Advances in Gastrointestinal and Liver Disease: From Physiological Mechanisms to Clinical Practice, 2nd Edition

Abstract submission deadline

25 July 2026

Manuscript submission deadline

20 December 2026

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Topic Information

Dear Colleagues,

The management of gastrointestinal and hepatic diseases is constantly evolving. The progressive understanding of pathogenic mechanisms has improved daily management, representing real translational medicine. For example, understanding the mechanisms underlying HCV virus infection has enabled the development of Direct-Acting Antivirals (DAAs), with a cure rate of 98%. However, patients with advanced liver disease, albeit cured from HCV infection, are still at risk of hepatocellular carcinoma (HCC) development. Therefore, these patients will remain a medical challenge for years to come. New antiviral agents are currently under development for the treatment of chronic delta hepatitis (CHD).

Hopefully, in the near future we will be able to at least control liver disease progression in patients with CHD, the most severe form of chronic viral hepatitis. In the coming decades, NAFLD/NASH will supplant viral hepatitis as the leading cause of chronic liver damage. Efforts are ongoing to identify novel biomarkers and tools for the detection of liver fibrosis and stratify the risk of liver disease progression. Moreover, novel molecules targeting several pathways involved in NAFLD onset and progression are under investigation. The decrease in the prevalence of Helicobacter pylori (H. pylori) infection, the widespread use of proton pump inhibitors, and the relative ease of access to gastroscopies have reduced the incidence of peptic disease and stomach cancer, which was once the main gastrointestinal pathology. In many areas of the world, however, H. pylori infection remains widespread, and there is still room for improvement in eradication strategies. Understanding the inflammatory pathways involved in inflammatory bowel disease has enabled the development of target therapies (anti-TNF, anti-IL12/23, anti-JAK, S1P1 modulators). Increased understanding of the microbiome will lead to applications that will go beyond the confines of the gut, although the COVID-19 pandemic will continue to affect the management of all diseases.

The objective of this Topic is to present the most up-to-date data on the pathogenesis and management of gastrointestinal and hepatological diseases, with a view to an increasingly personalized management of patients.

Dr. Davide Giuseppe Ribaldone
Dr. Gian Paolo Caviglia
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomedicines biomedicines	3.9	6.8	2013	17 Days	CHF 2600	Submit
Current Oncology curroncol	3.4	4.9	1994	21.5 Days	CHF 2200	Submit
Diagnostics diagnostics	3.3	5.9	2011	21 Days	CHF 2600	Submit
Journal of Clinical Medicine jcm	2.9	5.2	2012	17.7 Days	CHF 2600	Submit
Livers livers	2.4	3.2	2021	27.8 Days	CHF 1200	Submit
Transplantology transplantology	-	1.4	2020	38.9 Days	CHF 1000	Submit
Gastrointestinal Disorders gastrointestdisord	0.8	1.2	2019	19.2 Days	CHF 1400	Submit

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Published Papers (4 papers)

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All Biomedicines Current Oncology Diagnostics JCM Livers Transplantology Gastrointestinal Disorders

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10 pages, 2759 KB  

Open AccessCase Report

Steroid-Refractory Cholestatic Immune-Mediated Hepatitis Following Nivolumab Therapy in an Elderly Patient with Metastatic Melanoma: A Rare and Challenging Presentation

by Luis Posado-Dominguez, Jorge Feito-Perez, María Escribano-Iglesias, Miriam Bragado Pascual and Emilio Fonseca Sánchez

Curr. Oncol. 2025, 32(12), 663; https://doi.org/10.3390/curroncol32120663 - 27 Nov 2025

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Abstract

Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of advanced malignancies, but they may cause a wide range of immune-related adverse events (irAEs). Hepatic toxicity occurs in approximately 1–6% of patients treated with nivolumab and usually presents with a hepatocellular pattern responsive to [...] Read more.

Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of advanced malignancies, but they may cause a wide range of immune-related adverse events (irAEs). Hepatic toxicity occurs in approximately 1–6% of patients treated with nivolumab and usually presents with a hepatocellular pattern responsive to corticosteroids. The cholestatic-predominant immune-mediated hepatitis seems to respond poorly to immunosuppression. We describe an 87-year-old man with metastatic melanoma treated with nivolumab who developed steroid-refractory, cholestatic-predominant immune-mediated hepatitis after 18 cycles of therapy. Laboratory tests revealed a mixed but predominantly cholestatic pattern (ALT 585 U/L, GGT 2261 U/L, total bilirubin 2.0 mg/dL). Imaging excluded biliary obstruction or hepatic metastases. Liver biopsy showed acute lobular hepatitis with intracanalicular cholestasis and mild bile duct injury, consistent with immune-mediated, drug-induced injury (Ishak score 5). Mycophenolate mofetil produced only partial biochemical improvement. The patient died one month later from influenza A pneumonia in the context of combined immunosuppressive therapy. This case illustrates a cholestatic-predominant phenotype of nivolumab-induced hepatitis, characterized by poor corticosteroid response and incomplete recovery despite second-line immunosuppression. Recognition of this entity is essential, as early introduction of agents such as mycophenolate may improve outcomes. In elderly and frail patients, however, the risks of intensified immunosuppression must be carefully balanced against infection risk, highlighting the need for individualized management and vigilant monitoring. Full article

(This article belongs to the Topic Advances in Gastrointestinal and Liver Disease: From Physiological Mechanisms to Clinical Practice, 2nd Edition)

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14 pages, 530 KB  

Open AccessArticle

Adiposity and Metabolic Indices in the Diagnosis and Histological Stage Association of Metabolic Dysfunction-Associated Steatotic Liver Disease

by Lorena del Rocio Ibarra-Reynoso, Nemry Rodriguez-Hernandez, Maria-Luisa Lazo-de-la-Vega-Monroy, Juana Rosalba Garcia-Ramirez, Yeniley Ruiz-Noa, Benjamin Jordan-Perez, Serafin Garnelo-Cabañas, Veronica Muñoz-Cornejo and Monica del Carmen Preciado-Puga

J. Clin. Med. 2025, 14(23), 8365; https://doi.org/10.3390/jcm14238365 - 25 Nov 2025

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Background: Metabolic dysfunction-associated steatotic liver disease (MALSD) is defined as the excessive accumulation of triglycerides in the liver in the presence of at least one cardiometabolic risk factor and liver biopsy remains the diagnostic gold standard. This study aimed to evaluate the diagnostic [...] Read more.

Background: Metabolic dysfunction-associated steatotic liver disease (MALSD) is defined as the excessive accumulation of triglycerides in the liver in the presence of at least one cardiometabolic risk factor and liver biopsy remains the diagnostic gold standard. This study aimed to evaluate the diagnostic performance of adiposity and metabolism related indices for the non-invasive detection of MASLD and the metabolic dysfunction-associated steatohepatitis (MASH). Methods: A cross-sectional study was conducted in 161 Mexican adults undergoing laparoscopic cholecystectomy, during which liver biopsies were obtained for histological evaluation. Indices such as the Hepatic Steatosis Index (HSI), the Triglyceride–Glucose index (TyG), TyG-BMI (TyG adjusted for body mass index), and TyG-WC (TyG adjusted for waist circumference), among others, were calculated. Results: Of the 161 participants, 66 were diagnosed with MASLD, and 50 of them had histological evidence of MASH. All adiposity and metabolic indices evaluated were significantly higher in MASLD patients compared with controls. Logistic regression identified HSI, TyG, TyG-BMI, and TyG-WC as independently associated with MASLD and MASH, with TyG showing the strongest association. Correlation analyses demonstrated that TyG-BMI and TyG-WC were most strongly associated with histological features of MASH. Receiver operating characteristic curve analyses showed that TyG-WC had the highest diagnostic accuracy for MASLD (AUC 0.721, 95% CI 0.641–0.802) and MASH (AUC 0.735, 95% CI 0.648–0.823), while TyG-BMI displayed high sensitivity (0.758 for MASLD; 0.780 for MASH). Conclusions: Triglyceride–glucose-based indices, particularly TyG-WC and TyG-BMI, showed the highest diagnostic performance for detecting MASLD and MASH, suggesting that these indices may serve as practical, non-invasive tools for identifying individuals at risk. Full article

(This article belongs to the Topic Advances in Gastrointestinal and Liver Disease: From Physiological Mechanisms to Clinical Practice, 2nd Edition)

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16 pages, 1463 KB  

Open AccessReview

Macrophages in Autoimmune Liver Diseases: From Immune Homeostasis to Precision-Targeted Therapy

by Tianfu Liu, Yizhe Wang, Yichen Huang, Rui Zhao and Haili Shen

Biomedicines 2025, 13(10), 2520; https://doi.org/10.3390/biomedicines13102520 - 16 Oct 2025

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Abstract

Autoimmune liver diseases (AILDs) represent a diverse spectrum of chronic inflammatory conditions characterized primarily by compromised hepatic immune tolerance, including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). Recent evidence positions macrophages as pivotal players in AILDs pathogenesis, attributable [...] Read more.

Autoimmune liver diseases (AILDs) represent a diverse spectrum of chronic inflammatory conditions characterized primarily by compromised hepatic immune tolerance, including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC). Recent evidence positions macrophages as pivotal players in AILDs pathogenesis, attributable to their multifaceted roles in inflammation amplification, immune regulation, and fibrogenesis. In the context of AILDs, macrophages exhibit marked polarization imbalance, increased recruitment of monocytes, and impaired clearance of apoptotic cells. Through complex interactions with T lymphocytes and hepatic stellate cells, macrophages orchestrate a pathological milieu promoting inflammation and fibrosis. Notably, diverse programmed cell death (PCD) modalities—autophagy, necroptosis, pyroptosis, and ferroptosis—not only determine macrophage survival and functional phenotype but also significantly impact cytokine release, phenotypic plasticity, and the trajectory of immunopathological progression. This review synthesizes current understandings of macrophage-driven immunoregulatory mechanisms in AILDs, characterizes the regulatory attributes of various macrophage-related PCD processes, and evaluates their relevance in experimental disease models. Furthermore, we highlight recent advancements in biomarker identification and targeted therapeutic strategies. Comprehensive elucidation of the interplay between macrophage immunological activity and programmed cell death pathways promises to inform novel, personalized therapeutic approaches for patients with AILDs. Full article

(This article belongs to the Topic Advances in Gastrointestinal and Liver Disease: From Physiological Mechanisms to Clinical Practice, 2nd Edition)

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14 pages, 1397 KB  

Open AccessReview

The Emerging Role of CKAP4 in GI Cancer: From Molecular Pathways to Clinical Applications

by Markos Despotidis, Orestis Lyros, Tatiana S. Driva, Panagiotis Sakarellos, René Thieme, Andreas Mamilos, Stratigoula Sakellariou and Dimitrios Schizas

Curr. Oncol. 2025, 32(10), 561; https://doi.org/10.3390/curroncol32100561 - 7 Oct 2025

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Cytoskeleton-associated protein 4 (CKAP4) has emerged as a critical player in gastrointestinal (GI) cancer progression, diagnosis, and therapy. This comprehensive review synthesizes current knowledge on CKAP4′s multifaceted roles across GI malignancies, providing novel insights into its mechanisms of action and clinical potential. Its [...] Read more.

Cytoskeleton-associated protein 4 (CKAP4) has emerged as a critical player in gastrointestinal (GI) cancer progression, diagnosis, and therapy. This comprehensive review synthesizes current knowledge on CKAP4′s multifaceted roles across GI malignancies, providing novel insights into its mechanisms of action and clinical potential. Its interaction with DKK1 and subsequent activation of the PI3K/AKT pathway underscores its role in promoting tumor growth. This review also highlights novel insights into CKAP4′s mechanisms of action beyond the well-established DKK1-CKAP4 axis, including its interaction with integrin β1 and involvement in angiogenesis through the FMNL2/EGFL6/CKAP4/ERK pathway. CKAP4′s impact on tumor microenvironment and immune evasion is elucidated, offering a new perspective on its contribution to cancer progression. In addition, CKAP4 arises as a promising serum biomarker for early detection and prognosis across multiple GI cancers, emphasizing its potential superiority over traditional markers. The therapeutic potential of targeting CKAP4 is extensively explored, including novel approaches like anti-CKAP4 antibodies and aptamers, and their synergistic effects with existing treatments. By integrating findings from esophageal, gastric, pancreatic, and colorectal cancers, this review provides a unique, comprehensive overview of CKAP4 in GI oncology, underscoring CKAP4′s potential to revolutionize GI cancer diagnosis and treatment and paving the way for future translational research. Full article

(This article belongs to the Topic Advances in Gastrointestinal and Liver Disease: From Physiological Mechanisms to Clinical Practice, 2nd Edition)

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