An 89-year-old woman presented to the hospital with a chief complaint of fever and hematuria. Computed tomography revealed left hydronephrosis due to bladder cancer, along with common bile duct stones and marked dilation of the bile duct. Endoscopic ultrasonography-guided choledochoduodenostomy was attempted, but the common bile duct could not be visualized in close proximity to the duodenum. Instead, due to the gastroduodenal deformity, the common bile duct was in close proximity with the gastric antrum; therefore, the common bile duct was selected for puncture from the gastric antrum using a 19-gauge needle. However, the gastric wall and scope became separated during the dilation maneuver, making it difficult to dilate the fistula using a 6-Fr dilator and a 4-mm-diameter balloon dilation catheter, although it was possible to insert a tapered catheter with a 3.5-Fr tip under a 0.025-inch guidewire into the bile duct. The use of a stiff 0.035-inch guidewire allowed blunt dilation up to 9-Fr with a dilator, while simultaneously maintaining the distance between the gastric wall and the scope. Using this method, a 10-mm-diameter, 12-cm-long, partially covered metal stent was deployed successfully between the common bile duct and the posterior wall of the gastric antrum. Endoscopic ultrasonography-guided choledochogastrostomy (EUS-CGS) risks separating the gastrointestinal and biliary tracts during or after the procedure. In this case, the stiff guidewire enabled successful completion of the biliary procedures; thus, this guidewire can be used to safely manage difficult cases of EUS-CGS involving dilation of the fistula and stent deployment.

Autoimmune pancreatitis (AIP), which is considered the pancreatic expression of a systemic immunoglobulin G4-related disease, is characterized by excessive infiltration of plasmacytes bearing immunoglobulin G4 and a unique form of fibrosis in multiple organs. This relatively new disease entity has garnered great attention from clinicians, but its pathophysiology remains poorly understood. Recent discoveries indicate that plasmacytoid dendritic cell activation followed by robust production of type I interferon and interleukin-33 plays a key role in driving chronic fibro-inflammatory responses in both murine and human AIP. Furthermore, the compositional alterations in the gut microbiota, known as intestinal dysbiosis, triggered plasmacytoid dendritic cell-driven pathogenic type I interferon responses. Intestinal dysbiosis is associated with a breakdown in intestinal barrier function; thus, we examined whether the latter condition affects the development of experimental AIP. Our recent research has revealed that intestinal barrier disruption worsens experimental AIP by facilitating the translocation of pathogenic bacteria, such as Staphylococcus sciuri, to the pancreas from the gut. These results indicate the “gut-pancreas axis” underlies the immunopathogenesis of AIP, and the maintenance of intestinal barrier integrity can prevent the worsening of AIP by inhibiting pancreatic colonization by harmful gut bacteria. In this mini review, the interactions between AIP development and gut microbiota are discussed with the aim of providing useful information not only for researchers but also for clinicians.

Autoimmune pancreatitis (AIP), which is considered the pancreatic expression of a systemic immunoglobulin G4-related disease, is characterized by excessive infiltration of plasmacytes bearing immunoglobulin G4 and a unique form of fibrosis in multiple organs. This relatively new disease entity has garnered great attention from clinicians, but its pathophysiology remains poorly understood. Recent discoveries indicate that plasmacytoid dendritic cell activation followed by robust production of type I interferon and interleukin-33 plays a key role in driving chronic fibro-inflammatory responses in both murine and human AIP. Furthermore, the compositional alterations in the gut microbiota, known as intestinal dysbiosis, triggered plasmacytoid dendritic cell-driven pathogenic type I interferon responses. Intestinal dysbiosis is associated with a breakdown in intestinal barrier function; thus, we examined whether the latter condition affects the development of experimental AIP. Our recent research has revealed that intestinal barrier disruption worsens experimental AIP by facilitating the translocation of pathogenic bacteria, such as Staphylococcus sciuri, to the pancreas from the gut. These results indicate the “gut-pancreas axis” underlies the immunopathogenesis of AIP, and the maintenance of intestinal barrier integrity can prevent the worsening of AIP by inhibiting pancreatic colonization by harmful gut bacteria. In this mini review, the interactions between AIP development and gut microbiota are discussed with the aim of providing useful information not only for researchers but also for clinicians.

Autoimmune pancreatitis (AIP), which is considered the pancreatic expression of a systemic immunoglobulin G4-related disease, is characterized by excessive infiltration of plasmacytes bearing immunoglobulin G4 and a unique form of fibrosis in multiple organs. This relatively new disease entity has garnered great attention from clinicians, but its pathophysiology remains poorly understood. Recent discoveries indicate that plasmacytoid dendritic cell activation followed by robust production of type I interferon and interleukin-33 plays a key role in driving chronic fibro-inflammatory responses in both murine and human AIP. Furthermore, the compositional alterations in the gut microbiota, known as intestinal dysbiosis, triggered plasmacytoid dendritic cell-driven pathogenic type I interferon responses. Intestinal dysbiosis is associated with a breakdown in intestinal barrier function; thus, we examined whether the latter condition affects the development of experimental AIP. Our recent research has revealed that intestinal barrier disruption worsens experimental AIP by facilitating the translocation of pathogenic bacteria, such as Staphylococcus sciuri, to the pancreas from the gut. These results indicate the “gut-pancreas axis” underlies the immunopathogenesis of AIP, and the maintenance of intestinal barrier integrity can prevent the worsening of AIP by inhibiting pancreatic colonization by harmful gut bacteria. In this mini review, the interactions between AIP development and gut microbiota are discussed with the aim of providing useful information not only for researchers but also for clinicians.

An 89-year-old woman presented to the hospital with a chief complaint of fever and hematuria. Computed tomography revealed left hydronephrosis due to bladder cancer, along with common bile duct stones and marked dilation of the bile duct. Endoscopic ultrasonography-guided choledochoduodenostomy was attempted, but the common bile duct could not be visualized in close proximity to the duodenum. Instead, due to the gastroduodenal deformity, the common bile duct was in close proximity with the gastric antrum; therefore, the common bile duct was selected for puncture from the gastric antrum using a 19-gauge needle. However, the gastric wall and scope became separated during the dilation maneuver, making it difficult to dilate the fistula using a 6-Fr dilator and a 4-mm-diameter balloon dilation catheter, although it was possible to insert a tapered catheter with a 3.5-Fr tip under a 0.025-inch guidewire into the bile duct. The use of a stiff 0.035-inch guidewire allowed blunt dilation up to 9-Fr with a dilator, while simultaneously maintaining the distance between the gastric wall and the scope. Using this method, a 10-mm-diameter, 12-cm-long, partially covered metal stent was deployed successfully between the common bile duct and the posterior wall of the gastric antrum. Endoscopic ultrasonography-guided choledochogastrostomy (EUS-CGS) risks separating the gastrointestinal and biliary tracts during or after the procedure. In this case, the stiff guidewire enabled successful completion of the biliary procedures; thus, this guidewire can be used to safely manage difficult cases of EUS-CGS involving dilation of the fistula and stent deployment.

Autoimmune pancreatitis (AIP), which is considered the pancreatic expression of a systemic immunoglobulin G4-related disease, is characterized by excessive infiltration of plasmacytes bearing immunoglobulin G4 and a unique form of fibrosis in multiple organs. This relatively new disease entity has garnered great attention from clinicians, but its pathophysiology remains poorly understood. Recent discoveries indicate that plasmacytoid dendritic cell activation followed by robust production of type I interferon and interleukin-33 plays a key role in driving chronic fibro-inflammatory responses in both murine and human AIP. Furthermore, the compositional alterations in the gut microbiota, known as intestinal dysbiosis, triggered plasmacytoid dendritic cell-driven pathogenic type I interferon responses. Intestinal dysbiosis is associated with a breakdown in intestinal barrier function; thus, we examined whether the latter condition affects the development of experimental AIP. Our recent research has revealed that intestinal barrier disruption worsens experimental AIP by facilitating the translocation of pathogenic bacteria, such as Staphylococcus sciuri, to the pancreas from the gut. These results indicate the “gut-pancreas axis” underlies the immunopathogenesis of AIP, and the maintenance of intestinal barrier integrity can prevent the worsening of AIP by inhibiting pancreatic colonization by harmful gut bacteria. In this mini review, the interactions between AIP development and gut microbiota are discussed with the aim of providing useful information not only for researchers but also for clinicians.

An 89-year-old woman presented to the hospital with a chief complaint of fever and hematuria. Computed tomography revealed left hydronephrosis due to bladder cancer, along with common bile duct stones and marked dilation of the bile duct. Endoscopic ultrasonography-guided choledochoduodenostomy was attempted, but the common bile duct could not be visualized in close proximity to the duodenum. Instead, due to the gastroduodenal deformity, the common bile duct was in close proximity with the gastric antrum; therefore, the common bile duct was selected for puncture from the gastric antrum using a 19-gauge needle. However, the gastric wall and scope became separated during the dilation maneuver, making it difficult to dilate the fistula using a 6-Fr dilator and a 4-mm-diameter balloon dilation catheter, although it was possible to insert a tapered catheter with a 3.5-Fr tip under a 0.025-inch guidewire into the bile duct. The use of a stiff 0.035-inch guidewire allowed blunt dilation up to 9-Fr with a dilator, while simultaneously maintaining the distance between the gastric wall and the scope. Using this method, a 10-mm-diameter, 12-cm-long, partially covered metal stent was deployed successfully between the common bile duct and the posterior wall of the gastric antrum. Endoscopic ultrasonography-guided choledochogastrostomy (EUS-CGS) risks separating the gastrointestinal and biliary tracts during or after the procedure. In this case, the stiff guidewire enabled successful completion of the biliary procedures; thus, this guidewire can be used to safely manage difficult cases of EUS-CGS involving dilation of the fistula and stent deployment.

Background: /Aim: The aim of this study was to compare the therapeutic efficacy of ablation and surgery in solitary hepatocellular carcinoma (HCC) measuring ≤5 cm with a large HCC cohort database. Methods: The study included consecutive 2,067 patients with solitary HCC who were treated with either ablation (n=1,248) or surgery (n=819). Th e patients were divided into three groups based on the tumor size and compared the outcomes of the two therapies using propensity score matching. Results: No significant difference in recurrence-free survival (RFS) or overall survival (OS) was found between surgery and ablation groups for tumors measuring ≤2 cm or >2 cm but ≤3 cm. For tumors measuring >3 cm but ≤5 cm, RFS was significantly better with surgery than with ablation (3.6 and 2.0 years, respectively, P=0.0297). However, no significant difference in OS was found between surgery and ablation in this group (6.7 and 6.0 years, respectively, P=0.668). Conclusion The study suggests that surgery and ablation can be equally used as a treatment for solitary HCC no more than 3 cm in diameter. For HCCs measuring 3-5 cm, the OS was not different between therapies; thus, ablation and less invasive therapy can be considered a treatment option; however, special caution should be taken to prevent recurrence.

Background/Aims: This study aimed to evaluate the safety and efficacy of continuous propofol infusion for anesthesia during endoscopic ultrasonography (EUS). Methods: A total of 427 consecutive patients who underwent EUS between May 2018 and February 2019 were enrolled in this study. The patients were divided into two propofol infusion groups: continuous (n=207) and intermittent (n=220). The following parameters were compared: (1) propofol dose, (2) respiratory and circulatory depression, (3) body movement requiring discontinuation of the examination, (4) awakening score, and (5) patient satisfaction. Results: The median total maintenance dose of propofol was significantly higher in the continuous group than in the intermittent group (160.0 mg vs. 130.0 mg, respectively); however, the reduction in SpO2 was significantly lower in the continuous group (2.9% vs. 13.2%). Body movements occurred less frequently in the continuous group than in the intermittent group (40.1% vs. 49.5%, respectively). The rate of complete awakening was significantly higher in the continuous group than in the intermittent group. Finally, there was a significant difference in the percentage of patients who answered “absolutely yes” when asked about receiving EUS again: 52.7% in the continuous group vs. 34.3% in the intermittent group. Conclusions Continuous infusion resulted in stable sedation and reduced propofol-associated risks.

Background/Aims: This study aimed to evaluate the safety and efficacy of continuous propofol infusion for anesthesia during endoscopic ultrasonography (EUS). Methods: A total of 427 consecutive patients who underwent EUS between May 2018 and February 2019 were enrolled in this study. The patients were divided into two propofol infusion groups: continuous (n=207) and intermittent (n=220). The following parameters were compared: (1) propofol dose, (2) respiratory and circulatory depression, (3) body movement requiring discontinuation of the examination, (4) awakening score, and (5) patient satisfaction. Results: The median total maintenance dose of propofol was significantly higher in the continuous group than in the intermittent group (160.0 mg vs. 130.0 mg, respectively); however, the reduction in SpO2 was significantly lower in the continuous group (2.9% vs. 13.2%). Body movements occurred less frequently in the continuous group than in the intermittent group (40.1% vs. 49.5%, respectively). The rate of complete awakening was significantly higher in the continuous group than in the intermittent group. Finally, there was a significant difference in the percentage of patients who answered “absolutely yes” when asked about receiving EUS again: 52.7% in the continuous group vs. 34.3% in the intermittent group. Conclusions Continuous infusion resulted in stable sedation and reduced propofol-associated risks.