A 56-year-old female suffered from recurrent esophagogastric varices bleeding for 2 years due to cavernous transformation of the portal vein caused by hepatic hydatidosis. Multiple esophageal variceal ligations failed to prevent rebleeding. Transmesenteric vein extrahepatic portosystemic shunt was performed to decrease portal pressure gradient and prevent rebleeding.

Early pancreatic ductal adenocarcinoma (PDAC), including carcinoma in situ (CIS)/high-grade pancreatic intraepithelial neoplasia (PanIN) and very small invasive tumors, is increasingly recognized, but the significance of pancreatic parenchymal atrophy and delayed enhancement remains unsettled. This narrative review summarizes their pathological basis, technical determinants, observer variability, differential diagnoses, and evidence limitations across computed tomography (CT), magnetic resonance imaging (MRI)/magnetic resonance cholangiopancreatography (MRCP), endoscopic ultrasonography (EUS), and regionally variable pancreatic duct-oriented cytology pathways. Parenchymal atrophy should be distinguished from ductal abnormalities such as focal main pancreatic duct stenosis and perilesional branch-duct dilation, which depend heavily on technically optimized MRCP, including high-quality two-dimensional MRCP. Atrophy is a morphologic phenotype with heterogeneous substrates, whereas delayed enhancement more often reflects fibrosis-rich or inflammatory change and is not specific for PDAC, because focal autoimmune pancreatitis may show similar delayed enhancement. Reported prevalence and diagnostic value vary according to cohort spectrum, modality, phase definition, reader blinding, cytologic verification, and hindsight bias. Current evidence supports these signs as context-dependent clues, not diagnostic thresholds or management algorithms. Prospective pathology-linked studies with standardized protocols are needed.

Intestinal fibrosis is a common and severe complication in the progression of inflammatory bowel disease (IBD). Its pathological essence lies in the excessive synthesis and abnormal deposition of extracellular matrix (ECM) components within the intestinal tissue, leading to structural remodeling and dysfunction of the intestinal wall. As the disease progresses, fibrosis is primarily characterized by the pathological thickening of the muscularis propria, which subsequently triggers irreversible structural damage, such as intestinal strictures, severely impacting patients' quality of life and prognosis. Currently, clinical interventions for intestinal fibrosis are relatively limited, mainly relying on pharmacotherapy and surgical resection. However, existing drugs primarily focus on controlling the inflammatory response in IBD rather than directly targeting the fibrotic process, making it difficult to effectively block or reverse ECM accumulation. Although surgery can temporarily relieve obstruction, it is associated with a high postoperative recurrence rate and fails to fundamentally intervene in the pathological mechanisms of fibrosis. Therefore, a deeper understanding of the mechanisms underlying the initiation and progression of intestinal fibrosis is of great significance for developing specific anti-fibrotic therapeutic strategies and improving long-term patient outcomes. This review aims to systematically summarize the cellular and molecular mechanisms of intestinal fibrosis, with a focus on the roles of fibroblast activation, epithelial-mesenchymal transition, and immune microenvironment regulation in the fibrotic process. The goal is to provide a theoretical basis and novel research insights for the subsequent development of targeted drugs and the optimization of clinical treatment strategies.