MASLD and viral hepatitis overlap: An emerging dual burden in chronic liver disease

Abstract

The coexistence of metabolic dysfunction-associated steatotic liver disease (MASLD) and viral hepatitis has gained greater focus due to the global increase in chronic liver diseases. This convergence of conditions creates a unique clinical entity characterized by complex molecular interactions, difficult diagnosis, and treatment issues. The frequency of MASLD alongside viral hepatitis is becoming more prevalent. Overlapping pathogenic mechanisms, such as insulin resistance, activation of pro-inflammatory cytokines, hepatic steatosis, and persistent viral infection, establish a synergistic pathophysiological relationship that exacerbates fibrosis and liver damage. Non-invasive fibrosis assessments, multimodal imaging, and, in certain cases, liver biopsies are often required to achieve diagnostic accuracy. This review intends to examine the epidemiological overlap, shared pathophysiological mechanisms, diagnostic hurdles, and management challenges associated with the concurrent manifestation of MASLD and viral hepatitis.

Introduction

Overview of Liver Disease

Liver disease is a significant global health issue, causing nearly two million deaths each year, which accounts for about 4 percent of all global mortality. It is one of the top causes of death worldwide.^[1] Among the chronic liver disorders, chronic viral hepatitis (hepatitis B virus [HBV] and hepatitis C virus [HCV]) and metabolic dysfunction-associated steatotic liver disease (MASLD) are significant. In the past, people viewed viral hepatitis as an infectious disease. They saw MASLD as a liver problem tied to metabolic syndrome. However, it is now clear that both conditions can occur together. Despite the widespread use of HBV vaccines and the availability of effective direct-acting antivirals for HCV, it is still a major cause of morbidity and mortality.^[2] This trend is largely due to increasing rates of obesity, type 2 diabetes, and sedentary lifestyles.^[3]

Chronic Viral Hepatitis

Chronic viral hepatitis is a long-lasting infection caused by the HBV or the HCV. HBV chronically infects an estimated 350 to 400 million individuals globally and stays in liver cells as covalently closed circular DNA (cccDNA). This cccDNA acts as a stable viral template, posing a significant barrier to eradication.^[2,4] HCV affects approximately 58 million people globally.^[5] Both viruses lead to ongoing liver damage that can result in fibrosis, cirrhosis, and liver cancer. HBV infection alone increases the risk of liver-related death by more than three times, with an adjusted hazard ratio of 3.35.^[6] This risk rises more than twelvefold when MASLD is also present, highlighting the importance of early diagnosis and comprehensive management.^[6] In Pakistan, where HBV and HCV rates are moderate and hepatitis A and E are common, poor sanitation and inadequate healthcare systems hinder effective disease control.^[7]

Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)

In 2023, international societies (EASL, AASLD, ALEH, etc.) adopted a new nomenclature, replacing non-alcoholic fatty liver disease (NAFLD) with MASLD. According to the consensus definition, MASLD is diagnosed when there is evidence of hepatic steatosis (by imaging, histology, or non-invasive biomarker), at least one cardiometabolic risk factor (such as obesity or overweight, type 2 diabetes, elevated blood pressure, high triglycerides, or low HDL-cholesterol), and exclusion of harmful alcohol intake above established thresholds. MASLD is embedded under the umbrella term steatotic liver disease (SLD), which also includes related subtypes such as metabolic dysfunction- and alcohol-associated liver disease (MetALD) and cryptogenic steatotic liver disease. By using this definition, most patients previously labeled NAFLD meet criteria for MASLD.^[8,9] It is considered a hepatic manifestation of metabolic syndrome and is closely linked to obesity, insulin resistance, type 2 diabetes, high cholesterol, and high blood pressure. Worldwide, MASLD affects about 29.8 percent of adults in the general population, and prevalence is significantly higher in individuals with metabolic comorbidities—58.5 percent in those with diabetes, 74.1 percent in those with high blood pressure, and 47.4 percent in those who are obese.^[3] The global burden of this disease has nearly doubled in the past thirty years, increasing from 561 million cases in 1990 to 1.24 billion by 2019, and over 80 percent of countries have reported a rise in prevalence.^[10] The disease can range from simple fat accumulation to metabolic dysfunction-associated steatohepatitis (MASH), which may lead to fibrosis, cirrhosis, and liver cancer. At present, no medications have wide regulatory approval for treating MASLD. Lifestyle changes and managing metabolic risk factors remain the main approach to treatment.^[11]

Epidemiological Overlap and Synergistic Burden

Recent studies show that chronic viral hepatitis and MASLD frequently occur together and worsen liver damage.^[2,12] Among 425 inactive chronic hepatitis B (CHB) patients, 47.8% had concurrent MASLD, with 10.5% showing significant fibrosis compared to only 1.4% of those without fat in the liver.^[13] This indicates a much higher risk of cirrhosis when both conditions are present.^[13] Similarly, HCV genotype 3a-infected individuals show steatosis in nearly 48% of cases, associated with higher viral loads, more severe liver inflammation, and faster fibrosis progression.^[14] Mechanically, HBV’s X protein disrupts lipid metabolism, while HCV hinders lipid export. Insulin resistance and fat toxicity in MASLD trigger the release of inflammatory cytokines and activate stellate cells.^[5,15] Clinically, patients with both chronic viral hepatitis and MASLD experience faster scarring, significantly greater risks of cirrhosis and hepatocellular carcinoma, and higher liver-related death rates than those with single infections. This also presents greater challenges in diagnosis and treatment.^[6,16,17]

Regional and Demographic Variations

The prevalence of MASLD and its overlap with chronic viral hepatitis varies significantly across different populations. In Pakistan, MASLD impacts 75 percent of adults with type 2 diabetes. Of these, 22.5 percent progress to MASH. There are clear ethnic differences. Pathans have the highest rates of steatosis at 58.5 percent and NASH at 19.5 percent, compared to Punjabis at 44.5 percent and 10 percent, and Sindhis at 35.3 percent.^[18] These patterns reflect the country’s high metabolic burden, with 26.7 percent of adults having diabetes, and one in four considered obese.^[19] This variation, influenced by genetic, metabolic, and lifestyle factors, emphasizes the need for region-specific screening methods and combined antiviral and metabolic management strategies.^[16,20]

Knowledge Gaps and Rationale

Despite increasing evidence that CHB/HCV and MASLD together accelerate fibrosis, cirrhosis, and liver cancer, most studies still examine these conditions separately. There are significant gaps in understanding how they interact, identifying the best diagnostic methods—especially for non-obese MASLD in CHB—and developing effective combined treatment plans.^[21–23] Additionally, modeling studies indicate that cirrhosis linked to MASLD and liver-related deaths could more than double by 2030, especially in older populations.^[16]

Materials and Methods

A narrative review was conducted to explore the combined impact of MASLD and viral hepatitis in the same patient population. The focus was to illuminate their combined effects on liver pathology, the diagnostic challenges they present, and the management strategies available. The primary objective was to gather and synthesize current evidence from a variety of sources, including pre-clinical studies, clinical trials, systematic reviews, population-based analyses, and established clinical guidelines that pertain to this dual condition. A detailed literature search was done through electronic databases including PubMed, Scopus, ScienceDirect, and Google Scholar using specific keywords like [“MASLD,” “viral hepatitis,” “HCV,” “HBV,” “liver fibrosis,” “coexisting liver diseases,” “hepatocellular carcinoma,” “coexisting pathologies,” “dual etiology”] and Boolean operators [“AND” and “OR”] to refine the results. Additionally, “NAFLD” was also included as a keyword to capture relevant articles published before the 2023 nomenclature change, ensuring a comprehensive review.

Articles published in English from 2015–2023 involving patients having both NAFLD and viral hepatitis and from 2023–2025 having both MASLD and viral hepatitis were included, along with studies emphasizing clinical outcomes, diagnostic challenges, and therapeutic strategies; studies containing human subjects were also focused on. Conversely, studies having animal subjects with insufficient data on dual pathologies, editorials, case reports, studies exploring complications like hepatocellular carcinoma without the context of MASLD or viral hepatitis, and studies exploring liver diseases unrelated to MASLD or viral hepatitis were excluded.

Among the selected literature, particular attention was given to articles detailing the pathological interactions between these diseases, diagnostic methodologies, and the clinical consequences or complications that may arise. Relevant data from these included studies were thoroughly analyzed and categorized based on population characteristics, reported clinical and histological outcomes, diagnostic tools (such as liver biopsy, imaging, and biomarkers), and intervention strategies. All the data were compiled to identify the existing patterns, knowledge gaps, and potential clinical approaches for the management of patients suffering from both etiologies. This review also highlights the importance of future research and the need for updated clinical guidelines for this dual pathology.

Pathophysiological Crossroads in MASLD and Viral Hepatitis Coexistence

Chronic liver disease (CLD) is a serious health concern worldwide. The two primary causes of CLD around the world are viral hepatitis (HBV and HCV) and MASLD.^[24] Typically, viral hepatitis and MASLD have been studied separately, but several studies highlight the collaborative effect of viral hepatitis and MASLD. Higher complication rates and more complicated management of either disease arise when MASLD coexists with HBV or HCV in the same person.^[25]

The “Multiple-Hit” Pathogenesis of MASLD

MASLD includes a range of liver damage, from simple accumulation of fat in liver cells—steatosis—to more advanced forms of the disease, steatohepatitis, which can lead to fibrosis, cirrhosis, end-stage liver disease, and even hepatocellular carcinoma (HCC).^[26] It progresses according to the “multiple-hit” theory:

1. The “first hit” in MASLD is insulin resistance, obesity, type 2 diabetes, and metabolic syndrome. After the initial impact, the liver stores free fatty acids as triglycerides, which eventually results in typical steatosis.

2. “Multi-hits,” such as oxidative stress, inflammatory mediators, apoptosis, and mitochondrial dysfunction, cause disease progression and chronic liver damage (Fig. 1).^[27] The gut microbiota, as well as genetic and epigenetic factors, may also play an essential role; thus, the two-hit hypothesis is insufficient to explain the progression mechanism.^[28]

Figure 1.

Multiple-hit model depicting the interplay of metabolic insults, oxidative stress, and cytokine-mediated injury leading to fibrosis and eventual hepatocellular carcinoma (HCC) in metabolic dysfunction-associated steatotic liver disease (MASLD).

Immune Dysregulation and Inflammatory Pathways in MASLD

Activation of immune cells could exacerbate liver damage and inflammation in MASLD. Both the innate and adaptive immune systems play a significant role. The innate immune system cells include Kupffer cells, monocytes, macrophages, hepatic dendritic cells, neutrophils, and natural killer cells.^[27] In MASLD, innate immunity—particularly macrophages—plays a major role in promoting liver inflammation. MASH is caused by the activation of resident Kupffer cells (KCs) and the recruitment of monocytes, which both produce nitric oxide, ROS, and cytokines like TNF, IL-1β, IL-6, and TGF-β.^[29]

Adaptive immune system cells include CD4+ and CD8+ T cells (Th1, Th17, and regulatory T cells), B cells, and platelets.^[27] Additionally, KCs may stimulate Th17 differentiation by generating IL-23 or IL-6. Parallel to this, pathogen-associated molecular patterns (PAMPs) produced by the intestine activate B cells through TLR4, which can then either transform into plasma cells or be linked with MHC-II and trigger CD4+ T cells to produce interferon (IFN)-γ. In MASH, lipotoxicity can also change the Th17/Treg ratio by decreasing the frequency of intrahepatic CD4+ T cells. When Th17 activates neutrophils, they contribute to the inflammatory response by producing IL-17 and accumulating in the white adipose tissue (WAT), where they encourage lipolysis.^[30] The pathophysiology of MASLD is also influenced by insulin resistance, which is mainly caused by pro-inflammatory cytokines such as TNF-α, IL-1, and IL-6 (Fig. 2).^[31]

Figure 2.

Illustrating distinct immunopathogenic pathways for MASLD and Hepatitis B/C virus and their synergistic contribution to the development and progression of liver fibrosis.

Viral Immune Escape and Immune Exhaustion

Viral hepatitis exacerbates immunological imbalance through immune escape and exhaustion. Immunological imbalance at the Th17/IL-17 axis level plays a significant role in liver fibrogenesis after initial HCV or HBV injury. By recruiting neutrophils and monocytes, and by inducing the expression and production of interleukin-23 and IL-6 in the liver or peripheral cells, the Th17/IL-17 axis drives a chain of events that encourages a proinflammatory and profibrotic environment.^[32] Persistent exposure to viral factors, including hepatitis B and hepatitis C (HCV), causes CD8+ T cells to become functionally fatigued. The overexpression of inhibitory receptors such as PD-1 (programmed cell death protein 1) and/or Tim-3 (T-cell immunoglobulin and mucin domain-containing molecule-3) leads to immune exhaustion and subsequent downregulation of the host response by setting up chronic infection (Fig. 2).^[33,34]

Shared Molecular Mechanisms: Lipid Metabolism Disruption

Both HBV and HCV cause steatosis in MASLD patients by interfering with the liver’s lipid metabolism.

HCV: HCV affects multiple mechanisms of lipid metabolism within hepatocytes. It increases lipid biosynthesis, inhibits mitochondrial oxidation, and consequently lipid degradation. It also lowers the export of apolipoproteins, particularly very low-density lipoproteins (VLDL), leading to significant intracellular lipid accumulation and circulatory hypocholesterolemia and hypolipoproteinemia.^[35]

HBV: Hepatic lipogenesis, oxidative conversion of cholesterol to bile acids, hepatic lipid homeostasis, and therefore hepatic steatosis can all be impacted by the inhibition of peroxisome proliferator-activated receptors (PPARs) and signaling pathways (PI3K/AKT, LXR/SREBP, NF-κβ) by the HBV HBx protein. When the pre-S1 protein attaches to sodium taurocholate co-transporting polypeptide (NTCP), it most likely causes hepatic steatosis and changes in the metabolism of cholesterol. By influencing hepatic lipogenesis and hepatic stellate cells (HSCs) proliferation and survival, a differential expression of IL-13, G-CSF, CCL11, IL-6, and IL-4 may be linked to the development of hepatic steatosis and fibrosis in HBV patients.^[36]

Interplay Between MASLD and HBV/HCV Infection

Effect of MASLD on HBV/HCV Infection

Activation of the TLR4/Myd88 pathway in MASLD prevents HBV replication, and TLR (Toll-like receptors) induction contributes to HSC activation, thereby triggering inflammation-fibrosis-carcinoma (IFC). Palmitic acid, a saturated fatty acid, suppresses HBV-specific immunocytes, leading to insufficient immunological responses, which may be linked to a more severe course of HBV-related illness.^[36] The fatty liver has a sophisticated metabolic network that controls HCV replication. HCV uses lipid droplets for virion assembly and replication. Moreover, after being released from hepatocytes, mature HCVs in circulation are complexed with lipoproteins.^[37]

Effect of HBV/HCV on MASLD

The transcription of HBV DNA involves several transcription factors, such as CEBP, CREB, HNF3, HNF4, FXR, RXR, and PPAR. These transcription factors are involved in the metabolism of hepatic glucose, lipid, bile acid, and xenobiotics, and can either promote or inhibit hepatic cell regeneration, inflammation, fibrosis, and malignant transformation.^[37] As compared to patients with CHC alone, a study found that patients with simultaneous CHC and MASLD characteristics were more likely to have higher degrees of fibrosis.^[38]

Lipotoxicity and Hepatic Immune Modulation

The liver transforms triglycerides and free fatty acids into fatty acyl-CoA, which is subsequently carried to the mitochondria for β-oxidation, producing acetyl-CoA. However, a greater buildup of FFA (free fatty acids) results in:

1. Insufficient hepatic β-oxidation

2. Production of reactive oxygen species

3. Mitochondrial damage and mitophagy

4. Hepatocellular inflammation and oxidative stress^[27]

Reactive oxygen species (ROS) and lipid metabolites stimulate immune system cells, such as Kupffer cells, monocytes, and macrophages, which in turn release pro-inflammatory cytokines, including TNF-α, IL-10, and IL-17. By activating hepatic stellate cells, these cytokines exacerbate hepatic inflammation and promote the development of liver fibrosis.^[33]

Gut-Liver Axis and Systemic Inflammation

According to the recently proposed “intestinal-liver axis” notion, there is a connection between digestive tract disorders and liver illness.^[39] Due to intestinal damage and increased permeability caused by changes in gut microbiota, inflammatory factors (TNF-α, IL-1β, and IL-6) and lipopolysaccharides (LPS) are able to enter the bloodstream and make their way to the liver. Additionally, bile acid metabolism is disrupted by altered gut microbiota, which worsens oxidative stress and hepatic inflammation. This buildup of ROS triggers nuclear factor kappa B (NF-κB) signaling through TLR4, which leads to hepatocyte death and inflammation.^[40]

Clinical Implications of Dual Pathology

Patients with fatty liver who were infected with HBV were more likely to have advanced liver fibrosis, hepatic steatosis, hepatic inflammation, and hepatic ballooning than those with a simple chronic HBV infection. While fatty liver could predict considerable liver inflammation in chronic HBV infection on its own, it was not a risk factor for significant or advanced fibrosis.^[41] In patients with CHB undergoing antiviral therapy with nucleoside analogs (NAs), the coexistence of MASLD may reduce the virological response.^[17]

Diagnostic Challenges

Over the past decade, extensive research has evaluated many diagnostic techniques for staging chronic liver diseases and revealed their pros and cons.^[42]

Diagnostic Confusion / Overlapping Symptoms

In a clinical setting, there are several overlaps between the symptoms of MASLD and viral hepatitis. Despite a vast difference in the pathologic mechanisms of both diseases, patients often present with symptoms like fatigue, abdominal discomfort, icterus, ascites, and pruritus. These similar symptoms pose a challenge in diagnosing and contrasting both diseases.^[43,44] When comparing biomarkers, elevation of AST and ALT is a presentation of both diseases, which is why liver enzymes are not considered a useful diagnostic tool for MASLD in real-life practice.^[43] Moreover, oftentimes patients have advanced histological MASLD but are asymptomatic with normal liver function test (LFT) levels.^[42] In some patients, viral infections and MASLD act as a catalyst for disease progression, working in synergy and hastening the progression towards advanced liver pathologies.^[45,46] Secondly, viral infections may mimic the clinical presentations of MASLD, hindering the process of accurate diagnosis.^[42,47] In some cases, medications designed for MASLD management may interact with antiviral therapies, leading to a potential loss of efficacy and viral pathogenesis, which can lead to more severe consequences.^[45,47]

Imaging and Biomarkers in the Context of Coexisting Pathologies

Non-invasive markers are the first choice in the prediction of the severity of chronic liver diseases. This helps doctors to come up with a plan for treating the patient, such as deciding on aggressive treatments or simple monitoring.^[42] Other diagnostic tools, such as CTs or MRIs, are more sensitive and specific for advanced MASLD, but their main limitation is the fact that these tools cannot differentiate between MASLD and viral hepatitis, and cannot pinpoint the cause of these diseases, especially if they are secondary to some other pathology. CT is also contraindicated in pregnant women due to its harmful radiation.^[42,43,45]

The Role of Liver Biopsy and Non-Invasive Fibrosis Scores / When is the Liver Biopsy Justified?

Now the question arises, which tools are better at diagnosing liver pathologies than others? The answer to that is liver biopsy, which is considered the perfect gold standard test for MASLD. If these tests suggest a high-risk patient, i.e., they may have fibrosis or cirrhosis, then the next plan of action would be to go for a liver biopsy for definitive diagnosis.^[42,45] However, common practice is to use a combination of biomarkers and imaging techniques for accurate diagnosis, whereas liver biopsy is retained only for those patients who are at maximum severity.^[42,48] A liver biopsy accurately tells the staging, disease progression, and extent of the disease. However, it also has some downsides, such as being a very expensive and time-consuming procedure. It also poses a rare but life-threatening risk of complications and is not ideal in patients who are not at high risk.^[49]

Second in the list of better techniques is FibroScan or transient elastography. This technique uses ultrasound waves for diagnosis. With decent sensitivity, specificity, and its non-invasive nature, it is usually recommended.^[42,48,49] However, it is less effective in obese patients, and given that obesity is a risk factor for MASLD or any liver disease, the test often becomes insignificant.^[49] Fibrosis scores such as FIB-4, MASLD Fibrosis Score, and APRI (AST to platelet ratio index) are also proving to be a very useful diagnostic resource for liver diseases.^[50,51] Research shows that the MASLD Fibrosis Score is a validated biomarker, but it seems to perform better in the white population than in Asians, considering its limitations.^[42,50,52]

Treatment Challenges

Managing Antiviral Therapy in Metabolic Context

The management plans for patients with concurrent MASLD and viral infections also pose some serious challenges, as studies have shown that the treatment strategies for CHB may have adverse metabolic interactions with MASLD. For example, the standard treatment regimen for hepatitis B involves antivirals like tenofovir and entecavir. Tenofovir has been associated with kidney dysfunction, hypophosphatemia, and reduced bone mineral density.^[53] While some studies suggest entecavir may be associated with weight gain and glucose metabolism impairment, both of which may indirectly cause metabolic dysfunction.^[54] Similarly, HCV antivirals like ribavirin and interferon worsen insulin resistance.^[55,56] By contrast, direct-acting antivirals are generally associated with minimal adverse effects, but rapid HCV clearance may exacerbate underlying steatosis progression and unmask underlying MASLD.^[57] Moreover, the progression of one disease may impact the treatment of the other and vice versa, leading to unpredictability of the effect.^[25] Studies have stated that the impact of MASLD on antiviral treatments in CHB patients is controversial. Some argue that MASLD has a positive impact by increasing the clearance of HBsAg, while others suggest that MASLD has a negative impact by reducing HBV DNA suppression. While many studies found no clinically relevant association. Hence, close and timely monitoring of HBV DNA and ALT should be done for better intervention.^[58]

Lifestyle and Pharmacological Approaches in Dual Disease

Due to the complexities of management strategies in patients with concurrent MASLD and viral hepatitis, lifestyle modifications remain the best option, with weight loss being the first-line treatment.^[48] Other lifestyle modifications include exercise, cognitive behavioral therapy, and dietary changes such as hypocaloric diets and low fructose intake. Alcohol intake increases the chances of HCC and should be avoided.^[45,59] These lifestyle modifications should be emphasized and closely monitored in patients receiving long-term antiviral treatment. CHB or CHC antiviral therapy has been shown to adversely affect lipid metabolism, potentially aggravating the steatohepatic burden of these patients.^[60,61] As for therapeutic plans, there are no approved drugs for concurrent MASLD and viral hepatitis, but some drugs are given to support metabolic improvements, such as GLP agonists, which have demonstrated favorable effects on liver functional markers, reducing fibrosis, and reducing hepatic fat content in clinical trials,^[62] ezetimibe in reducing liver fat, and metformin for increasing insulin sensitivity.^[59] In addition, many patients with concurrent MASLD and CHB also have other comorbidities such as diabetes, hypertension, or dyslipidemia. Administration of these drugs along with those for liver disease may cause the phenomenon of polypharmacy, raising concerns regarding drug-drug interactions and cumulative hepatotoxicity. This risk should be carefully monitored and minimized in a clinical setting.^[63,64]

Future Targets: Dual-Action Therapeutics and Clinical Trials

Several investigations are currently underway in clinical trial phases, which may show promising results. One such study is the development of a drug named Lanifibranor, a pan-PPAR agonist, which has shown improvements in both MASLD and fibrosis.^[65] Another study is considering pegylated interferon, lamivudine (a reverse transcriptase inhibitor), and entecavir as a combination therapy for the treatment of CHB in MASLD patients. Some clinical trials have also investigated the role of FXR agonists in concurrent liver conditions, with positive outcomes reported. FXR agonists like tropifexor and obeticholic acid are shown to target steatosis, reduce viral replication, and have favorable results.^[66,67] Multiple other studies are also underway, and early data suggest potential benefits in the future (Fig. 3).^[68]

Figure 3.

Comprehensive framework of MASLD and HBV/HCV, illustrating disease evolution, oncogenic potential, and the key diagnostic, therapeutic, and preventive considerations.

Study Gaps and Future Research

Although increasing focus has been placed on the overlap between MASLD and viral hepatitis, some major aspects of the disease interaction are still not fully understood. Firstly, while previous experimental work has shown that HBV can interfere with metabolic pathways inside liver cells, including those related to glucose and amino acids, these findings have mostly been limited to laboratory studies and need further confirmation in human model.^[69] Secondly, some studies based on liver biopsy findings suggest that fatty liver may slow down the progression of fibrosis in HBV-infected individuals, which goes against earlier beliefs.^[21] These gaps highlight the need for well-designed, long-term studies that look at how both conditions interact over time, ideally using combined clinical, molecular, and imaging data. Research efforts should also focus on finding reliable tools for diagnosis and on testing treatment strategies that address both metabolic and viral factors at once.

Conclusion

As the prevalence of liver disease continues to grow globally, it has become increasingly crucial to comprehend the interaction between MASLD and viral hepatitis. These conditions have common underlying mechanisms, such as insulin resistance and the accumulation of fat in the liver, that not only speed up disease progression but also complicate diagnosis and treatment. When these diseases co-occur, the likelihood of severe complications, including liver cancer, rises significantly. Regrettably, existing diagnostic tools and treatments often do not adequately address both conditions simultaneously. There is a clear demand for a more integrated approach that aligns expertise from various fields of care to better assist patients dealing with this intricate overlap.

Conflict of Interest

The authors declare they have no conflicts of interest.

Financial Disclosure

The authors received no financial support for the research, authorship, and/or publication of this article.

Use of AI for Writing Assistance

The authors declare that no artificial intelligence (AI)-assisted technologies were used in the production of this manuscript.

Author Contributions

ME, IS, HA; Design – ME, KK; Supervision – ME; Data Collection and/or Processing – ME, DS; Analysis and/or Interpretation – ME, DS, KK; Literature Search – KK, HA, FY; Writing – ME, DS, IS, HA, FY; Critical Reviews KK, IS, HA, FY.

Peer-review

Externally peer-reviewed.