Portal hypertension from chronic liver disease leads to the formation of collateral blood vessels called spontaneous portosystemic shunts (SPSS). These shunts may form from existing vessels or through neo-angiogenesis. Their location affects clinical outcomes due to varying risks and complications. This review summarizes current knowledge on SPSS, covering their clinical impact and management strategies. Recent data suggest that SPSS increases the risk of variceal bleeding, regardless of shunt size. The size of the shunt is crucial in the rising incidence of hepatic encephalopathy (HE) linked to SPSS. It also increases the risk of portopulmonary hypertension and portal vein thrombosis. Detecting and assessing SPSS rely on computed tomography (CT) and magnetic resonance imaging. CT enables precise measurements and the prediction of cirrhosis progression. Management focuses on liver disease progression and SPSS-related complications, like HE, variceal bleeding, and portopulmonary hypertension. Interventional radiology techniques such as balloon-occluded, plug-assisted, and coil-assisted retrograde transvenous obliteration play a pivotal role. Surgical options are rare but are considered when other methods fail. Liver transplantation (LT) often resolves SPSS. Intraoperative SPSS ligation is still recommended in patients at high risk for developing HE or graft hypoperfusion.

Inflammatory bowel disease (IBD) represents heterogeneous and relapsing intestinal conditions with a severe impact on the quality of life of individuals and a continuously increasing prevalence. In recent years, the development of sequencing technology has provided new means of exploring the complex pathogenesis of IBD. An ideal solution is represented by the approach of precision medicine that investigates multiple cellular and molecular interactions, which are tools that perform a holistic, systematic, and impartial analysis of the genomic, transcriptomic, proteomic, metabolomic, and microbiomics sets. Hence, it has led to the orientation of current research towards the identification of new biomarkers that could be successfully used in the management of IBD patients. Multi-omics explores the dimension of variation in the characteristics of these diseases, offering the advantage of understanding the cellular and molecular mechanisms that affect intestinal homeostasis for a much better prediction of disease development and choice of treatment. This review focuses on the progress made in the field of prognostic and predictive biomarkers, highlighting the limitations, challenges, and also the opportunities associated with the application of genomics and epigenomics technologies in clinical practice.

Background: Although the current strategy in ulcerative colitis (UC) focuses on achieving endoscopic healing to improve long‐term outcomes, patients with persistent microscopic inflammation or intestinal barrier dysfunction remain at increased risk of relapse. Objective: We evaluated whether structural and functional abnormalities of the ileal and colonic mucosa assessed by probe‐based Confocal laser Endomicroscopy (pCLE) could predict the loss of therapeutic targets. Methods: The prospective single‐center study included 81 UC patients in clinical and endoscopic remission monitored for 24 months. At baseline, barrier dysfunction and histological inflammation (HI) were assessed through colonoscopy with pCLE and targeted biopsies from the terminal ileum, ascending colon, sigmoid, and rectum. Clinical evaluations were performed every 3 months. Results: The main predictors of loss of endoscopic remission were altered colonic permeability (Odds ratio OR = 3.85, 95% confidence interval CI 1.25–11.77, p = 0.018) and HI detected by pCLE (OR = 6.04, 95% CI 1.89–19.31, p = 0.002). Survival analysis demonstrated an increased risk of clinical relapse in patients with an altered barrier in the terminal ileum (Hazard ratio HR = 6.01, 95% CI 3.08–16.38, p < 0.001) or colon (HR = 6.51, 95% CI 2.08–17.21, p < 0.001). Persistent microscopic inflammation (Enhance index > 1) was significantly associated with unfavorable clinical outcome (HR = 3.39, 95% CI 1.23–8.38, p = 0.018). None of the 29 patients diagnosed with triple healing (histological healing associated with intact ileal and colonic permeability) at inclusion experienced relapse. Conclusions: Morphological and functional evaluation using pCLE offers superior prognostic value and is emerging as a possible therapeutic target for the prevention of clinical and endoscopic relapses in UC.

Background and Objectives: Current research approaches focusing on the human gut microbiota require complex in vitro systems that could provide sufficient viability and similarity with the conditions provided by the human intestine. As critical physiological functions, such as metabolic and inflammatory modulation, are associated with gut microbiota activity, complex host–microbiota interactions represent a pivotal new direction for therapeutic and nutritional interventions. However, there are several limitations to the current development of advanced in vitro models. Materials and Methods: A systematic review was performed according to the PRISMA guidelines for data collection and interpretation. Results: This manuscript summarizes the most advanced in vitro approaches for studying the gut microbiota, including batch fermentation models, dynamic fermentation models, and state-of-the-art technologies, such as organoids and gut-on-a-chip platforms. Each model offers beneficial study backgrounds, advantages, limitations, and the capacity to replicate the physiological complexity of the intestinal environment. However, due to the increased heterogeneity of the reported models, there is an urgent need for standardization. In this way, coherent regulatory frameworks are needed to guide the development and application of in vitro models. Conclusions: By consolidating knowledge and critically addressing current challenges, this study contributes to gut microbiota research by providing a direction for ethical, precise, and high-impact scientific studies.

Novel oncological therapies substantially improved the prognosis of cancer patients. Immunotherapies (immune checkpoint inhibitors) and targeted therapies (tyrosine kinase inhibitors) represent innovative strategies, which have revolutionized cancer patient’s approaches. However, the new treatments may bring additional adverse effects, therefore right selection, close monitoring, and appropriate clinical decisions in the event of a complication are of upmost importance in these patients' management. We present an elderly male patient undergoing treatment with alectinib - anaplastic lymphoma kinase (ALK) inhibitor for metastatic non-small cell lung cancer, who was diagnosed with acute liver failure by drug-induced liver injury, five months after the start of the therapy. After the other possible causes of hepatocellular injury were excluded, the drug was discontinued. Using corticotherapy and supportive measures, the evolution of the patient was favorable. Up to this moment, data showed that alectinib was less associated with liver function abnormalities compared to other ALK inhibitors, however most commonly of mild or moderate grade of severity, especially in the first two months of treatment. The case we report presented acute onset liver failure, with a relatively late occurrence during alectinib therapy. Timely recognition may improve patients’ prognosis, and monitoring must be carried out rigorously. Awareness and effective interdisciplinary communication among medical specialties play a pivotal role in the comprehensive care of cancer patients.

Background: Over the last two decades, therapy for benign esophageal strictures has shifted from empirical dilatations and surgery to evidence-based and complex endoscopic and surgical procedures, aiming to achieve long-term esophageal patency. Aim: The purpose of our study is to provide descriptive evidence regarding the appropriate tailored medical, endoscopic, and surgical management of benign esophageal strictures. Methods: This retrospective study includes patients with benign esophageal strictures; the data collected encompass the complete patient profiles, detailed etiologic and anatomic workups of the strictures, comprehensive imaging, as well as management and follow-up details. Technical and clinical success rates, adverse events, stricture patency, and the need for additional therapy have been evaluated. Results: Most of the strictures (80.2%) were complex, requiring advanced techniques for management. The primary treatment involved endoscopic dilation, performed with Savary-Gillard bougie dilators in 76.7% of cases and pneumatic balloon dilators in 23.3% of cases. Clinical success was achieved in 95.3% of patients, with a significant improvement in the Ogilvie dysphagia score. Patients with caustic strictures required repeated dilations over the years, compared to shorter intervals for peptic strictures. Adverse events were minimal (e.g., perforation 2.3% and bleeding 4.7%) and managed predominantly endoscopically. Refractory strictures (16.3%) required advanced interventions, including fully covered self-expandable metallic stents (fc-SEMS) and corticosteroid injections. Conclusions: Both our data and the current literature support the use of tailored endoscopic strategies as the first-choice options for managing benign esophageal strictures. Our results strongly suggest against one-size-fits-all therapeutic alternatives.