative characteristics are presented in Table 2.
Table 2. Comparative characteristics of MASLD phenotypes
|
Feature |
Classical metabolic |
Lean |
Met-ALD |
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Proportion among MASLD |
60–70% |
15–20% |
10–15% |
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BMI |
>30 kg/m² |
<25 kg/m² |
any |
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Fat distribution |
overt abdominal obesity |
visceral (hidden) |
often abdominal |
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Type 2 diabetes |
very common (40–50%) |
rare |
less common than classical |
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Hypertension/dyslipidemia |
very common |
less common |
common |
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PNPLA3 I148M |
population frequency |
significantly higher |
population frequency |
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Alcohol consumption |
none (<30/20 g/day) |
none (<30/20 g/day) |
moderate (30–60/20–40 g/day) |
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Dominant risk |
cardiovascular |
liver (fibrosis, HCC) |
mixed, with an accent on liver damage |
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Management priorities |
BP, lipids, glucose control; weight loss |
fibrosis screening, genetic counseling, visceral fat reduction |
complete alcohol cessation + metabolic control |
Figure 4 shows the estimated distribution of phenotypes in the MASLD patient population (Horn & Tacke, 2024; Zhou et al., 2026). The classical metabolic phenotype is dominant (60–70% of cases). However, the lean phenotype and Met-ALD together account for up to one third of patients and require special attention due to their higher risk of liver outcomes and, in the case of the lean phenotype, systematic underdiagnosis (Zhou et al., 2026).
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Figure 4. Distribution of phenotypes in the MASLD patient population Note: The lean phenotype is characterized by normal body mass index (<25 kg/m²) but the presence of visceral obesity and/or carriage of the pathogenic PNPLA3 I148M variant (Das, et al., 2025). The Met-ALD phenotype requires the presence of metabolic dysfunction and alcohol consumption at doses of 20–30 g/day for women and 30–60 g/day for men (Portincasa et al., 2024). |
The classical metabolic phenotype is the most common. Its key feature is a high frequency of cardiovascular events, which requires priority control of blood pressure, lipids, and glucose (Njei et al., 2024). The lean phenotype is characterized by normal BMI but a higher frequency of PNPLA3 I148M carriage and faster fibrosis progression (Das et al., 2025). These patients often remain undiagnosed due to the absence of overt signs of obesity (Ramandi et al., 2025). The Met-ALD phenotype is distinguished by the synergistic damaging effect of alcohol and metabolic disturbances (Portincasa et al., 2024). These patients have higher aminotransferase levels and a significantly higher risk of fibrosis and HCC than in isolated MASLD, while arterial hypertension and T2DM are less common (Babaei et al., 2023; Kusumawardani et al., 2023; Doddapanen et al., 2024; Joungtrakul & Smith, 2024; Shaji et al., 2024). The absolute priority for this group is complete alcohol cessation (Elmustafa et al., 2025).
The three phenotypes presented do not exhaust the full clinical diversity. Variants with dominant renal comorbidity, severe obstructive sleep apnea as the main driver, or combinations with hypothyroidism or polycystic ovary syndrome are possible (Njei et al., 2024). Nevertheless, identifying the three main phenotypes allows the physician to determine the priority specialty for coordinating patient management: cardiologist (classical metabolic phenotype), hepatologist and geneticist (lean phenotype), or addiction specialist (Met-ALD) (Powell et al., 2021; Elmustafa et al., 2025).
Results and Discussion
The present analysis confirms the initial thesis of heterogeneity within MASLD and the need for a stratified approach (Han et al., 2023). The traditional management model, focused primarily on liver tests and exclusion of alternative etiologies, is being replaced by a model in which comorbidity, genetic factors, and fibrosis stage are assessed together, and therapeutic priorities are determined by the dominant risk—cardiovascular, liver, or mixed (Eslam et al., 2022).
Data from large cohort studies allow us to state that fibrosis stage is the main predictor of liver outcomes. In contrast, cardiovascular outcomes are less dependent on fibrosis stage and are determined primarily by classical risk factors potentiated by MASLD-associated systemic inflammation (Badmus et al., 2023; Quek et al., 2023). This has two practical implications. A patient with MASLD and fibrosis F3–F4 requires aggressive monitoring of liver complications, including screening for hepatocellular carcinoma every 6 months (Koh et al., 2024). However, this does not negate the need for parallel control of blood pressure, lipid profile, and glycemia. A patient with MASLD and fibrosis F0–F2 should not be considered to have a “benign” course in terms of overall mortality. Their cardiovascular risk remains elevated, and it is this risk that will most likely determine the outcome (Kasper et al., 2021).
The introduction of the MASLD nomenclature represents a shift in diagnostic logic from exclusion to inclusion (Rinella et al., 2023; Kanwal et al., 2024). However, this shift raises several controversial issues. First, the threshold values for cardiometabolic factors adopted by the AASLD/EASL consensus are to some extent arbitrary. Their applicability across different racial and ethnic groups requires additional validation (Aboona et al., 2024). For example, the >94 cm waist circumference threshold for men, established for the European population, may be inadequate for individuals of Asian descent (Goedecke et al., 2022). Second, clinical studies conducted under the old NAFLD label now require careful interpretation, as the inclusion criteria may have systematically differed from those of the MASLD criteria (Guo et al., 2025). Third, the Met-ALD category introduces a new diagnostic threshold (20–30 g of ethanol per day), which is consensus-based and lacks a clear pathophysiological rationale (Zeng et al., 2024; Elmustafa et al., 2025).
Up to 22% of patients with confirmed steatotic liver disease have a normal BMI (Danpanichkul et al., 2025). In routine clinical practice, such patients are systematically underdiagnosed because physicians typically do not suspect fatty liver disease in a lean individual with normal or borderline liver tests (Ramandi et al., 2025). This delays diagnosis until the stage of established fibrosis (Zhou et al., 2026). The question of expanding indications for non-invasive fibrosis assessment (e.g., FIB-4 calculation) to all patients with metabolic disturbances regardless of BMI remains open (Sanyal et al., 2023). Several authors have proposed including the lean phenotype as a separate category in screening recommendations, but the evidence base for such recommendations is currently insufficient (Ampuero et al., 2024; Das et al., 2025).
Most of the data cited in this work comes from Western populations (USA, Europe) and Asian cohorts. Extrapolating these data to the Russian population requires caution (Zoncapè et al., 2024). The prevalence of obesity and T2DM in Russia is somewhat lower than in the USA, and the pattern of alcohol consumption has its own characteristics (Maevskaya et al., 2022). Specialized Russian cohort studies on MASLD are limited, underscoring the need for local epidemiological research (Li et al., 2024).
Based on the present analysis, the following algorithm for risk stratification and management of patients with MASLD is proposed (Figure 5). The algorithm includes four sequential steps: phenotype assessment, calculation of the FIB-4 index, elastography (if needed), and therapy selection based on the dominant risk (Bansal et al., 2025; EASL, 2024). The algorithm was developed taking into account the availability of the methods and can be implemented both at the primary care level and in specialized hepatology centers (Mózes et al., 2022).
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Figure 5. Management algorithm for patients with MASLD: risk stratification and patient routing. Abbreviations: BMI, body mass index; BP, blood pressure; HbA1c, glycated hemoglobin; AST, aspartate aminotransferase; ALT, alanine aminotransferase; HCC, hepatocellular carcinoma. Note: In patients with confirmed fibrosis F3–F4 (liver stiffness >12 kPa or FIB-4 >2.67 combined with clinical signs), liver ultrasound for HCC screening is indicated every 6 months, regardless of phenotype (Koh et al., 2024) |
The flowchart presents the sequence of steps from establishing a diagnosis of MASLD to selecting therapy and determining follow-up frequency (Arroyo-Fernández et al., 2023; Mislishayeva et al., 2023; Triantafyllopoulos et al., 2023; Lin & Mukai, 2024; Miranda et al., 2024; Prada et al., 2024). The algorithm includes four steps: (1) phenotype assessment based on anthropometric, laboratory, and anamnestic data; (2) determination of the priority specialty for coordinating management (cardiologist, hepatologist, addiction specialist) depending on phenotype; (3) non-invasive assessment of fibrosis stage using the FIB-4 index and, if necessary, elastography; (4) risk stratification and assignment of appropriate follow-up frequency (Hima et al., 2024; Ganea et al., 2024; Varoneckaitė et al., 2024).
Criteria and threshold values:
• FIB-4 < 1.3 — low risk of advanced fibrosis
• FIB-4 1.3–2.67 — gray zone, elastography required
• FIB-4 > 2.67 — high risk of advanced fibrosis (F3–F4)
• Liver stiffness < 8 kPa — low risk
• Liver stiffness 8–12 kPa — intermediate risk
• Liver stiffness > 12 kPa — high risk (F3–F4)
Limitations of the Work
This work has several limitations. First, it is a narrative review, not a systematic review with formal quality assessment of studies (Silva et al., 2025). Second, we deliberately did not address pharmacotherapy for MASLD (GLP-1 receptor agonists, ACC inhibitors, FXR agonists), as this is beyond the scope of our focus on patient profile and risk stratification (Wang et al., 2021). Third, the proposed phenotypes and algorithm require prospective validation in clinical studies (Wang et al., 2025). Nevertheless, we believe that the proposed model is practically applicable now, as it is based on routine parameters (FIB-4 is calculated from standard laboratory tests, elastography is widely available in regional centers, and phenotype identification requires only thorough history taking and basic examination) (Mózes et al., 2022; Kjaergaard et al., 2023).
Conclusion
Non-alcoholic fatty liver disease in its current conceptualization as MASLD is not an isolated hepatological disease but a systemic metabolic pathology in which the liver serves as one of several target organs. The prevalence of MASLD reaches 32% among adults worldwide. Incidence is steadily increasing, and the age of onset is decreasing. However, the main clinical significance of this disease is determined not so much by liver complications themselves, but by the fact that hepatic steatosis serves as a marker of severe insulin resistance, systemic inflammation, and atherogenic dyslipidemia — conditions that are direct causes of cardiovascular death, which ranks first in the mortality structure of patients with MASLD.
Prognosis in patients with MASLD is determined by the interaction of three groups of factors: fibrosis stage (main predictor of liver outcomes), comorbid profile (type 2 diabetes, arterial hypertension, dyslipidemia determine cardiovascular risk), and phenotype (classical metabolic, lean, or mixed Met-ALD). Ignoring any of these components leads to incomplete risk assessment and, consequently, to inadequate monitoring strategies.
Fibrosis stage should be assessed in every patient with MASLD using non-invasive methods (a two-step approach: calculate FIB-4, then elastography if needed). Patients with fibrosis F3–F4 require aggressive monitoring of liver complications (including HCC screening every 6 months), whereas patients with fibrosis F0–F2 can be followed in primary care but with mandatory control of cardiovascular risks.
Comorbid diseases (T2DM, arterial hypertension, dyslipidemia, obesity, obstructive sleep apnea, hypothyroidism, polycystic ovary syndrome) should be actively identified and treated. Prescribing statins and antihypertensive therapy in patients with MASLD is not only safe but necessary to reduce cardiovascular mortality.
Identifying three phenotypes — classical metabolic, lean (genetically driven), and Met-ALD — allows the physician to determine the priority specialty for coordinating patient management (cardiologist, hepatologist/geneticist, addiction specialist, respectively) and to select targeted therapy: control of cardiometabolic factors in the classical phenotype, aggressive fibrosis screening and genetic counseling in the lean phenotype, and complete alcohol cessation in the Met-ALD phenotype.
Lifestyle modification (weight loss of 5–10% for overweight patients, Mediterranean diet with restriction of fructose and simple sugars, physical activity of at least 150 minutes per week) has a higher level of evidence than any experimental pharmacological agent and should be recommended to all patients with MASLD.
The results of this work identify several areas requiring further study. First, validation of the proposed phenotypes and stratification algorithm is needed in prospective Russian cohorts, taking into account the characteristics of the Russian population (alcohol consumption patterns, prevalence of genetic polymorphisms, availability of diagnostic methods). Second, screening strategies for the lean phenotype of MASLD, which is currently systematically underdiagnosed, require development and clinical testing. Third, studies are needed to evaluate the efficacy and safety of new pharmacological agents in Russian populations, considering the comorbid background. Fourth, the development of Russian clinical guidelines for the management of patients with MASLD, adapted to local epidemiological and resource conditions, is advisable (Osonoi & Takebe, 2024; Zhang et al., 2026).
Contemporary management of a patient with MASLD is not about waiting for an "ideal" pharmacological agent. It is about systematic, consistent work with the patient's metabolic health, based on proper risk stratification and application of proven interventions. Weight loss, control of blood pressure, lipid profile, and glycemia, alcohol cessation, and regular physical activity currently have a higher level of evidence than any experimental therapy. The clinical task is not to limit oneself to documenting hepatic steatosis, but to assess the entire spectrum of metabolic disturbances, refer the patient to appropriate specialists in a timely manner, and not lose sight of the main threat — cardiovascular disease. Behind every liver disease stands a patient with their heart, blood vessels, kidneys, and long-term habits. One must treat the patient, not the organ.
Acknowledgments: The authors would like to thank the medical librarians at North Ossetian State Medical Academy (Vladikavkaz, Republic of North Ossetia-Alania, Russia) for their assistance with the literature search.
Conflict of interest: None
Financial support: None
Ethics statement: As this article is a narrative literature review and does not involve original data collection from human participants or animals, ethical approval was not required. All cited studies were conducted in accordance with their respective ethical standards and the principles of the Declaration of Helsinki.
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