Published online Mar 7, 2026. doi: 10.3748/wjg.v32.i9.115544
Revised: December 2, 2025
Accepted: January 14, 2026
Published online: March 7, 2026
Processing time: 131 Days and 2.7 Hours
Chronic hepatitis B (CHB) infection is a global public health burden, affecting over 250 million persons globally, and is associated with substantial morbidity and mortality due to cirrhosis, hepatic decompensation, and hepatocellular car
Core Tip: In context of a growing global burden of obesity and diabetes mellitus, metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic syndrome are increasingly observed in patients with chronic hepatitis B (CHB) virus infection. The relationship between hepatic steatosis and/or metabolic syndrome with CHB is complex and remains incompletely defined, although multiple cohort studies reveal an association with liver inflammation, liver fibrosis, hepatitis B virus (HBV)-related liver events such as cirrhosis, liver failure, and liver cancer, as well as biochemical and virologic response to antiviral therapy. Therefore, a dual diagnosis of MASLD and CHB, also termed met-HBV, may have important implications for management. Probable met-HBV can initially be identified on the basis of liver imaging, but a confirmed diagnosis can be established on vibration-controlled transient elastography-based controlled attenuation parameter score or liver biopsy. Patients diagnosed with met-HBV should undergo active management of MASLD and other manifestations of the metabolic syndrome. Future cohort studies and controlled trials are needed to inform evidence-based approaches to management.
- Citation: Bhatti TK, Lim JK. Diagnosis and management of metabolic dysfunction-associated steatohepatitis in patients with chronic hepatitis B infection. World J Gastroenterol 2026; 32(9): 115544
- URL: https://www.wjgnet.com/1007-9327/full/v32/i9/115544.htm
- DOI: https://dx.doi.org/10.3748/wjg.v32.i9.115544
Chronic hepatitis B (CHB) infection affects an estimated 254 million persons globally and is associated with substantial morbidity and mortality due to liver failure and hepatocellular carcinoma (HCC). Although CHB represents the key etiologic factor in the development of clinical liver events, many co-existing modifiable and non-modifiable risk factors may meaningfully contribute to these events, such as age, gender, hepatitis B virus (HBV) genotype, HBV viral load, hepatitis B e antigen (HBeAg) status, family history of HCC, alcohol, and hepatic steatosis. Of these, hepatic steatosis has been increasingly recognized as a potentially important co-factor in liver disease progression and liver cancer among patients with chronic HBV, particularly in context of the growing epidemic of obesity and metabolic syndrome. Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), formerly known as non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis, respectively, are characterized by hepatic steatosis in the absence of other liver disease etiologies or heavy alcohol consumption[1,2], with MASH representing a progressive variant of MASLD associated with histologic necroinflammation, liver cell damage, and fibrosis[1-3]. In contrast with NAFLD[3], a diagnosis of exclusion in patients with hepatic steatosis with no excessive alcohol consumption or competing etiologies, the terms metabolic dysfunction-associated fatty liver disease in 2020[4] and MASLD in 2023[3] represented diagnoses of inclusion, the former requiring at least one of overweight, obesity, or diabetes (and at least two additional metabolic risk factors), and the latter requiring at least one of five cardiometabolic risk factors, as well as exclusion of excessive alcohol intake or competing causes of steatosis.
MASH is increasingly recognized as a leading cause of cirrhosis, indication for liver transplantation, and source of significant financial and health burden in the United States and globally[5,6]. Whereas chronic hepatitis C virus infection has been associated with virally-mediated hepatic steatosis[7], HBV is not associated with de novo hepatic steatosis, but increasing data suggest that the co-existence of MASLD in patients with CHB may have important clinical implications for the natural history and clinical course of liver disease[8-11].
The latest meta-analysis revealed that 38% of individuals globally exhibited MASLD (2016-2019), representing a 50% rise during 1990-2006[5], and current models suggest a future increase in the prevalence of MASLD to 55.4% by 2040[12], particularly in geographies with an anticipated rise in cardiometabolic risk factors [obesity and type 2 diabetes mellitus (T2DM)] such as Asia and the Middle East and Northern Africa region[13-19]. A recent report of Global Burden of Disease data 2010-2021 reveal compelling evidence for the rising worldwide age-standardized rates of prevalence and incidence of MASLD, particularly in countries with varying sociodemographic indices such as China, Sudan, and India[20]. Among patients with chronic HBV, available data suggest that the estimated prevalence of hepatic steatosis is 30%-35%[8-10], including a meta-analysis of 98 studies and 484772 patients in whom hepatic steatosis was 34.9%[10].
Although limited data are available regarding the effect of HBV infection on hepatic steatosis[21,22], MASLD appears to be associated with lower levels of HBV viremia. Emerging data suggest that increasing levels of hepatic steatosis, as measured by controlled attenuation parameter (CAP) score on transient elastography, is associated with progressive fibrosis in patients with chronic HBV, as assessed by liver stiffness measurement (LSM)[23-25], although this relationship may be more significant in those with at minimum moderate to severe hepatic steatosis[26]. The strength of this association varies by study population, but ranges from hazard ratio (HR) of 1.96 (1.25-3.06)[23] to 3.26 (1.28-8.24)[24] to 3.60 (1.21-10.75)[25] and is observed both in patients who are treatment-naïve or on antiviral therapy with oral nucleos(t)ide (NUC) analogues[26]. Studies of patients with CHB who have undergone liver biopsy additionally reveal an association between histologically evident hepatic steatosis with significant liver inflammation and risk for advanced fibrosis[8,27,28].
The rising global prevalence of MASLD[5,29] among patients with CHB have heightened interest on its potential effect on HBV-related outcomes[30-34]. Available data have revealed mixed findings with regard to the relationship between hepatic steatosis, HBV infection, and liver outcomes[35-40].
Whereas the presence of CHB appears to be associated with poorer liver outcomes among patients with metabolic dysfunction-associated fatty liver disease[35], a large cohort study of 6786 patients with CHB revealed that fatty liver was not independently associated with cirrhosis or HCC risk among untreated patients, and was associated with a lower risk of cirrhosis [HR = 0.19, 95% confidence interval (CI): 0.12-0.33] and HCC (HR = 0.21, 95%CI: 0.09-0.51) among patients on antiviral therapy. In contrast, a large cohort study of 11502 patients with CHB with median 5.3 year follow-up revealed that whereas hepatic steatosis was not associated with cirrhosis complications, metabolic dysfunction was associated with an increased risk of cirrhosis [adjusted HR (aHR) = 1.82, 95%CI: 1.40-2.37] and cirrhosis complications (aHR = 1.30, 95%CI: 1.03-1.63), and among metabolic diseases, diabetes mellitus was associated with highest risk for cirrhosis complications (aHR = 2.87, 95%CI: 1.34-6.11)[40], signaling that metabolic syndrome rather than hepatic steatosis alone may represent the clinically important modifiable risk factor for liver events. Table 1 summarizes study evidence which characterize the risk of disease progression in patients with CHB and concurrent MASLD.
| Study population | SLD diagnosis | Viral suppression | Disease progression | Outcomes |
| 1202 CHB patients with or without steatosis[57] | VCTE | Lower median serum HBV DNA levels | Severe steatosis associated with increase severe fibrosis in treatment-naïve and treated patients | Fibrosis progression (increase) |
| 330 treatment-naive patients with CHB[58] | VCTE | HBsAg seroclearance | Persistent severe hepatic steatosis independently associated with fibrosis progression (OR = 2.379) | Fibrosis progression (increase) |
| 606 patients with CHB[62] | VCTE | HBsAg seroclearance | Severe steatosis associated with severe fibrosis in treatment-naive (OR = 3.60) and treated (OR: 1.95-2.79) patients | Fibrosis severity (increase) |
| Meta-analysis: 34 studies with 68268 CHB patients[63] | VCTE/biopsy-proven steatosis | HBsAg seroclearance (OR = 2.22) | Steatosis associated with cirrhosis (OR = 1.52) and HCC (OR = 1.59) | Cirrhosis (increase), HCC (increase) |
| 1089 patients with CHB[59] | Biopsy data | HBsAg seroclearance | Steatohepatitis + CHB more advanced fibrosis and shorter time to liver-related outcomes/death | Fibrosis (increase), outcomes worse |
| 197346 patients with CHB (South Korea NHIS)[64] | MASLD criteria | HBsAg seroclearance | Risk of HCC was 1.4-fold higher in CHB + MASLD | HCC (increase) |
| 11502 patients with CHB[65] | MASLD criteria | Lower HBV DNA levels | MASLD patients had higher risk of cirrhosis | Cirrhosis (increase) |
| 10546 treatment-naive CHB patients[66] | MASLD criteria | Fewer HBeAg positivity, lower HBV DNA levels | Steatosis + metabolic dysfunction increase risk of HCC (aHR 1.40 per dysfunction) | HCC (increase) |
The primary cause of death for persons with CHB is HCC[41], and established risk factors among patients receiving oral NUC therapy include cirrhosis, thrombocytopenia at baseline, male sex, and advanced age[42] and individual risk may be predicted using risk scores such as PAGE-B[43]. Among patients with CHB treated with oral antivirals, MASLD has been identified as an independent risk factor for HCC[44], with increasing evidence supporting a mechanistic link with MASLD/MASH and HCC carcinogenesis which may stem from insulin-resistance associated hepatic steatosis, lipotoxicity, endoplastic reticulum stress, inflammasome activation, and stellate cell activation[45-47]. MASLD also appears to serve as a co-factor in HCC development in more than half of cases in the presence of alternative primary liver disorders[48], which may have unique interaction in context of CHB which is strongly associated with HCC independent of cirrhosis due to HBV integration into the host hepatocyte genome, activation of HCC pathways through changes in genomic instability, p53 gene mutations, tumor suppressor genes, and telomerase reverse transcriptase gene activation[49-52] as well as HBV-mediated immune modulation of negative regulators of HCC such as interleukin-10 and transforming growth factor-β[53-56].
Distinct from the effects of severe hepatic steatosis on liver fibrosis and disease-based outcomes[57], MASLD has been associated with an increased likelihood of spontaneous hepatitis B surface antigen (HBsAg) clearance or functional cure[24,58]. These reports are supported by a meta-analysis comprising 34 studies and 68268 CHB patients which confirmed that hepatic steatosis was independently associated with HBsAg seroclearance (odds ratio = 2.22)[58], thus revealing a paradoxical relationship in context of the opposing effects on liver fibrosis, liver events, and mortality[32,58-63]. Furthermore, hepatic steatosis may adversely affect response to antiviral therapy with oral NUC analogues with poorer biochemical [alanine aminotransferase (ALT) normalization] and virologic response (suppression of HBV DNA, pregenomic RNA, quantitative HBsAg, and HBeAg loss/seroconversion)[64-66], as well as poorer improvement in liver stiffness score despite viral decline[67]. Real-world observational studies additionally reveal that diabetes mellitus and metabolic syndrome are also associated with poorer virologic response to oral NUC analogues[68].
Limited data addressing the impact of treatment of MASLD and other manifestations of the metabolic syndrome on HBV-related outcomes are presently available. Multiple studies have confirmed an association between diabetes mellitus and metabolic syndrome with an increased risk of HBV-related liver outcomes such as cirrhosis, HCC, and liver-related death[69-72]. However, prospective data to confirm benefit of treatment of diabetes, metabolic syndrome, or MASLD on HBV outcomes are lacking. One study has reported improvement in steatohepatitis with weight loss intervention in patients with CHB[73].
Future studies examining the impact of weight loss pharmacotherapy [e.g., glucagon-like peptide-1 receptor agonist (GLP1RA)], liver-directed MASH pharmacotherapy (e.g., resmetirom), and other anti-glycemic, lipid lowering, and antihypertensive treatment on HBV-related outcomes are needed. Despite limited evidence, due to the overlapping cardiometabolic risk profile of patients with CHB and hepatic steatosis, and the potential implications on liver outcomes, it is prudent to screen for metabolic syndrome and MASLD in this subpopulation, and consider individualized management of metabolic conditions if identified. Furthermore, this information may influence approach to HBV treatment. As per updated 2024 HBV guidelines of the World Health Organization (WHO)[74], antiviral therapy is recommended for HBsAg positive patients with MASLD or metabolic syndrome, independent of HBV DNA, serum ALT, or liver fibrosis stage.
Screening for concurrent MASLD and metabolic syndrome can be incorporated into standard workflows in the management of patients with CHB, including examination (body mass index, waist circumference, blood pressure), assessment of alcohol intake, laboratory testing (fasting glucose or glycosylated hemoglobin, lipid panel), and liver imaging with ultrasound, computed tomography, or magnetic resonance imaging (MRI), which are routinely performed in context of liver cancer surveillance. The presence of cardiometabolic risk factors should signal increased risk for concurrent MASLD and prompt further investigation.
Radiologic features consistent with hepatic steatosis (e.g., increased echogenicity) may identify patients with “probable met-HBV”. Vibration-controlled transient elastography (VCTE) is commonly used for fibrosis staging in CHB but additionally provides liver fat content assessment with CAP scoring. In a patient with CHB, the presence of at least one cardiometabolic risk factor plus clinically significant hepatic steatosis, based either on histologic grade 1 steatosis or greater (grade 1: 5%-33%, grade 2: 34%-66%, grade 3: > 66%), MRI-proton density fat fraction score ≥ 6.5% (grade 1: 6.5%-17.4%, grade 2: 17.5%-22.0%, grade 3: 22.1% or greater) or CAP score ≥ 238 dB/m (S1: 238-252 dB/m, S2: 253-282 dB/m, S3: 283 dB/m or greater), effectively rules in a diagnosis of “confirmed met-HBV”. Concurrent evidence of hepatic inflammation based on elevated liver transaminases, particularly in context of inactive or NUC-controlled CHB (e.g., HBV DNA < 2000 IU/mL) and absence of other precipitants (e.g., hepatotoxic medications, alcohol), effectively signals concurrent MASLD as the likely etiology.
As fibrosis staging is used as a criterion for HBV treatment eligibility in practice guidelines, attribution of key drivers of fibrosis development (concurrent MASLD vs CHB) directly impacts clinical decisions. All patients with CHB and suspected MASLD should undergo initial routine risk stratification with fibrosis-4 (FIB-4), with a score < 1.3 signaling low risk for advanced liver fibrosis. Among individuals with FIB-4 > 1.3, further risk stratification should be pursued with non-invasive tests (NITs) using serum fibrosis assays [e.g., enhanced liver fibrosis (ELF), Fibrotest, Fibrosure, Hepascore] and/or imaging-based elastography (e.g., VCTE, shear wave elastography, magnetic resonance elastography). Dual or sequential NITs combining elastography with serum fibrosis assays (e.g. Fibrotest, ELF) is preferred over a single NIT approach to corroborate fibrosis estimates, recognizing that established cut-offs for F2 fibrosis and cirrhosis were derived from patients with MASLD or CHB alone, and therefore modified cut-offs may be needed for patients with met-HBV[75]. Until additional data are available to inform evidence-based thresholds specific to met-HBV, we suggest the use of the established thresholds of LSM ≥ 8.0 kPa, ELF score ≥ 7.7, or equivalent to rule in F2 fibrosis or greater to identify potential candidates for MASLD pharmacotherapy. Furthermore, liver biopsy should be considered if there is significant discordance in these estimates and/or there remains uncertainty regarding primary drivers of liver injury and fibrosis.
Patients who are determined to have probable or confirmed met-HBV should be counseled regarding the potential implications of this dual liver diagnosis, and advised to pursue a holistic approach to improving liver health, including: (1) Lifestyle modification with diet and exercise as per practice guidelines for MASLD alone; (2) Individualized approach to medical, pharmacologic, endoscopic, or surgical weight loss based on presence of severe obesity and/or overall cardiometabolic risk profile; (3) Restriction of alcohol consumption for patients with elevated liver enzymes or significant fibrosis (F2 or greater), or elimination for patients with cirrhosis; (4) Restriction of potentially hepatotoxic medications or supplements; (5) Targeted treatment of relevant components of the metabolic syndrome (e.g., diabetes mellitus, hypertension, dyslipidemia) to reduce the risk for major adverse cardiovascular events; (6) Individualized approach to liver-directed treatment for MASH and F2-F3 fibrosis with resmetirom and/or semaglutide, particularly in patients with inactive or NUC-controlled CHB and evidence of significant liver inflammation and/or fibrosis; and (7) Individualized consideration for oral NUC therapy of HBV independent of other eligibility criteria, in accordance with 2024 WHO HBV guidelines. The WHO advises that the presence of comorbidities such as T2DM or MASLD should prompt consideration for antiviral therapy, due to the association between T2DM and MASLD on liver fibrosis progression and risk for HCC[76]. In lean non-diabetic patients diagnosed with met-HBV, consideration should be given for screening of other genetic and metabolic liver diseases associated with hepatic steatosis (e.g., Wilson’s disease, alpha-1 anti-trypsin deficiency).
Given limited data specific to this population, the management of patients undergoing liver-directed therapy for MASH in context of met-HBV with the two Food and Drug Administration-approved agents, oral thyroid hormone beta-receptor agonist resmetirom and/or the oral glucagon-like receptor-1 agonist semaglutide, should follow standard American Association for the Study of Liver Diseases guidance for patients with MASH alone, including regular monitoring of liver enzymes every 3-6 months and periodic assessments of CAP score and LSM on VCTE every 6-12 months[77,78]. Although patients with CHB were excluded in the phase 3 trials supporting regulatory approval, resmetirom and semaglutide may considered in the treatment of patients with met-HBV and F2-F3 fibrosis in the absence of independent drug-drug interactions or contraindications. Longitudinal assessment is needed in real-world studies to confirm safety, tolerability, and treatment response, and inform long-term management approach in this population. Among patients who are determined to have evidence of cirrhosis based on clinical markers, NITs, and/or liver biopsy, liver-directed MASLD treatment is not currently recommended, but these patients should be treated with oral NUC therapy and undergo routine cirrhosis management including HCC surveillance twice per year and assessment for clinically significant portal hypertension based on Baveno criteria and/or endoscopic evaluation for gastroesophageal varices. Finally, clinicians should incorporate a multidisciplinary patient-centered approach to management, including coordination of care between primary care, endocrinology, cardiology, and gastrointestinal/hepatology clinicians, and using shared decision making which prioritizes patient preference, and consideration of the impact of met-HBV and its treatment on health-related quality of life, patient-reported outcomes, and adherence to treatment. Figure 1 summarizes a suggested clinical algorithm for initial evaluation and management.
Metabolic syndrome and MASLD are common among patients with CHB, and may have important implications on virologic and other clinical outcomes. The complex interplay between metabolic syndrome, MASLD with or without steatohepatitis, and CHB remain incompletely understood and require further investigation to characterize the bidirectional effects and response to metabolic intervention. Available data are mixed but suggest that MASLD may contribute to an increased risk for liver events in patients with CHB, including cirrhosis, hepatic decompensation, and HCC. Adequately powered prospective cohort studies and controlled trials are needed to support evidence-based recommendations for evaluation and management. These studies should be supported by refined case definitions for met-HBV which account for the presence and severity of MASLD/MASH and other manifestations of the metabolic syndrome, and intersection with alcohol and other sources of hepatic steatosis. Validation studies in patients with met-HBV to derive modified cut-offs for risk stratification using NITs, including serum indices (e.g., FIB-4), serum assays (e.g., ELF), and liver elastography, ideally using liver histology and/or clinical outcome endpoints, would further support decisions regarding treatment initiation and longitudinal assessment of response. In the absence of available evidence, clinicians should consider routine assessment of risk factors for MASLD and metabolic syndrome, limited screening with labs and imaging, VCTE if available, and an individualized approach to metabolic interventions with lifestyle modification and/or pharmacotherapy. Finally, as the presence of HBV is exclusionary for enrollment in therapeutic trials for MASH, real-world observational cohort studies are needed to characterize the effects of GLP1RA, metabolic therapies targeting diabetes, hypertension, and dyslipidemia, and both current and future liver-directed MASH therapies on HBV-specific and overall liver outcomes. Such data will be necessary to inform evidence-based recommendations in future management guidelines.
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