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Hepatitis A virus (HAV) is a spherical, non-enveloped, linear-positive single-stranded RNA virus that belongs to the Picornaviridae family. The virus attacks the liver, which leads to inflammation and the onset of jaundice. It represents a disease of the pediatric population and, in most cases, it causes an acute self-limited illness, but rarely a fulminant condition. HAV spreads from person to person through the fecal-oral route and ingestion of contaminated food or drink. It is highly endemic in large geographical areas of the world, including the Indian subcontinent, where most of the population is exposed to the virus in childhood. Most of the viral infections at this age cause asymptomatic disease that provides lifelong protection against HAV. However, our recent study showed an increased incidence of HAV infection in the adult population. This signifies a change in the pattern of age-specific seroprevalence of antibodies for hepatitis A and a huge number of non-immune susceptible individuals. Molecular epidemiological studies define various aspects of viral infection and transmission. Sequence characterization based on the VP1/P2A junction region confirmed IIIA and IA as the predominant genotypes circulating in the Indian subcontinent. The duration of the viremia is dependent on the host, and viral genotypes have no role in the severity of the disease. A mutational study confirmed the lack of genetic variations among Indian strains. Due to the high endemicity of this disease in the Indian subcontinent, vaccination is not recommended. However, individuals who are susceptible and seronegative for HAV-IgG should be targeted for vaccination. It will be a rational and cost-effective approach.
Hepatitis A virus (HAV) is a spherical, non-enveloped, linear-positive single-stranded RNA virus that belongs to the Picornaviridae family. The virus attacks the liver, which leads to inflammation and the onset of jaundice. It represents a disease of the pediatric population and, in most cases, it causes an acute self-limited illness, but rarely a fulminant condition. HAV spreads from person to person through the fecal-oral route and ingestion of contaminated food or drink. It is highly endemic in large geographical areas of the world, including the Indian subcontinent, where most of the population is exposed to the virus in childhood. Most of the viral infections at this age cause asymptomatic disease that provides lifelong protection against HAV. However, our recent study showed an increased incidence of HAV infection in the adult population. This signifies a change in the pattern of age-specific seroprevalence of antibodies for hepatitis A and a huge number of non-immune susceptible individuals. Molecular epidemiological studies define various aspects of viral infection and transmission. Sequence characterization based on the VP1/P2A junction region confirmed IIIA and IA as the predominant genotypes circulating in the Indian subcontinent. The duration of the viremia is dependent on the host, and viral genotypes have no role in the severity of the disease. A mutational study confirmed the lack of genetic variations among Indian strains. Due to the high endemicity of this disease in the Indian subcontinent, vaccination is not recommended. However, individuals who are susceptible and seronegative for HAV-IgG should be targeted for vaccination. It will be a rational and cost-effective approach.
DOI: https://doi.org/10.37349/edd.2025.100593
This article belongs to the special issue Viral Hepatitis
This article evaluates contemporary and evolving surgical techniques in diverticulitis management. A comprehensive literature search was conducted using PubMed on guidelines for articles on surgical interventions for diverticulitis. The relevant data were extracted and synthesized to identify trends, advancements, and gaps in the current understanding of surgical interventions for diverticulitis. Many patients with uncomplicated diverticulitis can achieve favourable outcomes through conservative management strategies. Surgical interventions are increasingly tailored based on individual risk profiles and disease severity. Recent methods for managing diverticulitis highlight the significance of personalized treatment, which can lead to faster recovery times and better overall quality of life. More patients are now considered appropriate candidates for primary anastomosis, with or without a stoma in place of Hartmann’s procedure, where reversal is often tricky. Additionally, minimally invasive surgical techniques are being employed more frequently.
This article evaluates contemporary and evolving surgical techniques in diverticulitis management. A comprehensive literature search was conducted using PubMed on guidelines for articles on surgical interventions for diverticulitis. The relevant data were extracted and synthesized to identify trends, advancements, and gaps in the current understanding of surgical interventions for diverticulitis. Many patients with uncomplicated diverticulitis can achieve favourable outcomes through conservative management strategies. Surgical interventions are increasingly tailored based on individual risk profiles and disease severity. Recent methods for managing diverticulitis highlight the significance of personalized treatment, which can lead to faster recovery times and better overall quality of life. More patients are now considered appropriate candidates for primary anastomosis, with or without a stoma in place of Hartmann’s procedure, where reversal is often tricky. Additionally, minimally invasive surgical techniques are being employed more frequently.
DOI: https://doi.org/10.37349/edd.2025.100592
This article belongs to the special issue Diverticulitis: Pathomechanism, Diagnosis and Treatment
Aim:
The current state of the problem of stomach and duodenal diseases presupposes a mandatory examination of patients for the presence of Helicobacter pylori infection. Highly specific and sensitive diagnostic methods are known and applied, however, the problem of removal from clinical laboratories, isolation, including during a pandemic, dictates the search for new solutions.
Methods:
Mobile diagnostic solutions based on portable devices with highly sensitive quartz piezoelectric sensors were investigated using a variety of devices (1–8 sensor elements) and data processing algorithms.
Results:
A three-year volunteer monitoring study demonstrated that sensor arrays are informative for exhaled air and volatile skin compound analysis, enabling both point diagnostics and long-term tracking.
Conclusions:
The study demonstrates the significant potential of sensor libraries in non-invasive diagnostics, particularly through the innovative application of facial skin projection for volatile marker detection. Three diagnostic approaches have been presented for assessing stomach and esophageal conditions via non-invasive monitoring of exhaled air composition and volatile skin compounds. The authors’ extensive experience in breath urease testing for both adults and children enabled purposeful modifications of diagnostic devices and data processing algorithms. A three-year volunteer monitoring study during anti-Helicobacter therapy and dietary interventions revealed high stability and informativeness of the urease test utilizing chemical sensor arrays. Notably, this research represents the first demonstration of facial organ projection as a method for stomach condition assessment and volatile molecule monitoring without sample collection, showcasing promising prospects for future diagnostic applications.
Aim:
The current state of the problem of stomach and duodenal diseases presupposes a mandatory examination of patients for the presence of Helicobacter pylori infection. Highly specific and sensitive diagnostic methods are known and applied, however, the problem of removal from clinical laboratories, isolation, including during a pandemic, dictates the search for new solutions.
Methods:
Mobile diagnostic solutions based on portable devices with highly sensitive quartz piezoelectric sensors were investigated using a variety of devices (1–8 sensor elements) and data processing algorithms.
Results:
A three-year volunteer monitoring study demonstrated that sensor arrays are informative for exhaled air and volatile skin compound analysis, enabling both point diagnostics and long-term tracking.
Conclusions:
The study demonstrates the significant potential of sensor libraries in non-invasive diagnostics, particularly through the innovative application of facial skin projection for volatile marker detection. Three diagnostic approaches have been presented for assessing stomach and esophageal conditions via non-invasive monitoring of exhaled air composition and volatile skin compounds. The authors’ extensive experience in breath urease testing for both adults and children enabled purposeful modifications of diagnostic devices and data processing algorithms. A three-year volunteer monitoring study during anti-Helicobacter therapy and dietary interventions revealed high stability and informativeness of the urease test utilizing chemical sensor arrays. Notably, this research represents the first demonstration of facial organ projection as a method for stomach condition assessment and volatile molecule monitoring without sample collection, showcasing promising prospects for future diagnostic applications.
DOI: https://doi.org/10.37349/edd.2025.100591
This article belongs to the special issue Helicobacter Pylori and Infection: Genomics, Diagnosis, Pathogenesis, Antibiotic Resistance, Microbiota, Cancer, Prevention and Therapeutics
Peroxisome proliferator-activated receptors (PPARs) comprise three isoforms: PPARα, PPARβ/δ, and PPARγ, which regulate the expression of genes involved in fatty acid uptake, β-oxidation, adipogenesis, gluconeogenesis, and insulin sensitivity. Type 2 diabetes (T2D), often accompanied by other features of metabolic syndrome, contributes to vasculopathy, end-stage organ failure, and cancer. Metabolic dysfunction-associated steatotic liver disease (MASLD) refers to steatotic liver disease in the presence of cardiometabolic risk factor(s) and without excessive alcohol consumption. MASLD is prevalent among adults with T2D and carries a high risk of liver fibrosis, metabolic dysfunction-associated steatohepatitis (MASH), cirrhosis and incident T2D. In MASLD, the liver becomes a hub of lipid toxicity, oxidative stress, and fibrotic signalling whenever T2D disrupts hormonal and adipokine signalling, increases free fatty acid flux, and promotes chronic inflammation. MASLD, therefore, results from an impairment of the protection physiologically offered by PPARs through fatty acid oxidation, lipid storage in the adipose tissue, and mitigation of insulin resistance and pro-inflammatory cascades. By examining the molecular mechanisms of PPARα, PPARβ/δ, and PPARγ, as well as their interactions with cofactors like PGC-1α, and their crosstalk with pathways like sterol regulatory element-binding protein (SREBP), NF-κB, AMP-activated protein kinase (AMPK), and adipokines, researchers and clinicians can better understand how T2D-related MASLD can be prevented or treated. Single PPAR agonists, such as fibrates and glitazones, have limited clinical efficacy in achieving hard liver histology endpoints like MASH resolution and fibrosis regression in humans. However, the Pan-PPAR agonist Lanifibranor at the highest doses shows promise in ameliorating these outcomes in subjects with non-cirrhotic MASH. This suggests that activating all three PPAR isoforms together enhances their therapeutic effects on various cells and target organs, restoring insulin resistance, improving gluco-lipidic homeostasis, while inhibiting pro-inflammatory and pro-fibrogenic pathways. Analysis of unresolved issues should dictate the research agenda.
Peroxisome proliferator-activated receptors (PPARs) comprise three isoforms: PPARα, PPARβ/δ, and PPARγ, which regulate the expression of genes involved in fatty acid uptake, β-oxidation, adipogenesis, gluconeogenesis, and insulin sensitivity. Type 2 diabetes (T2D), often accompanied by other features of metabolic syndrome, contributes to vasculopathy, end-stage organ failure, and cancer. Metabolic dysfunction-associated steatotic liver disease (MASLD) refers to steatotic liver disease in the presence of cardiometabolic risk factor(s) and without excessive alcohol consumption. MASLD is prevalent among adults with T2D and carries a high risk of liver fibrosis, metabolic dysfunction-associated steatohepatitis (MASH), cirrhosis and incident T2D. In MASLD, the liver becomes a hub of lipid toxicity, oxidative stress, and fibrotic signalling whenever T2D disrupts hormonal and adipokine signalling, increases free fatty acid flux, and promotes chronic inflammation. MASLD, therefore, results from an impairment of the protection physiologically offered by PPARs through fatty acid oxidation, lipid storage in the adipose tissue, and mitigation of insulin resistance and pro-inflammatory cascades. By examining the molecular mechanisms of PPARα, PPARβ/δ, and PPARγ, as well as their interactions with cofactors like PGC-1α, and their crosstalk with pathways like sterol regulatory element-binding protein (SREBP), NF-κB, AMP-activated protein kinase (AMPK), and adipokines, researchers and clinicians can better understand how T2D-related MASLD can be prevented or treated. Single PPAR agonists, such as fibrates and glitazones, have limited clinical efficacy in achieving hard liver histology endpoints like MASH resolution and fibrosis regression in humans. However, the Pan-PPAR agonist Lanifibranor at the highest doses shows promise in ameliorating these outcomes in subjects with non-cirrhotic MASH. This suggests that activating all three PPAR isoforms together enhances their therapeutic effects on various cells and target organs, restoring insulin resistance, improving gluco-lipidic homeostasis, while inhibiting pro-inflammatory and pro-fibrogenic pathways. Analysis of unresolved issues should dictate the research agenda.
DOI: https://doi.org/10.37349/edd.2025.100590
This article belongs to the special issue Nuclear Receptors and the Digestive Tract: from Molecular Physiology to Clinics via Pharmacology
Amyloidosis is a rare disease, corresponding to a deposition of proteins in various tissues. Amyloid light-chain (AL) amyloidosis can involve the liver in 17% to 45% of patients. Diagnosis of liver disease is based on specific criteria, coupling alkaline phosphatases and hepatomegaly. Liver stiffness is altered in cases of heart involvement, and overall, in cases of liver involvement. Liver biopsy is generally avoided due to an important bleeding risk. Treatment is essentially based on stem cell transplantation and chemotherapy, with large progress during the last decade. Liver involvement recovery is generally diagnosed with a reduction in alkaline phosphatases and in liver size.
Amyloidosis is a rare disease, corresponding to a deposition of proteins in various tissues. Amyloid light-chain (AL) amyloidosis can involve the liver in 17% to 45% of patients. Diagnosis of liver disease is based on specific criteria, coupling alkaline phosphatases and hepatomegaly. Liver stiffness is altered in cases of heart involvement, and overall, in cases of liver involvement. Liver biopsy is generally avoided due to an important bleeding risk. Treatment is essentially based on stem cell transplantation and chemotherapy, with large progress during the last decade. Liver involvement recovery is generally diagnosed with a reduction in alkaline phosphatases and in liver size.
DOI: https://doi.org/10.37349/edd.2025.100589
Hepatocellular carcinoma (HCC) ranks as the sixth most diagnosed cancer and the third most common cancer-related death globally. The underlying precise molecular mechanisms for its progression remain poorly understood. Interestingly, approximately 90% of HCC-related deaths are not due to the primary tumor itself but rather to its difficult-to-treat metastatic spread. Despite sorafenib being the first-line therapy for HCC, challenges such as drug resistance, frequent recurrence, and metastasis contribute to poor prognosis. In this context, alternative therapeutic strategies are urgently needed. A broad spectrum of phytochemicals, including polyphenolic derivatives, flavonoids, carotenoids, alkaloids, terpenes, lignans, and saponins, has shown considerable promise as potential anti-cancer agents, both in vitro and in vivo. These natural plant-derived compounds exhibit distinct and overlapping mechanisms of action, characterized by their antioxidant, anti-inflammatory, and anti-cancer properties, offering a novel approach to HCC treatment. An extensive literature search was conducted from 2010 to 2024 using reputable electronic databases such as MEDLINE, Embase, Google Scholar, Science Direct, and other reliable sources using different keywords, including HCC, medicinal plants in HCC, HCC metastasis, and mechanism of action of medicinal plants in HCC, among others. This comprehensive review aims to summarize the potential role of plant-based bioactive components in combating HCC through various cellular mechanisms, highlighting their therapeutic potential in the management of both primary and metastatic disease.
Hepatocellular carcinoma (HCC) ranks as the sixth most diagnosed cancer and the third most common cancer-related death globally. The underlying precise molecular mechanisms for its progression remain poorly understood. Interestingly, approximately 90% of HCC-related deaths are not due to the primary tumor itself but rather to its difficult-to-treat metastatic spread. Despite sorafenib being the first-line therapy for HCC, challenges such as drug resistance, frequent recurrence, and metastasis contribute to poor prognosis. In this context, alternative therapeutic strategies are urgently needed. A broad spectrum of phytochemicals, including polyphenolic derivatives, flavonoids, carotenoids, alkaloids, terpenes, lignans, and saponins, has shown considerable promise as potential anti-cancer agents, both in vitro and in vivo. These natural plant-derived compounds exhibit distinct and overlapping mechanisms of action, characterized by their antioxidant, anti-inflammatory, and anti-cancer properties, offering a novel approach to HCC treatment. An extensive literature search was conducted from 2010 to 2024 using reputable electronic databases such as MEDLINE, Embase, Google Scholar, Science Direct, and other reliable sources using different keywords, including HCC, medicinal plants in HCC, HCC metastasis, and mechanism of action of medicinal plants in HCC, among others. This comprehensive review aims to summarize the potential role of plant-based bioactive components in combating HCC through various cellular mechanisms, highlighting their therapeutic potential in the management of both primary and metastatic disease.
DOI: https://doi.org/10.37349/edd.2025.100588
Brazil ranks second globally in absolute liver transplants and leads pediatric transplantation in Latin America. This scoping review aims to map the results and perspectives of pediatric liver transplantation in Brazil from 2000 to 2022. A scoping review was conducted following the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews Checklist (PRISMA-ScR) guidelines, using PubMed, Virtual Health Library (VHL), and ScienceDirect. From 293 records, 26 studies were included based on predefined criteria. The review focused on clinical indications, techniques, outcomes, and regional disparities. Results: Of the 26 included studies, 10 (38%) reported survival rates, showing 1-, 5-, and 10-year survival of 89.3%, 78.1%, and 68.5% for deceased donors and 93.1%, 85.7%, and 67.5% for living donors, respectively. Eleven studies (42%) discussed living donor liver transplantation (LDLT), which accounts for 53.4% of pediatric transplants. Eight studies (31%) detailed postoperative complications, such as vascular (up to 19%) and biliary (15.7%) issues, rejection (~ 50%), and infections. The COVID-19 pandemic led to a 20.6% reduction in transplant activity and increased waiting list mortality from 8.4% to 11.9%. Despite Brazil’s leadership in pediatric liver transplants, challenges persist, including donor shortages, diagnostic delays, geographic concentration in São Paulo (66%), and limited data systematization. These factors hinder equitable access and optimal outcomes across the country. To improve pediatric liver transplantation in Brazil, actions are needed to strengthen donor registration systems, decentralize services, enhance team training, and adopt techniques like split liver transplantation. Expanding national databases and prognostic tools will help address disparities and improve care.
Brazil ranks second globally in absolute liver transplants and leads pediatric transplantation in Latin America. This scoping review aims to map the results and perspectives of pediatric liver transplantation in Brazil from 2000 to 2022. A scoping review was conducted following the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews Checklist (PRISMA-ScR) guidelines, using PubMed, Virtual Health Library (VHL), and ScienceDirect. From 293 records, 26 studies were included based on predefined criteria. The review focused on clinical indications, techniques, outcomes, and regional disparities. Results: Of the 26 included studies, 10 (38%) reported survival rates, showing 1-, 5-, and 10-year survival of 89.3%, 78.1%, and 68.5% for deceased donors and 93.1%, 85.7%, and 67.5% for living donors, respectively. Eleven studies (42%) discussed living donor liver transplantation (LDLT), which accounts for 53.4% of pediatric transplants. Eight studies (31%) detailed postoperative complications, such as vascular (up to 19%) and biliary (15.7%) issues, rejection (~ 50%), and infections. The COVID-19 pandemic led to a 20.6% reduction in transplant activity and increased waiting list mortality from 8.4% to 11.9%. Despite Brazil’s leadership in pediatric liver transplants, challenges persist, including donor shortages, diagnostic delays, geographic concentration in São Paulo (66%), and limited data systematization. These factors hinder equitable access and optimal outcomes across the country. To improve pediatric liver transplantation in Brazil, actions are needed to strengthen donor registration systems, decentralize services, enhance team training, and adopt techniques like split liver transplantation. Expanding national databases and prognostic tools will help address disparities and improve care.
DOI: https://doi.org/10.37349/edd.2025.100587
Here, the history of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis nomenclatures is summarized. Metabolic dysfunction-associated fatty liver disease (MAFLD) was coined in 2020, and metabolic dysfunction-associated steatotic liver disease (MASLD) was proposed in 2023. With this backset, the present article aims at reviewing the similarities and differences between MAFLD and MASLD through a systematic analysis of published comparative studies. MAFLD and MASLD have a complex disease spectrum comprising, further to all-cause mortality, hepatic (fibrosis, cirrhosis, and primary liver cancer) and extrahepatic outcomes (major adverse cardiovascular events, chronic kidney disease, extrahepatic cancers, type 2 diabetes, and vascular dementia). Comparative studies document that—due to its superior ability to identify liver fibrosis—MAFLD better captures mortality owing to all-causes, hepatic and extrahepatic outcomes, which are strongly associated with the severity of liver fibrosis. Moreover, MASLD is inappropriate in pediatric care, lacks specificity, tends to overdiagnosis, does not consider coexistent viral hepatitis or lean subjects, and amplifies disease heterogeneity. Collectively, the evidence presented in this narrative review supports an urgent need for the development of evidence-based guideline statements. This novel developmental process should involve not only a systematic review of the evidence, with equal contribution from all the world’s regions of stakeholders and clinical panelists, but also should use quantitative data to identify an objective-level consensus to guarantee wide adoption of the process outcomes.
Here, the history of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis nomenclatures is summarized. Metabolic dysfunction-associated fatty liver disease (MAFLD) was coined in 2020, and metabolic dysfunction-associated steatotic liver disease (MASLD) was proposed in 2023. With this backset, the present article aims at reviewing the similarities and differences between MAFLD and MASLD through a systematic analysis of published comparative studies. MAFLD and MASLD have a complex disease spectrum comprising, further to all-cause mortality, hepatic (fibrosis, cirrhosis, and primary liver cancer) and extrahepatic outcomes (major adverse cardiovascular events, chronic kidney disease, extrahepatic cancers, type 2 diabetes, and vascular dementia). Comparative studies document that—due to its superior ability to identify liver fibrosis—MAFLD better captures mortality owing to all-causes, hepatic and extrahepatic outcomes, which are strongly associated with the severity of liver fibrosis. Moreover, MASLD is inappropriate in pediatric care, lacks specificity, tends to overdiagnosis, does not consider coexistent viral hepatitis or lean subjects, and amplifies disease heterogeneity. Collectively, the evidence presented in this narrative review supports an urgent need for the development of evidence-based guideline statements. This novel developmental process should involve not only a systematic review of the evidence, with equal contribution from all the world’s regions of stakeholders and clinical panelists, but also should use quantitative data to identify an objective-level consensus to guarantee wide adoption of the process outcomes.
DOI: https://doi.org/10.37349/edd.2025.100586
This article addresses the current understanding of the bidirectional relationship between iron metabolism and the gut microbiota. Both iron deficiency and iron overload in the gut can negatively affect the composition and function of the intestinal microbiota. Conversely, beneficial members of the colonic microbiota play a key role in enhancing systemic iron absorption. Particular attention is given to the potential use of microbiota-modulating agents for the correction of colonic dysbiosis as part of a comprehensive therapeutic approach to iron deficiency/overload conditions. Therefore, these interventions, by supporting microbiota restoration and reduction of intestinal inflammation, may also offer novel therapeutic avenues for disorders of iron metabolism.
This article addresses the current understanding of the bidirectional relationship between iron metabolism and the gut microbiota. Both iron deficiency and iron overload in the gut can negatively affect the composition and function of the intestinal microbiota. Conversely, beneficial members of the colonic microbiota play a key role in enhancing systemic iron absorption. Particular attention is given to the potential use of microbiota-modulating agents for the correction of colonic dysbiosis as part of a comprehensive therapeutic approach to iron deficiency/overload conditions. Therefore, these interventions, by supporting microbiota restoration and reduction of intestinal inflammation, may also offer novel therapeutic avenues for disorders of iron metabolism.
DOI: https://doi.org/10.37349/edd.2025.100585
This article belongs to the special issue Gut Microbiota towards Personalized Medicine in Metabolic Disease
Celiac disease is an immune-mediated disorder with significant metabolic implications. Several factors have been proposed to explain the association between celiac disease in patients following a gluten-free diet and metabolic disorders, including metabolic syndrome. Growing evidence suggests a pivotal role of gut microbiome dysbiosis in the onset of celiac disease and its associated metabolic disturbances. The present narrative review examines (i) the connections between celiac disease and metabolism-related comorbidities, including metabolic syndrome and metabolic dysfunction-associated steatotic liver disease; (ii) the role of the gut microbiome in celiac disease, including the outcomes of gut microbiome dysbiosis in celiac children and adults; and (iii) the potential of microbial therapeutic strategies within the context of personalized medicine for patients with celiac disease and comorbid metabolic conditions. A synthesis of existing studies highlights several protective factors and interventions for future celiac disease prevention research. Adopting plant-based, health-promoting dietary patterns such as the Mediterranean or vegetarian diet within the first two years of life reduces celiac disease risk. These fiber- and phytochemical-rich diets support beneficial gut microbiota growth and short-chain fatty acid production, which maintain intestinal barrier integrity by enhancing mucus and tight junction proteins. Short-chain fatty acids also modulate immunity by inducing Tregs that secrete IL-10, suppressing pro-inflammatory Th1 responses and autoantibody production. Precision probiotics offer diverse therapeutic benefits in celiac disease by reducing inflammation, restoring beneficial microbes, and degrading immunogenic gliadin peptides. Postbiotics complement these effects by reinforcing barrier integrity and counteracting gliadin-induced inflammation. Thus, integrating clinical models with microbial biomarkers promises to improve celiac disease diagnosis and monitoring, enabling better risk stratification, earlier detection, and personalized management of this heterogeneous disease.
Celiac disease is an immune-mediated disorder with significant metabolic implications. Several factors have been proposed to explain the association between celiac disease in patients following a gluten-free diet and metabolic disorders, including metabolic syndrome. Growing evidence suggests a pivotal role of gut microbiome dysbiosis in the onset of celiac disease and its associated metabolic disturbances. The present narrative review examines (i) the connections between celiac disease and metabolism-related comorbidities, including metabolic syndrome and metabolic dysfunction-associated steatotic liver disease; (ii) the role of the gut microbiome in celiac disease, including the outcomes of gut microbiome dysbiosis in celiac children and adults; and (iii) the potential of microbial therapeutic strategies within the context of personalized medicine for patients with celiac disease and comorbid metabolic conditions. A synthesis of existing studies highlights several protective factors and interventions for future celiac disease prevention research. Adopting plant-based, health-promoting dietary patterns such as the Mediterranean or vegetarian diet within the first two years of life reduces celiac disease risk. These fiber- and phytochemical-rich diets support beneficial gut microbiota growth and short-chain fatty acid production, which maintain intestinal barrier integrity by enhancing mucus and tight junction proteins. Short-chain fatty acids also modulate immunity by inducing Tregs that secrete IL-10, suppressing pro-inflammatory Th1 responses and autoantibody production. Precision probiotics offer diverse therapeutic benefits in celiac disease by reducing inflammation, restoring beneficial microbes, and degrading immunogenic gliadin peptides. Postbiotics complement these effects by reinforcing barrier integrity and counteracting gliadin-induced inflammation. Thus, integrating clinical models with microbial biomarkers promises to improve celiac disease diagnosis and monitoring, enabling better risk stratification, earlier detection, and personalized management of this heterogeneous disease.
DOI: https://doi.org/10.37349/edd.2025.100584
This article belongs to the special issue Gut Microbiota towards Personalized Medicine in Metabolic Disease
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease worldwide. Its prevalence is increasing due to its close relationship with obesity, insulin resistance, and other metabolic disorders. In this context, the gut-liver axis has been identified as a fundamental regulator in the progression of MASLD, integrating metabolic, immunological, and inflammatory signals that influence hepatic homeostasis. This article reviews the interconnection between the intestine and the liver in the onset and progression of MASLD, highlighting the roles of cholesterol and its metabolism, intestinal barrier permeability, microbiota, and hepatic signaling pathways. We analyze how intestinal dysbiosis and alterations in the enterohepatic circulation of bile acids affect cholesterol absorption and metabolism. Furthermore, we address the influence of endotoxin translocation, activation of the innate immune system, and the interaction of key transcription factors on disease progression from steatosis to advanced fibrosis and hepatocellular carcinoma (HCC). Finally, therapeutic strategies, including pharmacological, dietary, and immunomodulation-based approaches, are discussed to regulate cholesterol metabolism, modulate the intestinal microbiota, and restore gut-liver axis homeostasis. Integrating this knowledge could open new perspectives for treating and preventing MASLD, addressing the disease from a broader and multidisciplinary viewpoint.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease worldwide. Its prevalence is increasing due to its close relationship with obesity, insulin resistance, and other metabolic disorders. In this context, the gut-liver axis has been identified as a fundamental regulator in the progression of MASLD, integrating metabolic, immunological, and inflammatory signals that influence hepatic homeostasis. This article reviews the interconnection between the intestine and the liver in the onset and progression of MASLD, highlighting the roles of cholesterol and its metabolism, intestinal barrier permeability, microbiota, and hepatic signaling pathways. We analyze how intestinal dysbiosis and alterations in the enterohepatic circulation of bile acids affect cholesterol absorption and metabolism. Furthermore, we address the influence of endotoxin translocation, activation of the innate immune system, and the interaction of key transcription factors on disease progression from steatosis to advanced fibrosis and hepatocellular carcinoma (HCC). Finally, therapeutic strategies, including pharmacological, dietary, and immunomodulation-based approaches, are discussed to regulate cholesterol metabolism, modulate the intestinal microbiota, and restore gut-liver axis homeostasis. Integrating this knowledge could open new perspectives for treating and preventing MASLD, addressing the disease from a broader and multidisciplinary viewpoint.
DOI: https://doi.org/10.37349/edd.2025.100583
This article belongs to the special issue The Role of Gut Microbiota in the Pathogenesis and Management of Metabolic-Associated Steatotic Liver Disease (MASLD)
Minimal hepatic encephalopathy (MHE) is often the least recognized form of hepatic encephalopathy, affecting up to 80% of people living with liver cirrhosis. While the signs can be quite subtle, MHE can seriously disrupt cognitive functions such as attention and memory. This disruption can impact daily life, potentially leading to an increased risk of accidents. Unfortunately, many health care providers might overlook the diagnosis because the symptoms can be vague, and identifying MHE usually requires specific tests like the psychometric hepatic encephalopathy score (PHES). Several factors contribute to MHE, including elevated ammonia levels, systemic inflammation, and issues with the gut-brain connection. It’s crucial to identify and treat MHE quickly, as it can progress to overt hepatic encephalopathy (OHE), which presents much more severe symptoms and is associated with higher mortality rates. Current treatment approaches often include medications like lactulose and rifaximin, along with cognitive rehabilitation and dietary changes. Emerging treatments that focus on gut health, such as probiotics, are showing potential in helping to lower ammonia levels. This review brings together the latest research on MHE, pointing out significant gaps in how we diagnose it and the potential of new therapies like synbiotics. By looking at recent multicenter studies, we aim to offer practical insights that could help prevent the progression to OHE, ultimately improving patient outcomes.
Minimal hepatic encephalopathy (MHE) is often the least recognized form of hepatic encephalopathy, affecting up to 80% of people living with liver cirrhosis. While the signs can be quite subtle, MHE can seriously disrupt cognitive functions such as attention and memory. This disruption can impact daily life, potentially leading to an increased risk of accidents. Unfortunately, many health care providers might overlook the diagnosis because the symptoms can be vague, and identifying MHE usually requires specific tests like the psychometric hepatic encephalopathy score (PHES). Several factors contribute to MHE, including elevated ammonia levels, systemic inflammation, and issues with the gut-brain connection. It’s crucial to identify and treat MHE quickly, as it can progress to overt hepatic encephalopathy (OHE), which presents much more severe symptoms and is associated with higher mortality rates. Current treatment approaches often include medications like lactulose and rifaximin, along with cognitive rehabilitation and dietary changes. Emerging treatments that focus on gut health, such as probiotics, are showing potential in helping to lower ammonia levels. This review brings together the latest research on MHE, pointing out significant gaps in how we diagnose it and the potential of new therapies like synbiotics. By looking at recent multicenter studies, we aim to offer practical insights that could help prevent the progression to OHE, ultimately improving patient outcomes.
DOI: https://doi.org/10.37349/edd.2025.100582
Aim:
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a widespread chronic liver condition associated with liver inflammation, fibrosis, and various metabolic disorders. Although cholic acid (CA), a primary bile acid (BA), is known to reduce steatosis when added to a high-fat diet, it may exacerbate hepatocellular injury by promoting oxidative stress and inflammation. Therefore, regulating BA-induced liver toxicity is crucial. Dimethyl fumarate (DMF) is an FDA-approved drug known to activate the nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2), a transcription factor that induces cytoprotective genes involved in cellular stress. The present study aimed to investigate whether DMF supplementation could attenuate CA-induced liver injury in high-fat diet-fed mice.
Methods:
To induce liver injury, high-fat diet with and without CA were compared for liver damage and liver fat gain. Following the establishment of the toxic but antisteatotic effect of CA, C57BL/6j mice were fed a high-fat diet supplemented with 0.5% CA (HFDCA) with or without DMF (0.3 mg/mL or 0.6 mg/mL), which was administered via drinking water for 7 weeks.
Results:
CA was found to be an accelerator of high-fat diet to induce liver damage, but prevented liver fat accumulation. HFDCA mice showed signs of liver damage, including elevated liver enzymes and liver enlargement. However, DMF treatment activated the Nrf2 pathway and partially mitigated the hepatotoxic effect of CA/high-fat diet, although some doses exhibited pro-oxidant effects.
Conclusions:
The findings suggest that DMF, as an activator of Nrf2, has potential as a therapeutic agent for liver diseases related to high-fat diets and BA-induced injury, though careful dosage management is crucial to maximize its benefits and mitigate BA toxicity.
Aim:
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a widespread chronic liver condition associated with liver inflammation, fibrosis, and various metabolic disorders. Although cholic acid (CA), a primary bile acid (BA), is known to reduce steatosis when added to a high-fat diet, it may exacerbate hepatocellular injury by promoting oxidative stress and inflammation. Therefore, regulating BA-induced liver toxicity is crucial. Dimethyl fumarate (DMF) is an FDA-approved drug known to activate the nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2), a transcription factor that induces cytoprotective genes involved in cellular stress. The present study aimed to investigate whether DMF supplementation could attenuate CA-induced liver injury in high-fat diet-fed mice.
Methods:
To induce liver injury, high-fat diet with and without CA were compared for liver damage and liver fat gain. Following the establishment of the toxic but antisteatotic effect of CA, C57BL/6j mice were fed a high-fat diet supplemented with 0.5% CA (HFDCA) with or without DMF (0.3 mg/mL or 0.6 mg/mL), which was administered via drinking water for 7 weeks.
Results:
CA was found to be an accelerator of high-fat diet to induce liver damage, but prevented liver fat accumulation. HFDCA mice showed signs of liver damage, including elevated liver enzymes and liver enlargement. However, DMF treatment activated the Nrf2 pathway and partially mitigated the hepatotoxic effect of CA/high-fat diet, although some doses exhibited pro-oxidant effects.
Conclusions:
The findings suggest that DMF, as an activator of Nrf2, has potential as a therapeutic agent for liver diseases related to high-fat diets and BA-induced injury, though careful dosage management is crucial to maximize its benefits and mitigate BA toxicity.
DOI: https://doi.org/10.37349/edd.2025.100581
This article belongs to the special issue Gastrointestinal Diseases, Cholesterol, Oxysterols, and Bile Acids
The liver operates as a highly coordinated microsystem, where various liver cell types engage in dynamic interactions to maintain homeostasis. This intercellular cooperation resembles sociological models of sustainable cooperation, encompassing mechanisms such as resource sharing, communication networks, and conflict resolution. However, both in biology and sociology, cooperation can break down due to external pressures and self-serving behaviors. In metabolic dysfunction-associated steatotic liver disease (MASLD), chronic metabolic stress disrupts this equilibrium, leading to endothelial dysfunction, immune overactivation, and fibrosis—akin to sociological models of systemic collapse. A common model in sociology, Hardin’s Tragedy of the Commons, describes how individuals overexploit shared resources when acting in self-interest, ultimately leading to resource depletion. Similarly, under metabolic stress, hepatic cells prioritize short-term survival by increasing lipid storage, inflammatory signaling, and extracellular matrix (ECM) production. This self-serving response, much like free-riding in societal systems, exacerbates dysfunction, reinforcing a cycle of fibrosis and organ failure. Moreover, the failure in MASLD extends beyond the liver itself. The liver’s cooperative role is integral to its participation in inter-organ axes, including those with the cardiovascular, gut, brain, and kidney systems. While the analogy has limitations—cells do not possess intent as humans do—the fundamental principle of cooperation breakdown leading to systemic instability holds across disciplines. An interdisciplinary approach integrating biological and sociological insights offers novel perspectives for therapeutic innovation. Sociological frameworks provide concepts such as incentive structures and collective action, which can be applied to cellular behavior. By restoring cooperative cellular networks, therapies like extracellular vesicle (EV) treatment, ECM remodeling, and receptor (ant)agonists mimic interventions in social systems that rebuild trust and sustainability. This review explores how biological and sociological models of cooperation breakdown align and how regenerative medicine can leverage these insights to develop strategies that restore cellular equilibrium and halt disease progression.
The liver operates as a highly coordinated microsystem, where various liver cell types engage in dynamic interactions to maintain homeostasis. This intercellular cooperation resembles sociological models of sustainable cooperation, encompassing mechanisms such as resource sharing, communication networks, and conflict resolution. However, both in biology and sociology, cooperation can break down due to external pressures and self-serving behaviors. In metabolic dysfunction-associated steatotic liver disease (MASLD), chronic metabolic stress disrupts this equilibrium, leading to endothelial dysfunction, immune overactivation, and fibrosis—akin to sociological models of systemic collapse. A common model in sociology, Hardin’s Tragedy of the Commons, describes how individuals overexploit shared resources when acting in self-interest, ultimately leading to resource depletion. Similarly, under metabolic stress, hepatic cells prioritize short-term survival by increasing lipid storage, inflammatory signaling, and extracellular matrix (ECM) production. This self-serving response, much like free-riding in societal systems, exacerbates dysfunction, reinforcing a cycle of fibrosis and organ failure. Moreover, the failure in MASLD extends beyond the liver itself. The liver’s cooperative role is integral to its participation in inter-organ axes, including those with the cardiovascular, gut, brain, and kidney systems. While the analogy has limitations—cells do not possess intent as humans do—the fundamental principle of cooperation breakdown leading to systemic instability holds across disciplines. An interdisciplinary approach integrating biological and sociological insights offers novel perspectives for therapeutic innovation. Sociological frameworks provide concepts such as incentive structures and collective action, which can be applied to cellular behavior. By restoring cooperative cellular networks, therapies like extracellular vesicle (EV) treatment, ECM remodeling, and receptor (ant)agonists mimic interventions in social systems that rebuild trust and sustainability. This review explores how biological and sociological models of cooperation breakdown align and how regenerative medicine can leverage these insights to develop strategies that restore cellular equilibrium and halt disease progression.
DOI: https://doi.org/10.37349/edd.2025.100580
As the most prevalent hepatic disorder worldwide, metabolic dysfunction-associated steatotic liver disease (MASLD) afflicts over one-third of the global population, representing a significant public health challenge. The multifactorial pathogenesis of this condition is principally rooted in metabolic dysregulation. It is notable that emerging evidence highlights a critical role for gut microbiota (GM) in disease initiation and progression. This comprehensive review elaborates some representative GM species that influence hepatic lipid metabolism and elucidates the mechanisms through which GM dysbiosis exacerbates MASLD pathogenesis. Importantly, the positive or negative effects of intestinal bacterial communities on MASLD are largely dependent on their special metabolites, such as short chain fatty acids, ethanol, and trimethylamine N-oxide. Current therapeutic strategies targeting GM modulation, including prebiotics, probiotics, fecal microbiota transplantation, specific medicines, and bacteriphages, demonstrate promising efficacy that partially restores microbial equilibrium and mitigates hepatic steatosis. Although limitations still persist in achieving sustained clinical remission, the expanding frontier of microbiome research continues to refine our understanding of host-microbiota crosstalk in MASLD. Future investigations integrating multiple approaches and longitudinal clinical data hold potential to unravel complex microbial networks, paving the way for innovative therapeutic breakthroughs in metabolic liver disease management.
As the most prevalent hepatic disorder worldwide, metabolic dysfunction-associated steatotic liver disease (MASLD) afflicts over one-third of the global population, representing a significant public health challenge. The multifactorial pathogenesis of this condition is principally rooted in metabolic dysregulation. It is notable that emerging evidence highlights a critical role for gut microbiota (GM) in disease initiation and progression. This comprehensive review elaborates some representative GM species that influence hepatic lipid metabolism and elucidates the mechanisms through which GM dysbiosis exacerbates MASLD pathogenesis. Importantly, the positive or negative effects of intestinal bacterial communities on MASLD are largely dependent on their special metabolites, such as short chain fatty acids, ethanol, and trimethylamine N-oxide. Current therapeutic strategies targeting GM modulation, including prebiotics, probiotics, fecal microbiota transplantation, specific medicines, and bacteriphages, demonstrate promising efficacy that partially restores microbial equilibrium and mitigates hepatic steatosis. Although limitations still persist in achieving sustained clinical remission, the expanding frontier of microbiome research continues to refine our understanding of host-microbiota crosstalk in MASLD. Future investigations integrating multiple approaches and longitudinal clinical data hold potential to unravel complex microbial networks, paving the way for innovative therapeutic breakthroughs in metabolic liver disease management.
DOI: https://doi.org/10.37349/edd.2025.100579
This article belongs to the special issue The Role of Gut Microbiota in the Pathogenesis and Management of Metabolic-Associated Steatotic Liver Disease (MASLD)
The changing management paradigm of acute complicated diverticulitis and the elective indications for surgery have evolved in the last decade based on reported evidence-based data. Recently, it has been demonstrated that randomized controlled trials (RCTs), the highest trial format in the hierarchy of evidence-based reporting, suffer from a ‘crisis of replicability’. The development of a fragility index (FI) quantitatively defines the robustness of an RCT by shifting the number of participants in a trial into a different binary group in an effort to influence reported statistical significance (the lower the FI the greater the study fragility). The only available report on FI in diverticular management showed that in an eclectic range of RCT’s comparing intervention and non-intervention, two-thirds of the studies had an FI ≤ 1 where statistical recalculation using Fisher’s Exact test rendered one-quarter of previously positive studies non-significant. Comparisons between studies and units are still dependent upon sample sizes and the numbers lost to follow-up even when some of the FI progeny (including a reverse FI, a fragility quotient dividing the FI by the sample size, or other incidence or generalized FI metrics) are utilized in assessment. Future analyses need to define all comparisons rather than cherry-picking examples where a p value approaches significance. Despite the fact that no FI value defines the strength of a RCT, its use attempts to link the reported p value with the sample size and the statistical power of the study. Positive findings in diverticular trials are then considered not so much definitive as rather provocateurs encouraging further similarly designed studies in different environments. Minimizing patient loss in treatment arms and reporting the reasons for drop-out, strictly adhering to randomization, consistent blinding, and group allocation concealment can all improve the logistical running of an RCT initially designed to evaluate some potentially important new treatment.
The changing management paradigm of acute complicated diverticulitis and the elective indications for surgery have evolved in the last decade based on reported evidence-based data. Recently, it has been demonstrated that randomized controlled trials (RCTs), the highest trial format in the hierarchy of evidence-based reporting, suffer from a ‘crisis of replicability’. The development of a fragility index (FI) quantitatively defines the robustness of an RCT by shifting the number of participants in a trial into a different binary group in an effort to influence reported statistical significance (the lower the FI the greater the study fragility). The only available report on FI in diverticular management showed that in an eclectic range of RCT’s comparing intervention and non-intervention, two-thirds of the studies had an FI ≤ 1 where statistical recalculation using Fisher’s Exact test rendered one-quarter of previously positive studies non-significant. Comparisons between studies and units are still dependent upon sample sizes and the numbers lost to follow-up even when some of the FI progeny (including a reverse FI, a fragility quotient dividing the FI by the sample size, or other incidence or generalized FI metrics) are utilized in assessment. Future analyses need to define all comparisons rather than cherry-picking examples where a p value approaches significance. Despite the fact that no FI value defines the strength of a RCT, its use attempts to link the reported p value with the sample size and the statistical power of the study. Positive findings in diverticular trials are then considered not so much definitive as rather provocateurs encouraging further similarly designed studies in different environments. Minimizing patient loss in treatment arms and reporting the reasons for drop-out, strictly adhering to randomization, consistent blinding, and group allocation concealment can all improve the logistical running of an RCT initially designed to evaluate some potentially important new treatment.
DOI: https://doi.org/10.37349/edd.2025.100578
This article belongs to the special issue Diverticulitis: Pathomechanism, Diagnosis and Treatment
Yu JW et al. (World J Gastroenterol. 2025;31:105188. DOI: 10.3748/wjg.v31.i16.105188) used male Sprague-Dawley rats fed a high-fat diet for 8 weeks to recapitulate metabolic dysfunction-associated steatotic liver disease (MASLD) experimentally. MASLD rats were randomized to receive either the duodenal mucosal ablation (DMA) using irreversible electroporation (IRE) during laparotomy or sham DMA. Data have shown that DMA was associated with duodenal thickening compared to the control group, crypts were narrower and shallower crypts and villi slimmer than sham DMA group. Moreover, the DMA group exhibited improved liver histology compared to the sham group though accompanied by inconsistent variations in blood lipid values and statistically non-significant variations in surrogate indices of MASLD. Thirdly, DMA rats had lower serum concentrations of gut hormones with crucial metabolic functions, lower lipopolysaccharide serum level, increased duodenal expression and immunofluorescence staining intensity of gut hormones expression, and higher expression of zonula occludens-1 and claudin than sham-rats. The study by Yu, et al. has innovative findings and is properly designed to illustrate the pathomechanisms underlying improved MASLD histology after DMA with IRE. However, this paper also has some methodological limitations that prompt additional studies in animal models and, ideally, in humans to be conducted as soon as safety and feasibility are demonstrated.
Yu JW et al. (World J Gastroenterol. 2025;31:105188. DOI: 10.3748/wjg.v31.i16.105188) used male Sprague-Dawley rats fed a high-fat diet for 8 weeks to recapitulate metabolic dysfunction-associated steatotic liver disease (MASLD) experimentally. MASLD rats were randomized to receive either the duodenal mucosal ablation (DMA) using irreversible electroporation (IRE) during laparotomy or sham DMA. Data have shown that DMA was associated with duodenal thickening compared to the control group, crypts were narrower and shallower crypts and villi slimmer than sham DMA group. Moreover, the DMA group exhibited improved liver histology compared to the sham group though accompanied by inconsistent variations in blood lipid values and statistically non-significant variations in surrogate indices of MASLD. Thirdly, DMA rats had lower serum concentrations of gut hormones with crucial metabolic functions, lower lipopolysaccharide serum level, increased duodenal expression and immunofluorescence staining intensity of gut hormones expression, and higher expression of zonula occludens-1 and claudin than sham-rats. The study by Yu, et al. has innovative findings and is properly designed to illustrate the pathomechanisms underlying improved MASLD histology after DMA with IRE. However, this paper also has some methodological limitations that prompt additional studies in animal models and, ideally, in humans to be conducted as soon as safety and feasibility are demonstrated.
DOI: https://doi.org/10.37349/edd.2025.100577
Background:
Esophageal varices (EV) and gastric varices (GV) are the most common portal hypertension complications in liver cirrhosis patients. Esophagogastroduodenoscopy (EGD) is the main standard procedure for variceal screening and treatment. Nonetheless, luminal evaluation sometimes cannot accurately evaluate the size of varices. Recently, endoscopic ultrasound (EUS) has been studied for EV and GV evaluation.
Methods:
Literature search was performed from PubMed, Scopus, and Cochrane Library databases until December 2022. Two independent reviewers (C.R.A.L. and T.P.) independently obtained and evaluated the selected studies according to pre-determined eligibility criteria.
Results:
Ten studies (four observational studies, three randomized controlled trials, and three retrospective reviews of case series) describing 593 patients met our eligibility criteria. Eight out of ten studies evaluated utilization of EUS for coil embolization and/or cyanoacrylate injection. All studies demonstrated excellent technical success rate of the procedure with good therapeutic efficacy, in terms of lowering the risk of recurrent bleeding. Significantly better findings were observed from groups treated with combination of coil and cyanoacrylate glue injection in comparison to monotherapy. One study also highlighted the higher possibility of developing pulmonary embolism in groups treated with conventional cyanoacrylate injection.
Discussion:
EUS-guided combination therapy appears to be a safe and effective modality for treating patients with gastric variceal bleeding with high number of complete obliteration and low risk of gastric variceal rebleeding. Further meta-analysis large-scale randomized clinical trials are still required to confirm these findings.
Background:
Esophageal varices (EV) and gastric varices (GV) are the most common portal hypertension complications in liver cirrhosis patients. Esophagogastroduodenoscopy (EGD) is the main standard procedure for variceal screening and treatment. Nonetheless, luminal evaluation sometimes cannot accurately evaluate the size of varices. Recently, endoscopic ultrasound (EUS) has been studied for EV and GV evaluation.
Methods:
Literature search was performed from PubMed, Scopus, and Cochrane Library databases until December 2022. Two independent reviewers (C.R.A.L. and T.P.) independently obtained and evaluated the selected studies according to pre-determined eligibility criteria.
Results:
Ten studies (four observational studies, three randomized controlled trials, and three retrospective reviews of case series) describing 593 patients met our eligibility criteria. Eight out of ten studies evaluated utilization of EUS for coil embolization and/or cyanoacrylate injection. All studies demonstrated excellent technical success rate of the procedure with good therapeutic efficacy, in terms of lowering the risk of recurrent bleeding. Significantly better findings were observed from groups treated with combination of coil and cyanoacrylate glue injection in comparison to monotherapy. One study also highlighted the higher possibility of developing pulmonary embolism in groups treated with conventional cyanoacrylate injection.
Discussion:
EUS-guided combination therapy appears to be a safe and effective modality for treating patients with gastric variceal bleeding with high number of complete obliteration and low risk of gastric variceal rebleeding. Further meta-analysis large-scale randomized clinical trials are still required to confirm these findings.
DOI: https://doi.org/10.37349/edd.2025.100576
Metabolic associated steatotic liver disease (MASLD) stands as the most common hepatic disorder in both developed and developing countries. The global increasing rates in obesity rates are fuelling an increase in MASLD cases. Fibroscan, a transient elastography device, is a research-based, noninvasive method for assessing liver fibrosis. Accurately measuring the extent of fibrosis presents difficulties in a cohort of individuals who are severely obese with a body mass index (BMI) ≥ 40 kg/m2, particularly regarding the reliability and applicability of the XL probe. This study’s objective is to evaluate the precision of fibroscan in morbidly obese individuals with a BMI ≥ 40 kg/m2. We explored Google, PubMed, and Medline to gather information on fibroscan and its application for measuring fibrosis levels in morbidly obese patients ≥ 40 kg/m2 who have MASLD. The fibrosis levels obtained from the fibroscan do not consistently correlate with the clinical or histopathological data, which are essential for accurately determining liver stiffness measurement (LSM) cutoff values and/or ranges for these patients with either significant or advanced fibrosis. Additional prospective multicenter studies are necessary to better establish LSM cutoff values and/or ranges for patients suffering from significant or advanced fibrosis due to morbid obesity.
Metabolic associated steatotic liver disease (MASLD) stands as the most common hepatic disorder in both developed and developing countries. The global increasing rates in obesity rates are fuelling an increase in MASLD cases. Fibroscan, a transient elastography device, is a research-based, noninvasive method for assessing liver fibrosis. Accurately measuring the extent of fibrosis presents difficulties in a cohort of individuals who are severely obese with a body mass index (BMI) ≥ 40 kg/m2, particularly regarding the reliability and applicability of the XL probe. This study’s objective is to evaluate the precision of fibroscan in morbidly obese individuals with a BMI ≥ 40 kg/m2. We explored Google, PubMed, and Medline to gather information on fibroscan and its application for measuring fibrosis levels in morbidly obese patients ≥ 40 kg/m2 who have MASLD. The fibrosis levels obtained from the fibroscan do not consistently correlate with the clinical or histopathological data, which are essential for accurately determining liver stiffness measurement (LSM) cutoff values and/or ranges for these patients with either significant or advanced fibrosis. Additional prospective multicenter studies are necessary to better establish LSM cutoff values and/or ranges for patients suffering from significant or advanced fibrosis due to morbid obesity.
DOI: https://doi.org/10.37349/edd.2025.100575
Aim:
Our previous study provided evidence that systemic zonula occludens (ZO) 1 levels are elevated in cirrhotic and hepatocellular carcinoma (HCC) patients. Here, we aimed to evaluate serum ZO-1 levels in patients with decompensated alcoholic cirrhosis (DCAC) with hepatorenal syndrome (HRS) and compare its diagnostic potential with the well-established HRS biomarker, cystatin C.
Methods:
A total of 36 DCAC patients with HRS and 40 healthy volunteers were recruited. Serum ZO-1, cystatin C, and clinical chemistry parameters were analysed.
Results:
Compared to control subjects, DCAC patients with HRS exhibited significantly higher ZO-1 levels (7.059 ± 0.29 vs. 0.788 ± 0.11; p < 0.0001) and cystatin C levels (2.97 ± 0.24 vs. 1.59 ± 0.04; p < 0.0001). Serum ZO-1 correlated positively with cystatin C (r = 0.561, p < 0.0001), serum creatinine (r = 0.779, p < 0.0001), and MELD-Na (r = 0.850, p < 0.0001). Moreover, ZO-1 demonstrated a higher area under the curve (AUC) than cystatin C, indicating a better diagnostic potential for HRS in DCAC patients.
Conclusions:
These findings suggest that ZO-1 may serve as a valuable biomarker for HRS in DCAC patients. However, further validation in a larger cohort is necessary to confirm its clinical utility.
Aim:
Our previous study provided evidence that systemic zonula occludens (ZO) 1 levels are elevated in cirrhotic and hepatocellular carcinoma (HCC) patients. Here, we aimed to evaluate serum ZO-1 levels in patients with decompensated alcoholic cirrhosis (DCAC) with hepatorenal syndrome (HRS) and compare its diagnostic potential with the well-established HRS biomarker, cystatin C.
Methods:
A total of 36 DCAC patients with HRS and 40 healthy volunteers were recruited. Serum ZO-1, cystatin C, and clinical chemistry parameters were analysed.
Results:
Compared to control subjects, DCAC patients with HRS exhibited significantly higher ZO-1 levels (7.059 ± 0.29 vs. 0.788 ± 0.11; p < 0.0001) and cystatin C levels (2.97 ± 0.24 vs. 1.59 ± 0.04; p < 0.0001). Serum ZO-1 correlated positively with cystatin C (r = 0.561, p < 0.0001), serum creatinine (r = 0.779, p < 0.0001), and MELD-Na (r = 0.850, p < 0.0001). Moreover, ZO-1 demonstrated a higher area under the curve (AUC) than cystatin C, indicating a better diagnostic potential for HRS in DCAC patients.
Conclusions:
These findings suggest that ZO-1 may serve as a valuable biomarker for HRS in DCAC patients. However, further validation in a larger cohort is necessary to confirm its clinical utility.
DOI: https://doi.org/10.37349/edd.2025.100574
This article belongs to the special issue Cirrhosis and Its Complications
