Over the past decade， with the continuous development of direct cholangioscopy and pancreatoscopy， they have been widely used in the diagnosis and treatment of various pancreaticobiliary diseases. In October 2025， United European Gastroenterology released the consensus recommendations for direct cholangioscopy and pancreatoscopy， including general recommendations for direct cholangioscopy and pancreatoscopy and specific recommendations for biliopancreatic duct stones， biliary strictures， and other indications， with an aim to provide standard guidance for the clinical diagnosis and treatment of pancreaticobiliary diseases. This article gives an excerpt of the key recommendations in the consensus.

Objective: To analyze the temporal changes in lipid levels in patients following acute pancreatitis(AP) and explore the factors associated with post-AP serum triglyceride( TG) level changes. Methods: Patients diag- nosed with AP were included in this study. Clinical data were collected retrospectively , and lipid profile data from follow-up visits after discharge were tracked. Kaplan-Meier(K-M) curves were used to stratify follow-up duration ,iodine content detection. Thyroid volume was measured using a fully digital ultrasound imaging system , and goiter prevalence was calculated. Results: A total of 141 patients with 306 follow⁃up visits were included. Spearman correlation analysis showed a mild increase in lipid levels over time post⁃discharge : TG( r = 0. 159 , P = 0. 005) , total cholesterol(TC)( r = 0. 231 , P < 0. 000 1) , high⁃density lipoprotein cholesterol( HDL⁃C) ( r = 0. 181 , P = 0. 002) , and apolipoproteinA1 ( ApoA1) ( r = 0. 371 , P <0. 000 1) . In the univariate linear mixed model , male gender(β = 0. 160 ,P = 0. 007) , body mass index(BMI) (β= 0. 017 , P = 0. 007) , diabetes history(β = 0. 138 , P = 0. 030) , smoking history(β = 0. 166 ,P = 0. 004) , and recurrent AP(β = 0. 119 , P = 0. 029) were significantly associated with Lg(TG) levels (P < 0. 05) . In the multivariate model , BMI( β = 0. 019 , P = 0. 042) , smoking history ( β = 0. 155 , P = 0. 049 ) , and recurrent AP( β =0. 148 , P = 0. 032) remained significantly positively correlated with changes in Lg(TG) levels after AP , albeit with a low correlation strength (r < 0. 200) . Conclusion Lipid levels , including TG , TC , HDL⁃C and ApoA1 , tend to increase over time in AP patients after discharge , with this trend being more pronounced in those with hypertriglyceridemic acute pancreatitis. Post⁃AP TG levels are significantly influenced by BMI at the time of onset , smoking history and recurrent AP.

Diabetes of the exocrine pancreas(DEP)used to be called pancreatic diabetes,pancreatogenic diabetes or type 3c diabetes mellitus.Currently,the incidence of DEP is higher than that of type 1 diabetes mellitus.The pathogenesis and clinical manifestations of DEP are related to primary pancreatic diseases.In terms of management,we need to consider both pancreatic endocrine and exocrine functions,and comprehensively treat diabetes mellitus and primary pancreatic diseases.By now,there has been no guideline related to DEP;its diagnostic criteria,differentiation with type 2 diabetes mellitus,and selection of hypoglycemic programs are challenges in clinical practice.This article reviews the clinical studies related to DEP,and summarizes the evolution of its terminology,pathogenesis,clinical manifestations,complications,diagnosis,treatment and management.

Fibrosis is a pathological condition characterized by the excessive deposition of extracellular matrix due to the imbalance between injury and repair.It can affect multiple organs,including the heart,lungs,liver,kidneys,and pancreas.The progression of fibrosis is usually slow and difficult to reverse,and it can severely impair organ functions.In industrialized countries,deaths caused by fibrosis account for up to 45％,resulting in a tremendous disease burden.Thus,there is an urgent need for drugs that can reverse or delay the progression of fibrosis.In recent years,remarkable progress has been made in the research on the pathogenesis of fibrosis in different organs,and relevant drugs targeting fibrosis are also under active development.This article briefly summarizes the drugs currently marketed and drugs at the clinical trial stage for treating fibrosis.

The transformation from inflammation to cancer is a complex pathological process, in which the inflammatory state progresses to the formation of malignant tumors. Chronic pancreatitis (CP) is a progressively inflammatory and fibrosing disease, predominantly featuring acinar cell atrophy owing to the cellular damage and fibrosis of the pancreatic parenchyma. This review centers on elucidating how prolonged exposure to a chronic inflammatory environment prompts adaptive changes in acinar cells, which may ultimately lead to their conversion into cancerous cells. By delving into the pivotal role of acinar-to-ductal metaplasia, this article investigates the multi-stage pathway of CP progression into pancreatic cancer, as well as the underlying molecular regulatory networks. We aim to light on the profound mechanisms of CP's inflammation-driven carcinogenic transformation, and thus provide a scientific foundation for devising innovative preventive strategies and therapeutic interventions targeted at mitigating or halting this lethal conversion process.

Objective:To analyze the mutation spectrum and regional distribution of susceptibility pathogenic genes in Chinese chronic pancreatitis (CP) patients.Methods:A retrospective analysis was conducted on 1 758 sporadic CP patients who underwent gene sequencing for pathogenic mutations of four major susceptibility genes ( SPINK1, PRSS1, CTRC, and CFTR) at the First Affiliated Hospital of Naval Medical University from December 2010 to November 2022. Pathogenic mutations of four major susceptibility genes were detected by using the next-generation sequencing, and both known and novel pathogenic mutations were validated by Sanger sequencing. The ethnic and regional distributions of pathogenic mutations across different ethnic groups were compared. The ArcMap 10.7 software was used to provide the distribution map of common CP pathogenic mutations in China, and regional differences of these mutations were assessed. According to seven major geographical regions in China, we also evaluated the enrichment differences of CP pathogenic mutations in North China region, Northeast China region, East China region, Central China region, South China region, Southwest China region, and Northwest China region. Results:Among 1 758 CP patients, 50.23% (883/1 758) carried pathogenic mutations, and the SPINK1 pathogenic mutations were most predominated (39.31%). Among them, c.194+2T>C mutations accounted for 94.21% of all SPINK1 mutations. 32.59% (573/1 758) of patients carried single heterozygous mutation of one susceptibility gene, and 4.61% carried homozygous mutation of SPINK1 c.194+2T>C. There was no statistically significant difference on the overall pathogenic mutation carrying rate between Han and ethnic minority patients, whereas the mutation carrying rate of SPINK1 c.194+2T>C was significantly higher among Han patients than among ethnic minorities (37.48% vs 20.00%, P<0.05). Among 31 provinces and cities, the mutation carrying rate of CP patients in Tianjin, Guangdong, Yunnan, Hubei and Anhui were all higher than 60.00%. The SPINK1 mutations accounted for the highest proportion of pathogenic mutations across all provinces (33.33% to 61.54%), and SPINK1 c.194+2T>C was the most prevalent mutation. The mutation carrying rate of SPINK1 c.194+2T>C was higher than 40.00% in Jilin, Liaoning, Tianjin, Anhui, Jiangxi, Hubei, Henan, and Guangdong. Distribution analysis of seven geographic regions showed that the overall carrying rate of pathogenic mutations in North China region was significantly lower than that in Central China region (represented by Henan, Hubei, and Hunan; 38.38% vs 58.15%), and the differences were statistically significant ( P<0.05). Additionally, although the carrying rate of SPINK1 c.194+2T>C was highest in Central (41.85%) and Northeast China region (38.78%), no significant differences were found among different regions. Conclusions:Genetic factors was the main etiology of CP in China, with SPINK1 c.194+2T>C mutations being most prevalent. The carrying rates of common susceptibility genes of CP were highest in Central China region as well as SPINK1 c.194+2T>C mutation.

Objective:To analyze the mutation spectrum and regional distribution of susceptibility pathogenic genes in Chinese chronic pancreatitis (CP) patients.Methods:A retrospective analysis was conducted on 1 758 sporadic CP patients who underwent gene sequencing for pathogenic mutations of four major susceptibility genes ( SPINK1, PRSS1, CTRC, and CFTR) at the First Affiliated Hospital of Naval Medical University from December 2010 to November 2022. Pathogenic mutations of four major susceptibility genes were detected by using the next-generation sequencing, and both known and novel pathogenic mutations were validated by Sanger sequencing. The ethnic and regional distributions of pathogenic mutations across different ethnic groups were compared. The ArcMap 10.7 software was used to provide the distribution map of common CP pathogenic mutations in China, and regional differences of these mutations were assessed. According to seven major geographical regions in China, we also evaluated the enrichment differences of CP pathogenic mutations in North China region, Northeast China region, East China region, Central China region, South China region, Southwest China region, and Northwest China region. Results:Among 1 758 CP patients, 50.23% (883/1 758) carried pathogenic mutations, and the SPINK1 pathogenic mutations were most predominated (39.31%). Among them, c.194+2T>C mutations accounted for 94.21% of all SPINK1 mutations. 32.59% (573/1 758) of patients carried single heterozygous mutation of one susceptibility gene, and 4.61% carried homozygous mutation of SPINK1 c.194+2T>C. There was no statistically significant difference on the overall pathogenic mutation carrying rate between Han and ethnic minority patients, whereas the mutation carrying rate of SPINK1 c.194+2T>C was significantly higher among Han patients than among ethnic minorities (37.48% vs 20.00%, P<0.05). Among 31 provinces and cities, the mutation carrying rate of CP patients in Tianjin, Guangdong, Yunnan, Hubei and Anhui were all higher than 60.00%. The SPINK1 mutations accounted for the highest proportion of pathogenic mutations across all provinces (33.33% to 61.54%), and SPINK1 c.194+2T>C was the most prevalent mutation. The mutation carrying rate of SPINK1 c.194+2T>C was higher than 40.00% in Jilin, Liaoning, Tianjin, Anhui, Jiangxi, Hubei, Henan, and Guangdong. Distribution analysis of seven geographic regions showed that the overall carrying rate of pathogenic mutations in North China region was significantly lower than that in Central China region (represented by Henan, Hubei, and Hunan; 38.38% vs 58.15%), and the differences were statistically significant ( P<0.05). Additionally, although the carrying rate of SPINK1 c.194+2T>C was highest in Central (41.85%) and Northeast China region (38.78%), no significant differences were found among different regions. Conclusions:Genetic factors was the main etiology of CP in China, with SPINK1 c.194+2T>C mutations being most prevalent. The carrying rates of common susceptibility genes of CP were highest in Central China region as well as SPINK1 c.194+2T>C mutation.

Dyspepsia is a common group of clinical symptoms and can be classified into organic and functional dyspepsia. Patients with chronic pancreatitis （CP） often have the symptoms of dyspepsia such as fatty diarrhea， abdominal distention， and abdominal pain， and most patients have pancreatic exocrine insufficiency （PEI）， which belongs to organic dyspepsia. In clinical practice， the diagnosis of PEI and dyspepsia requires a comprehensive assessment of clinical manifestations， nutritional status， and pancreatic exocrine function， and an individualized treatment regimen should be developed based on such factors. However， some patients with normal exocrine function may have the symptoms of dyspepsia， and the diagnosis and treatment of such patients are still difficulties in clinical practice. This article reviews the advances in the diagnosis and treatment of dyspepsia in CP patients.

With the increase in global life expectancy, the incidence of neurodegenerative diseases is increasing year by year. Studies have confirmed that patients with different types of neurodegenerative diseases have circadian rhythm disorder and gut microbiota dysregulation. The occurrence of neurodegenerative diseases and circadian rhythm disorder are mutually causal, and in this causal relationship, gut microbiota may play an important role. Gut microbiota affects the communication between gut and brain through "microbiota ⁃ gut ⁃ brain axis", and can affect neural development. Gut microbiota dysregulation can increase the risk of neurodegenerative diseases. At the same time, the diurnal fluctuation of gut microbiota themselves is also regulated by the host biological clock. This article reviewed the progress of research on relationship of circadian rhythm disorder and gut microbiota involved in neurodegenerative diseases.

Objective:To identify the risk factors and develop nomogram for idiopathic chronic pancreatitis (ICP) patients with common bile duct stricture (CBDS).Methods:The clinical data of 1 633 ICP patients admitted to the Department of Gastroenterology of First Affiliated Hospital of Naval Medical University from January 2000 to December 2013 were collected retrospectively and prospectively. The patients were classified into CBDS group ( n=259) and non-CBDS group ( n=1 374) according to whether CBDS occurred. The cumulative incidence of CBDS after the onset and diagnosis of ICP were calculated by Kaplan-Meier method. After excluding patients who had developed CBDS before/or at the diagnosis of ICP, the remaining patients were randomly divided into the training set and the validation set. The univariate and multivariate Cox proportional hazards regression analysis were used to establish a risk predicting nomogram for CBDS after ICP onset. Its clinical application value was evaluated through the consistency index (C index). Results:15.9%(259/1 633) of patients developed CBDS after the onset of ICP. The cumulative incidence of CBDS at 3, 5, and 10 years after the onset of ICP was 9.6% (95% CI 0.082-0.111), 11.2% (95% CI 0.097-0.129) and 16.2% (95% CI 0.142-0.184), respectively. 9.4%(143/1 517) of patients developed CBDS after the diagnosis of ICP. The cumulative incidence of CBDS at 3, 5, and 10 years after the diagnosis of ICP was 8.3% (95% CI 0.069-0.099), 8.9% (95% CI 0.074-0.105) and 13.3% (95% CI 0.110-0.162), respectively. Univariate analysis found that factors including gender, age at onset of ICP, age at diagnosis of ICP, being adolescents at onset of ICP, smoking history, alcohol intake, initial manifestations, pancreatic duct stones, fatty steatorrhea, main pancreatic duct (MPD) morphology and pain type were significantly different between CBDS group and non-CBDS group. Multivariate analysis showed that male ( HR 2.134, 95% CI 1.336-3.408), age at diagnosis of ICP ( HR 1.038, 95% CI 1.024-1.052), first manifestation (pancreatic abdominal pain) and main duct morphology (complex lesion) were identified as independent risk factors for CBDS in ICP patients. A nomogram for predicting CBDS after ICP diagnosis was established based on the above four variables. The nomogram had a C-index of 0.740 (95% CI 0.700-0.790) for internal validation in the training set and 0.650 (95% CI 0.570-0.730) for external validation in the validation set. Conclusions:The nomogram established in this study can evaluate the risk of developing CBDS in ICP patients, benefit the early diagnosis and timely intervention of CBDS in clinical practice, and prevent potential related complications.