Gastroenterology Insights

12 pages, 1213 KiB

Open AccessSystematic Review

New Onset Inflammatory Bowel Disease Risk Following Bariatric Surgery: A Systematic Review and Meta-Analysis of Observational Studies

by Wafa A. Aldhaleei, Tarek Odah, Nader Bakheet, Heather Jett, Jana G. Hashash, Michael B. Wallace, Vivek Kumbhari, Francis A. Farraye and Akshaya Srikanth Bhagavathula

Gastroenterol. Insights 2024, 15(3), 708-719; https://doi.org/10.3390/gastroent15030050 - 14 Aug 2024

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Abstract

Background: While bariatric surgery may reduce obesity-associated inflammation, alterations in gut microbiome and nutrition could impact inflammatory bowel disease (IBD) risk. This study aimed to investigate the association between bariatric surgery and new onset IBD. Methods: A systematic review and meta-analysis of observational [...] Read more.

Background: While bariatric surgery may reduce obesity-associated inflammation, alterations in gut microbiome and nutrition could impact inflammatory bowel disease (IBD) risk. This study aimed to investigate the association between bariatric surgery and new onset IBD. Methods: A systematic review and meta-analysis of observational studies was conducted from inception to 31 January 2024. Risk estimates were pooled using a DerSimonian and Laird random-effects model, and adjusted hazards ratios (HRs) with corresponding 95% confidence interval (CI) were reported. The modified Newcastle-Ottawa Quality Assessment Scale (NOS) was used to examine the risk of bias. Results: Of 98 articles screened, four studies comprising 4,727,600 participants were included in the systematic review and two studies in the meta-analysis. Included studies had high quality and low risk of bias according to NOS. The pooled analysis revealed a significant risk of new onset IBD (HR: 1.28, 95% CI: 1.04–1.53, I² = 74.9%), particularly Crohn’s disease (HR: 1.75, 1.59–1.92, I² = 0), following bariatric surgery, but no significant risk of ulcerative colitis (HR: 0.93, 0.75–1.11, I² = 11.5%). Conclusions: This meta-analysis found that bariatric surgery was associated with a higher risk of developing Crohn’s disease. Patients should be counseled on IBD risk pre-surgery, and symptomatic patients should be evaluated post-surgery to enable early diagnosis and management. Full article

(This article belongs to the Special Issue Recent Advances in the Management of Gastrointestinal Disorders)

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32 pages, 4820 KiB

Open AccessReview

Hepatitis C Virus: History and Current Knowledge

by Skender Topi, Elona Gaxhja, Ioannis Alexandros Charitos, Marica Colella and Luigi Santacroce

Gastroenterol. Insights 2024, 15(3), 676-707; https://doi.org/10.3390/gastroent15030049 - 8 Aug 2024

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Abstract

According to the World Health Organization (WHO), the incidence of HCV remains high (around 1.5 million new patients every year), and 80% of patients with acute infection will progress to chronic hepatitis and develop cirrhosis and even liver cancer. Furthermore, some extrahepatic pathologies [...] Read more.

According to the World Health Organization (WHO), the incidence of HCV remains high (around 1.5 million new patients every year), and 80% of patients with acute infection will progress to chronic hepatitis and develop cirrhosis and even liver cancer. Furthermore, some extrahepatic pathologies may be correlated with HCV (such as mixed cryoglobulinemia, porphyria cutanea tarda, lichen planus, glomerulonephritis, Sjogren’s syndrome, Hodgkin and non-Hodgkin cell lymphoma, and others). In view of these secondary complications, together with the substantial risk of liver damage, the objective of this review was to research and suggest, based on the scientific evidence, the appropriate clinical use of drugs with direct antiviral action (AAD) according to the criteria of international medical organizations. This is to maximize the clinical benefits for patients and to facilitate access to DAA therapy for all patients with chronic hepatitis C. According to the WHO, no vaccine is currently available, and therapies using new antivirals and their combinations are now an effective and safer solution for patients than they have been in the past with the use of interferons. This study aims to analyse the history and knowledge of the pathogenic biomolecular mechanisms and current therapies for HCV. Full article

(This article belongs to the Special Issue Novelties in Diagnostics and Therapeutics in Hepatology: 2nd Edition)

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15 pages, 1996 KiB

Open AccessReview

Mucosal Immunity and Trained Innate Immunity of the Gut

by Tsvetelina Velikova, Issa El Kaouri, Konstantina Bakopoulou, Milena Gulinac, Kremena Naydenova, Martin Dimitrov, Milena Peruhova and Snezhina Lazova

Gastroenterol. Insights 2024, 15(3), 661-675; https://doi.org/10.3390/gastroent15030048 - 2 Aug 2024

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Abstract

Mucosal immunity and trained innate immunity of the gut play a pivotal role in maintaining intestinal homeostasis and defending against microbial pathogens. This review provides an overview of the mechanisms underlying mucosal immunity and the concept of trained innate immunity in the gut. [...] Read more.

Mucosal immunity and trained innate immunity of the gut play a pivotal role in maintaining intestinal homeostasis and defending against microbial pathogens. This review provides an overview of the mechanisms underlying mucosal immunity and the concept of trained innate immunity in the gut. We discuss the interaction between gut microbiota and the host immune system, highlighting the role of epithelial cells, dendritic cells, and innate lymphoid cells, as well as the novel concept of trained innate immunity and its role in perpetuating or attenuating gut inflammation. We also comment on the current models for investigating mucosal immunity, their limitations, and how they can be overcome. Additionally, we explore the potential therapeutic implications of modulating mucosal immunity and trained innate immunity in gastrointestinal diseases. Only by elucidating the mechanisms underlying mucosal immunity and the concept of trained innate immunity, innovative approaches to modulate immune responses and restore intestinal homeostasis in the context of gastrointestinal disorders could be implemented. Full article

(This article belongs to the Section Gastrointestinal Disease)

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14 pages, 1409 KiB

Open AccessReview

Dietary Supplements as Concentrated Sources of Nutrients with a Nutritional or Physiological Effect for Children with Inflammatory Bowel Disease

by Rayna Shentova, Antoaneta Mihova and Tsvetelina Velikova

Gastroenterol. Insights 2024, 15(3), 647-660; https://doi.org/10.3390/gastroent15030047 - 31 Jul 2024

Viewed by 331

Abstract

The consequences of inflammatory bowel disease (IBD) in children are connected to possible detrimental impacts on growth, development, psychosocial function, and general well-being. Therefore, the primary management plan in pediatric IBD is to achieve the long-term control of intestinal inflammation while also monitoring [...] Read more.

The consequences of inflammatory bowel disease (IBD) in children are connected to possible detrimental impacts on growth, development, psychosocial function, and general well-being. Therefore, the primary management plan in pediatric IBD is to achieve the long-term control of intestinal inflammation while also monitoring potential disease complications and therapeutic adverse effects, where nutritional management is of utmost importance. This review explores the role of dietary supplements as concentrated sources of nutrients with nutritional and/or physiological effects on children with IBD. While dietary supplements are commonly used in pediatric IBD management, their efficacy and, for some of them, safety remain subjects of debate. We provide an overview of the types of dietary supplements available and their potential benefits and risks in pediatric IBD patients. Additionally, we discuss the evidence supporting the use of specific supplements, their mechanisms of action, and considerations for clinical practice. Understanding the role of dietary supplements in pediatric IBD management is crucial for optimizing patient care and outcomes. Full article

(This article belongs to the Section Gastrointestinal Disease)

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15 pages, 3910 KiB

Open AccessReview

Primary Signet-Ring-Cell Carcinoma in the Colorectum: A Case-Based Literature Review

by Milena Gulinac, Niya Mileva, Dimitrina Miteva, Tsvetelina Velikova and Dorian Dikov

Gastroenterol. Insights 2024, 15(3), 632-646; https://doi.org/10.3390/gastroent15030046 - 28 Jul 2024

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Abstract

Primary colorectal signet-ring-cell carcinoma of the colon and rectum (PSRCCR) is an extremely rare subtype of mucinous adenocarcinoma with a reported rate of less than 1%. This low rate is mainly because it is generally diagnosed at advanced stages. The most common stage [...] Read more.

Primary colorectal signet-ring-cell carcinoma of the colon and rectum (PSRCCR) is an extremely rare subtype of mucinous adenocarcinoma with a reported rate of less than 1%. This low rate is mainly because it is generally diagnosed at advanced stages. The most common stage at which it is diagnosed for the first time is III or IV, with a lower median survival than other histological subtypes. To diagnose PSRCCR of the colon, at least half of the tumor must be consistent with a signet-ring-cell pattern. This review aims to provide a comprehensive overview of PSRCCR by synthesizing the existing literature and clinical data. Our objective was to elucidate the clinical features, diagnostic challenges, histopathological characteristics, molecular alterations, treatment modalities, and prognostic factors associated with this carcinoma. Additionally, we highlighted the significance of early detection, accurate diagnosis, and personalized therapeutic approaches in improving outcomes for patients with this challenging malignancy. By presenting a case report on the topic, we aimed to enhance understanding among clinicians, pathologists, and researchers, ultimately contributing to optimized management strategies and improved patient care for PSRCCR. Full article

(This article belongs to the Section Gastrointestinal Disease)

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18 pages, 6739 KiB

Open AccessArticle

Differential Effects of Somatostatin on TNF Receptors and Apoptosis in Hepatocellular Carcinoma Cell Lines

by Maria Georgiadou, George Notas, Ioannis Tsomidis, Argyro Voumbouraki, Ioannis Drygiannakis, George Emmanouil and Elias Kouroumalis

Gastroenterol. Insights 2024, 15(3), 614-631; https://doi.org/10.3390/gastroent15030045 - 4 Jul 2024

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Abstract

The anti-tumoral activity of somatostatin has been demonstrated in both animal experiments and human tumors. Clinical trials have reported conflicting results. We therefore hypothesized that somatostatin might have different effects in various hepatocellular carcinoma cells. Their clarification would possibly allow for the better [...] Read more.

The anti-tumoral activity of somatostatin has been demonstrated in both animal experiments and human tumors. Clinical trials have reported conflicting results. We therefore hypothesized that somatostatin might have different effects in various hepatocellular carcinoma cells. Their clarification would possibly allow for the better selection of patients suitable for the optimal treatment results. We studied the mRNA and protein expression of TNF receptors and the TNFa-induced apoptosis using the HepG2 and the Hep3B human hepatocellular carcinoma cells after incubation with the somatostatin analog octreotide. RT-PCR, Western blot, and parameters associated with apoptosis (NF-kB nuclear translocation, P65 Ser536 and P65 Ser468 phosphorylation, DNA fragmentation) were assessed. Only TNFR1 was constitutively present in the two cell lines. Octreotide incubation led to an earlier reduction in TNFR1 mRNA and protein in HepG2 compared to Hep3B cells (1 h and 6–12 h, respectively). NF-kB translocation to the nucleus was induced by TNFa and was more prominent in Hep3B. Translocation was unaffected by octreotide. Serine phosphorylation was significantly induced by TNFa and was more evident in the Hep3B cells. TNFa-induced Ser536 phosphorylation was inhibited by octreotide only in the HepG2 cells. DNA fragmentation was not influenced by either octreotide or TNFa in the HepG2 cells, but TNFa induced fragmentation in the Hep3B cells (1.8-fold increase) verified by the TUNEL index (43 compared to 19 for the HepG2 cells). Octreotide and TNFa co-incubation induced apoptosis in the HepG2 cells (1.7-fold increase compared to controls) but inhibited apoptosis in the Hep3B cells. We conclude that: (1) octreotide reduced TNFR1 receptor expression in both cell lines, (2) parameters of apoptosis were differentially affected by octreotide in the two cell lines, and (3) this might be a partial explanation for the conflicting results of somatostatin analog treatment in human hepatocellular carcinoma trials. Full article

(This article belongs to the Section Liver)

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15 pages, 703 KiB

Open AccessReview

Anabolic Androgenic Steroids and Hepatocellular Adenoma and Carcinoma: Molecular Mechanisms and Clinical Implications

by Luca Ielasi, Enrico Fulco, Nicola Reggidori, Marco Domenicali and Francesco Giuseppe Foschi

Gastroenterol. Insights 2024, 15(3), 599-613; https://doi.org/10.3390/gastroent15030044 - 4 Jul 2024

Viewed by 1274

Abstract

Anabolic androgenic steroids (AAS) are a class of hormones that are used for hormonal replacement therapy in cases of male hypogonadism and for a few other medical conditions, mainly anemias, as well as for the female-to-male transition process. At the same time, AAS [...] Read more.

Anabolic androgenic steroids (AAS) are a class of hormones that are used for hormonal replacement therapy in cases of male hypogonadism and for a few other medical conditions, mainly anemias, as well as for the female-to-male transition process. At the same time, AAS are widely abused for their muscle-building and strength-increasing properties. Among their side effects, androgens can exert a toxic effect on the liver, causing hepatotoxicity, but they can also induce hepatocyte proliferation and malignant transformation. Hepatocellular adenoma (HCA) and hepatocellular carcinoma (HCC) are two primary liver lesions that have been described as potentially related to AAS. This review provides an up-to-date analysis of how androgens can induce liver carcinogenesis and a comprehensive overview on the available data in the literature about AAS and primary liver tumors. Full article

(This article belongs to the Special Issue Feature Papers in Liver Research)

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11 pages, 2857 KiB

Open AccessArticle

Grading of Fatty Liver Based on Computed Tomography Hounsfield Unit Values versus Ultrasonography Grading

by Sultan Abdulwadoud Alshoabi, Reyan Mohammed Alharbi, Rufaydah Bader Algohani, Shahad Abdullah Alahmadi, Maryam Ahmed, Samah F. Faqeeh, Dalal Alahmadi, Abdulaziz A. Qurashi, Fahad H. Alhazmi, Rakan Mohammed Alrehaili and Abdulrahman Khalil Almughathawi

Gastroenterol. Insights 2024, 15(3), 588-598; https://doi.org/10.3390/gastroent15030043 - 4 Jul 2024

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Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) ranges from hepatic steatosis to nonalcoholic steatohepatitis and may lead to liver cirrhosis. This study aimed to assess the feasibility of numerical grading MASLD using noncontrast computed tomography (NCCT). Methods: In a retrospective study of 166 [...] Read more.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) ranges from hepatic steatosis to nonalcoholic steatohepatitis and may lead to liver cirrhosis. This study aimed to assess the feasibility of numerical grading MASLD using noncontrast computed tomography (NCCT). Methods: In a retrospective study of 166 patients diagnosed with MASLD between June 2020 and January 2024, MASLD was graded by ultrasonography, and liver density was measured on NCCT. The MASLD grades and NCCT densities were compared. Results: The MASLD grades were distributed as follows: grade 0 (n = 79, 47.6%), grade 2 (n = 48, 28.9%), grade 1 (n = 25, 15.1%), and grade 3 (n = 14, 8.4%). The mean liver density was 57.75 Hounsfield units (HU) ± 6.18 (range: 48.9–78.2), 51.1 HU ± 4.7 (range: 41.4–59.7), 39.3 ± 6.4 (range: 21.4–48.9), and 22.87 ± 7.5 (range: 12–36.4) in the grade 0, grade 1, grade 2, and grade 3 patients, respectively. An analysis of variance test showed significant variance in the distribution of mean liver density in the different MASLD grades (p < 0.001). Conclusions: After ultrasonography diagnosis of MASLD, NCCT offers an objective, numerical, and calculable method for MASLD grading that is available for radiologists, radiologic technologists, and interested physicians away from experience dependence. NCCT determined that grade 2 had a specific density from 36.4 to 41.4 HU that significantly overlapped with grade 1 (41.4–48.9) HU and with grade 3 (21.4–36.4 HU). Grade 1 showed a significant overlap with the normal liver (48.9–59.7 HU). Full article

(This article belongs to the Section Gastrointestinal and Hepato-Biliary Imaging)

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14 pages, 4016 KiB

Open AccessArticle

Mitigative Effect of Graphene Oxide Nanoparticles in Maintaining Gut–Liver Homeostasis against Alcohol Injury

by Hiral Aghara, Prashsti Chadha and Palash Mandal

Gastroenterol. Insights 2024, 15(3), 574-587; https://doi.org/10.3390/gastroent15030042 - 2 Jul 2024

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Abstract

Alcoholic liver disease (ALD) develops when the immunotolerant environment of the liver is compromised due to excessive alcohol consumption. ALD progression involves variations in the expressions of multiple genes, resulting in liver inflammation and the development of a leaky gut. It is still [...] Read more.

Alcoholic liver disease (ALD) develops when the immunotolerant environment of the liver is compromised due to excessive alcohol consumption. ALD progression involves variations in the expressions of multiple genes, resulting in liver inflammation and the development of a leaky gut. It is still unclear which molecular mechanism is involved in ALD progression, and due to that, there are currently no FDA-approved drugs available for its treatment. In this study, the protective effects of graphene oxide (GO) nanoparticles were investigated against ethanol-induced damage in the gut–liver axis in in vitro. GO was synthesized using a modified Hummer’s method, and characterization was performed. Given the general concerns regarding nanoparticle toxicity, assessments of cell viability, lipid accumulation, DNA damage, cell death, and the generation of reactive oxygen species (ROS) were conducted using various techniques. Furthermore, the gene expressions of pro- and anti-inflammatory cytokines were determined using RT-qPCR. The findings reveal that GO promoted cell viability even against ethanol treatment. Additionally, lipid accumulation significantly decreased when cells were treated with GO alongside ethanol compared to ethanol treatment alone, with similar trends observed for other assays. A gene expression analysis indicated that GO treatment reduced the expression of proinflammatory cytokines while enhancing the expression of antioxidant genes. Moreover, GO treatment led to improvements in gut integrity and a reduction in proinflammatory cytokines in colon cells damaged by ethanol. These findings suggest that GO holds promise as a drug carrier, exhibiting no observed toxic effects. By shedding light on the protective effects of GO against ethanol-induced damage, this study contributes to the burgeoning field of nanoparticle-mediated therapy for ALD. Full article

(This article belongs to the Section Liver)

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19 pages, 2672 KiB

Open AccessReview

Exploring Gut–Brain Interaction Disorders: Mechanisms and Translational Therapies Crossing Neurology to Gastroenterology

by Georgi V. Vasilev, Dimitrina Miteva, Milena Gulinac, Lyubomir Chervenkov, Meglena Kitanova and Tsvetelina Velikova

Gastroenterol. Insights 2024, 15(3), 555-573; https://doi.org/10.3390/gastroent15030041 - 2 Jul 2024

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Abstract

The bidirectional communication network between the gut and the brain, known as the gut–brain axis, plays a crucial role in health and disease. This review explores the mechanisms underlying gut–brain interaction disorders and highlights translational therapies bridging neurology and gastroenterology. Mechanisms encompass anatomical, [...] Read more.

The bidirectional communication network between the gut and the brain, known as the gut–brain axis, plays a crucial role in health and disease. This review explores the mechanisms underlying gut–brain interaction disorders and highlights translational therapies bridging neurology and gastroenterology. Mechanisms encompass anatomical, endocrine, humoral, metabolic, and immune pathways, with the gut microbiota exerting profound influence. Clinical evidence links gut microbiota fluctuations to mood disorders, GI disruptions, and neurodevelopmental conditions, emphasizing the microbiome’s pivotal role in shaping brain–gut interactions. Pharmacological therapies such as amitriptyline and selective serotonin reuptake inhibitors modulate neurotransmitter activity, offering relief in functional gastrointestinal disorders like irritable bowel syndrome (IBS). Non-pharmacological interventions like cognitive–behavioral therapy and hypnotherapy address maladaptive thoughts and induce relaxation, alleviating gastrointestinal symptoms exacerbated by stress. Emerging therapies include gut microbiota modulation, dietary interventions, vagus nerve stimulation, and intestinal barrier modulation, offering novel approaches to manage neurological disorders via the gastrointestinal tract. Understanding and harnessing the gut–brain axis holds promise for personalized therapeutic strategies in neurogastroenterology. Full article

(This article belongs to the Section Gastrointestinal Disease)

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14 pages, 7521 KiB

Open AccessArticle

Evaluation of Immunological Response to TLR2 and α-SMA in Crohn’s Disease and Ulcerative Colitis

by Anthea Miller, Giorgia Pia Lombardo, Giuseppina Rizzo, Magdalena Kotanska, Giuseppinella Melita, Socrate Pallio, Alba Migliorato, Giuseppina Cutroneo and Simona Pergolizzi

Gastroenterol. Insights 2024, 15(3), 541-554; https://doi.org/10.3390/gastroent15030040 - 28 Jun 2024

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Abstract

Inflammatory bowel diseases (IBDs) represent multifactorial chronic inflammatory conditions of the gastrointestinal tract. The main IBDs are Crohn’s disease (CD) and ulcerative colitis (UC). CD may cause perforation, stricture or transmural inflammation, which can occur discontinuously in the entire gastrointestinal tract (GIT). UC [...] Read more.

Inflammatory bowel diseases (IBDs) represent multifactorial chronic inflammatory conditions of the gastrointestinal tract. The main IBDs are Crohn’s disease (CD) and ulcerative colitis (UC). CD may cause perforation, stricture or transmural inflammation, which can occur discontinuously in the entire gastrointestinal tract (GIT). UC leads to mucosal inflammation as well as mucosal atrophy in the rectum and the colon. Innate immunity is considered the first line of defense against microbial invasion; among Toll-like receptors, TLR2 is the most important for defense against mycobacterial infection. TLR2 has been reported to have a lot of functions in infectious diseases and in other pathologies, such as chronic and acute inflammatory diseases. Alfa-Smooth Muscle Actin (α-SMA) is an important biomarker in IBDs. All myofibroblasts express α-SMA, which has been found to be upregulated in CD and UC. Paraformaldehyde-fixed intestinal tissues, from patients with CD and patients with UC, were analyzed by immunostaining for TLR2 and α-SMA. Our results showed that, in the samples obtained from UC patients with inflamed mucosa, TLR2-positive epithelial cells concentrated on the mucosal surface and scattered immune cells in the connective tissue; furthermore, numerous α-SMA-positive cells (subepithelial myofibroblasts) were detected in the lamina propria and around glands, while some myofibroblasts co-localizing with α-SMA and TLR2 could be inflammatory macrophages. In CD patients, TLR2-positive enterocytes and α-SMA-positive myofibroblasts in the lamina propria of the villus have been observed. In control samples, a low positivity to α-SMA and TLR2 was observed in subepithelial myofibroblasts and scattered immune cells of the lamina propria. These data showed the recall of α-SMA-positive myofibroblasts during the inflammatory state; in addition, TLR2 expression has been observed to change in the intestinal epithelium in IBDs, demonstrating that alterations in the innate system response may contribute to the pathogenesis of these diseases. Full article

(This article belongs to the Section Gastrointestinal Disease)

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11 pages, 1609 KiB

Open AccessArticle

The Severity of Gastrointestinal Disorders and Autistic-Like Behaviors Could Be Associated with a Selective Humoral Response to Bovine Milk Caseins: A Case Series

by Ángel F. Valenzuela-Zamora, Rocío Campos-Vega, José A. López-Diaz and Abraham Wall-Medrano

Gastroenterol. Insights 2024, 15(3), 530-540; https://doi.org/10.3390/gastroent15030039 - 26 Jun 2024

Viewed by 1247

Abstract

Severe gastrointestinal symptoms (GIS) and food hypersensitivity are tightly associated in young individuals with autism spectrum disorders (ASD). Here, we explored the relationship of GIS (gastrointestinal severity index, ROMA IV criteria, Bristol scale), ASD-like behaviors (Childhood Autism Rating Scale), and certain sociodemographic/clinical traits [...] Read more.

Severe gastrointestinal symptoms (GIS) and food hypersensitivity are tightly associated in young individuals with autism spectrum disorders (ASD). Here, we explored the relationship of GIS (gastrointestinal severity index, ROMA IV criteria, Bristol scale), ASD-like behaviors (Childhood Autism Rating Scale), and certain sociodemographic/clinical traits (epidemiological survey) with serum immunoreactivity (IgG, IgA, IgE titers) towards bovine milk caseins (BMC; by ELISA) and subfractions (by immunoblotting) in thirty-one pediatric patients (~3–15 y, 77% male) with mild-to-severe GIS and ASD-like behaviors. In total, 42%, 25%, and 23% of all participants exhibited no (IgG−/IgA−), mono (IgG+/IgA−), or dual (IgG+/IgA+) immunoreactivity to BMC, respectively; the trend was significantly associated with the severity of the GIS and ASD-like behaviors, regurgitations, and self-reported allergies (OR: 1 → (1.9–3.1) → 13.5–16.0)]. No IgE+ response to BMC was found. Dual responders were α > κ > β-casein, though nonspecific reactivity to other protein fractions was also observed. The IgA+ > IgG+ but not IgE+ response to BMC (mainly α-casein) seems to be related to the severity of GIS and ASD-like behaviors, although a larger number of ASD patients are needed to draw a causal association. Full article

(This article belongs to the Special Issue Recent Advances in the Management of Gastrointestinal Disorders)

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11 pages, 874 KiB

Open AccessArticle

Repeated Previous Transarterial Treatments Negatively Affect Survival in Patients with Hepatocellular Carcinoma Receiving Sorafenib

by Bernardo Stefanini, Luca Ielasi, Andrea Casadei-Gardini, Michele Piscopo, Raffaella Tortora, Lorenzo Lani, Tiziana Pressiani, Vito Sansone, Rodolfo Sacco, Giulia Magini, Matteo Renzulli, Francesco Giuseppe Foschi, Fabio Piscaglia, Francesco Tovoli and Alessandro Granito

Gastroenterol. Insights 2024, 15(3), 519-529; https://doi.org/10.3390/gastroent15030038 - 22 Jun 2024

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Abstract

Background: Transarterial chemoembolisation (TACE) and radioembolisation (TARE) can lead to the deterioration of liver function, especially in cases of a high tumour burden, potentially lessening the benefits of subsequent systemic treatments. We aimed to verify whether a high number of previous transarterial treatments [...] Read more.

Background: Transarterial chemoembolisation (TACE) and radioembolisation (TARE) can lead to the deterioration of liver function, especially in cases of a high tumour burden, potentially lessening the benefits of subsequent systemic treatments. We aimed to verify whether a high number of previous transarterial treatments modified the outcomes of patients who received sorafenib as a frontline systemic treatment. Methods: A retrospective analysis of a large multicenter dataset containing prospectively collected data of sorafenib-treated patients was conducted. Results: Data from 696 patients were analysed, with 139 patients having received >two transarterial procedures before starting sorafenib. A propensity score matched 139 identified pairs of patients. Having received >two locoregional treatments was independently associated with a shorter survival (hazard ratio 1.325, 95% confidence interval 1.018–1.725, p = 0.039). This pattern was confirmed amongst responders to sorafenib, but not in progressors. A trend toward a higher rate of the permanent discontinuation of sorafenib due to liver failure (18.7 vs. 10.8%, p = 0.089) and a lower rate of eligibility for second-line treatments (24.5 vs. 17.3%, p = 0.184) was observed in patients who had received >two transarterial procedures. Conclusions: Repeated endovascular treatments negatively impacted the survival of HCC patients, especially sorafenib-responders. An early switch to systemic therapies should be considered in cases that are unlikely to respond. Full article

(This article belongs to the Section Liver)

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Gastroenterol. Insights, Volume 15, Issue 3 (September 2024) – 13 articles

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