I. Introduction
Steatotic liver disease (SLD) encompasses a spectrum of liver conditions characterized by the accumulation of triglycerides in hepatocytes. Among these, metabolic dysfunction-associated steatotic liver disease (MASLD) has recently emerged as the most prevalent chronic liver disease worldwide, largely driven by the rising prevalence of obesity and metabolic dysfunction1. The global prevalence of MASLD is currently estimated at approximately 38% among adults2. In South Korea, our previous analysis revealed an increasing trend, with MASLD affecting over 40% of adult men and more than 20% of adult women3.
In 2023, the term nonalcoholic fatty liver disease (NAFLD) was officially replaced by MASLD4. This nomenclature change reflects a paradigm shift in understanding the disease, which is no longer defined merely by the absence of alcohol intake, but rather recognized as a liver condition fundamentally linked to metabolic dysfunction5. The updated terminology underscores the central role of metabolic dysfunction-involving obesity, insulin resistance, dyslipidemia, and/or hypertension-in the pathogenesis and progression of MASLD6.
The clinical importance of MASLD lies in its impact both intrahepatically and extrahepatically. Within the liver, MASLD can progress from simple steatosis (termed MASL) to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma (HCC)7. Among these stages, the development of MASH is particularly critical, as it substantially increases the risk of liver-related mortality8. Beyond the liver, MASLD is strongly associated with an increased risk of cardiovascular disease, chronic kidney disease, and endocrine disorders, reflecting its systemic nature9. Notably, cardiovascular complications are the leading cause of death in patients with MASLD, far surpassing liver-related mortality10.
Given this evolving clinical landscape, Korean medicine practitioners must recognize MASLD as a major health concern11. This case report aims to illustrate the clinical spectrum of MASLD by comparing two patients-one with MASL and the other with MASH-from both intrahepatic and extrahepatic perspectives. The authors hope this report will assist Korean medicine physicians in distinguishing between clinical phenotypes and underscore the importance of personalized diagnostic and therapeutic strategies tailored to each patient’s metabolic and hepatic profile.
II. Report of the Cases
1. Medical history and characteristics
The first case involves a 51-year-old man with a body mass index (BMI) of 29.9. He reported no subjective symptoms such as fatigue, headache, or dyspepsia, except for mild right knee pain. He had been gradually gaining weight since graduating from high school, with a more rapid increase of 20 kg over the past decade, primarily due to frequent consumption of instant foods and late-night snacks He was unaware of his weight gain and did not engage in regular physical activity. He had never been prescribed medications for any component of metabolic syndrome, despite presenting with a systolic blood pressure of 160 mmHg and diastolic pressure of 91 mmHg on the day of hospital visit. He denied alcohol or tobacco use and had no notable family history of chronic disease.
The second case concerns a 54-year-old man with a BMI of 35.1, indicating severe obesity. He had been obese since adolescence but gained an additional 8 kg over the past two years after transitioning to a sedentary, high-stress office job. He had been taking medications for hypertension and hyperlipidemia for four years and experienced chronic fatigue and lethargy. He did not drink alcohol but had a history of heavy smoking (1.5 packs per day) until quitting two months prior to presentation. He did not engage in regular physical activity. His father had a history of cardiovascular disease and hypertension. This case report has been approved by IRB of Daejeon University Hospital (# DJDSKH-25-E-06-20).
2. Laboratory findings
Laboratory testing revealed contrasting hepatic enzyme profiles between the two patients. The first patient showed normal aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels (13 IU/L and 16 IU/L, respectively), whereas the second patient exhibited elevated levels of both enzymes (80 ΠU/L each for AST and ALT). Both patients had borderline HbA1c levels (6.0% and 5.8%) and exhibited significant insulin resistance, with homeostatic model assessment for insulin resistance (HOMA-IR) scores of 4.0 and 8.2, respectively. Interestingly, the first patient demonstrated a notably higher level of high-sensitivity C-reactive protein (hs-CRP, 4.3 mg/L) compared to the second patient (1.0 mg/L) (Fig. 1C).
Fig. 1
Comparative summary of key clinical parameters in two patients with MASLD.
The upper panel presents FibroScan-based assessments of hepatic steatosis and fibrosis in the two patients. Steatosis is quantified by the controlled attenuation parameter (CAP, dB/m), and fibrosis by liver stiffness measurement (LSM, kPa) (Panels A and B). The lower panel summarizes key metabolic dysfunction-associated parameters, including blood chemistry, insulin resistance, and inflammatory markers (Panel C).
3. Assessment of fatty liver and fibrotic change
Transient elastography (FibroScan) was used to assess hepatic steatosis and fibrosis via the controlled attenuation parameter (CAP) and liver stiffness measurement (LSM). The first patient showed severe hepatic steatosis (CAP 336 dB/m) without evidence of fibrosis (LSM 3.4 kPa). In contrast, the second patient had both severe steatosis (CAP 393 dB/m) and advanced hepatic fibrosis (LSM 13.4 kPa)(Fig. 1A). Based on these results, the first patient was diagnosed with MASL, while the second patient was classified as having MASH with hepatic fibrosis (Fig. 1A and B).
III. Discussion
These two cases illustrate the clinical heterogeneity of MASLD and underscore the necessity for a dual-perspective evaluation-addressing both intrahepatic and extrahepatic risks-for effective risk stratification and management.
The first patient, a 51-year-old man, exhibited simple steatosis (MASL) with no biochemical or imaging evidence of inflammation or fibrosis (AST/ALT within normal range, LSM 3.4 kPa). However, he had several significant cardiometabolic risk factors, including hypertension (160/91 mmHg), borderline HbA1c (6.0%), insulin resistance (HOMA-IR 4.02), and markedly elevated hs-CRP (4.3 mg/L). Despite the minimal hepatic damage, his systemic inflammatory burden and untreated metabolic syndrome placed him at high cardiovascular risk (Fig. 1C). The second patient, a 54-year-old man, met the diagnostic criteria for MASH due to markedly elevated liver enzymes (AST/ALT 80 IU/L) and advanced liver stiffness (LSM 13.4 kPa). While he had severe steatosis (CAP 393), his extrahepatic metabolic parameters were relatively well-managed through ongoing treatment for hypertension and dyslipidemia. His hs-CRP level remained within normal limits (1.0 mg/L) (Fig. 1C). Therefore, while the second patient had a greater hepatic disease burden, his cardiovascular risk was better addressed. These two patients exemplify distinct phenotypes within the MASLD spectrum-one dominated by hepatic complications (e.g., fibrosis, cirrhosis), and the other by systemic metabolic and cardiovascular threats (e.g., atherosclerosis, myocardial infarction).
Such diverse clinical phenotypes and health-related risks mandate a comprehensive, individualized approach to the assessment and management of individuals with MASLD12. Progression from MASLD to MASH, characterized by hepatic inflammation, is a key determinant of the development of cirrhosis and hepatocellular carcinoma (HCC), which are linked to liver-related mortality13. Although serum aminotransferases (AST and ALT) are traditionally used to assess liver damage, they correlate poorly with histologic severity in MASLD. Many patients with advanced steatohepatitis or fibrosis maintain normal or mildly elevated enzyme levels. Additionally, these enzymes are acutely responsive to lifestyle changes, such as weight loss, fasting, or alcohol abstinence, and may thus mask ongoing disease progression14.
In contrast, liver fibrosis reflects a chronic and cumulative response to metabolic liver injury. A meta-analysis by Dulai et al. identified fibrosis stage as the strongest independent predictor of both liver-related and all-cause mortality in MASLD, with hazard ratios increasing from F1 to F4 (HR up to 6.40 for cirrhosis)15. Therefore, fibrosis assessment—not transaminase levels or the degree of steatosis—should be the cornerstone for prognostication and clinical decision-making in MASLD. FibroScan offers a reliable, noninvasive method for assessing both steatosis (via CAP) and fibrosis (via LSM), with reported sensitivity and specificity of 85% and 90%, which is superior to abdominal ultrasound or blood biomarkers in stratifying hepatic risk16. In the second case, significant fibrosis was detected despite relatively modest metabolic parameters, reaffirming the necessity of direct fibrosis evaluation (Fig. 1B).
While MASLD originates in the liver, its most fatal consequences are cardiovascular. Large-scale cohort studies reveal that cardiovascular disease accounts for nearly 38% of MASLD-related deaths, compared to only 4.8% due to liver disease17. This highlights the need to evaluate and manage systemic inflammation, insulin resistance, blood pressure, and lipid profiles in these patients. Among extrahepatic markers, hs-CRP can serve as a predictor of future cardiovascular events, although its interpretability is limited by susceptibility to fluctuation from acute inflammation or tissue injury18. The first patient had significantly elevated hs-CRP (4.3 mg/L) and LDL-cholesterol (187 mg/dL), compared to normal levels in the second patient (1.0 mg/L and 87 mg/dL, respectively) (Fig. 1C). A large cohort study showed that combined elevation of hs-CRP (≥3.0 mg/L) and LDL-C (≥130 mg/dL) is associated with a 1.5-fold increased risk for ischemic heart disease and stroke19. Thus, even in the absence of fibrosis (Fig. 1A), the first patient clearly requires aggressive cardiovascular risk management, including treatment for hypertension, dyslipidemia, and insulin resistance. Of cause, we have to notice
These contrasting cases illustrate the complexity of MASLD and emphasize the need to move beyond a liver-centric paradigm to a comprehensive, patient-centered approach. Normal liver enzymes or absence of symptoms should not result in clinical complacency. Instead, objective assessments, such as the stage of fibrosis and biomarkers (e.g., HOMA-IR, hs-CRP), must be incorporated into the routine evaluation of MASLD patients.
IV. Conclusion
This case report provides Korean medicine practitioners with a clinical framework for distinguishing between MASLD patients at risk of hepatic disease progression and those with predominant cardiovascular risk. Such differentiation is essential for establishing integrative treatment strategies-including personalized diagnosis, preventive counseling, and interventions ranging from herbal prescriptions to nutritional and lifestyle modifications.
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