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A man in his 50s underwent endoscopic submucosal dissection (ESD) for a rectal tumor measuring 28 mm. He was not taking any antithrombotic medication. On the third, 11th, 18th, and 24th days after the procedure, bleeding was observed from different areas of the ulcer bed margin and was managed with hemostatic forceps. Despite epithelization and ulcer healing, delayed bleeding recurred, with the fourth episode being severe, marked by significant bleeding and a decrease in serum hemoglobin level. Although clip closure of the ulcer bed and the application of PuraStat were attempted, they failed to prevent recurrent bleeding. Therefore, polyglycolic acid (PGA) sheets were applied to the ulcer bed during the fourth episode. Four days later, PGA sheets remained on the ulcer bed without any signs of bleeding, and healing continued. No further bleeding episodes occurred. The fact that continuous hemostasis was achieved after application of the PGA sheet without complications suggested that this approach may be an option in future cases of refractory delayed bleeding after rectal ESD.

T. Iida, H. Chiba, A. Hirohata, et al., “Electrolyte Depletion Syndrome due to a 28 cm Rectal Villous Tumor: Successful Endoscopic Resection of One of the Largest Tumors Reported to Date—A Case Report,” DEN Open 6 (2026): e70197.

In paragraph 5 of the “Case Report” section, the statement: “The depth of submucosal invasion was measured at 800 µm, with no evidence of lymphovascular invasion. Both the horizontal and vertical resection margins were free of tumor involvement, and curative resection was thus achieved (Figure 2).” was incorrect. The correct description should read: “The depth of submucosal invasion was measured at 800 µm, with no evidence of lymphovascular invasion, and budding grade 1. Although the pathological margin was positive for carcinoma and unclear for adenoma, the resection was considered curative based on endoscopic findings (Figure 2).”

We would like to add the following acknowledgment in relation to the valuable comments provided regarding this lesion.

“Acknowledgments” section, the statement: “The authors wish to thank all the clinical staff who contributed to this paper, and we would like to express our sincere gratitude to Dr. Hiroshi Kawachi (Department of Pathology, Omori Red Cross Hospital, Tokyo, Japan/Department of Pathology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan) for the detailed pathological diagnosis of this case, and to all the pathology staff for their invaluable support.”

We apologize for this error.

Endoscopic mucosal resection (EMR) has been widely adopted as an endoscopic treatment for colorectal tumors. However, in non-lifting lesions, EMR often becomes technically challenging, leading to piecemeal resection or residual tumor. Recently, underwater EMR (UEMR) has been developed as a novel technique that allows mucosal and submucosal layers to float under water, facilitating snare resection without submucosal injection. UEMR has been reported to improve en bloc resection rates and shorten procedure time compared with conventional EMR, and its usefulness has been demonstrated in non-lifting and residual lesions. We encountered a case in which a 78-year-old woman had a small IIa+IIc-type lesion of the sigmoid colon that could not be completely removed by EMR at a previous hospital due to non-lifting and snare slippage, resulting in only partial resection. She was subsequently referred to our hospital for further treatment. At our hospital, UEMR was successfully performed, achieving en bloc resection. Histopathological examination revealed well-differentiated tubular adenocarcinoma with 560 µm submucosal invasion, negative resection margins, and no lymphovascular invasion, thus fulfilling the criteria for curative resection. This case highlights the illustrative and educational significance of applying UEMR, rather than endoscopic submucosal dissection, to achieve a safe and time-efficient curative resection for a small non-lifting colorectal carcinoma. UEMR may represent a potential salvage option in selected EMR-difficult cases, although further accumulation of cases is warranted to clarify its role.

While hepatocellular carcinoma (HCC) often invades the portal or hepatic vein to form tumor thrombus, tumor thrombus in the bile duct is rare. In such cases, differentiation from intrahepatic cholangiocarcinoma is difficult, and the tumor often appears as a smooth, yellowish-white, polypoid mass within the bile duct lumen. We report herein a case of obstructive jaundice due to bile duct tumor thrombus of HCC diagnosed by peroral cholangioscopy (POCS). A 64-year-old man presented with epigastralgia and jaundice. Contrast-enhanced computed tomography revealed an irregular mass with hypoenhancement in liver segment S8, along with dilatation of the right intrahepatic bile duct due to the invading tumor. The hepatic mass was poorly visualized on ultrasound, making percutaneous liver tumor biopsy difficult. POCS was performed after endoscopic retrograde cholangiopancreatography for biopsy of the intrahepatic bile duct tumor thrombus. POCS clearly revealed a smooth, yellowish-white, polypoid tumor in the right intrahepatic bile duct, and a biopsy of the tumor was performed under POCS. Based on the pathological findings, HCC was diagnosed, and chemotherapy with atezolizumab and bevacizumab was initiated.

Endoscopic submucosal dissection (ESD) is widely used for early esophageal cancer, even in patients with liver cirrhosis (LC). Corticosteroids, administered orally or by local injection, are often used to prevent post-ESD esophageal stricture. However, their safety in patients with decompensated LC and refractory ascites remains unclear. A man in his 70s with alcohol-related decompensated LC and refractory ascites underwent ESD for subcircumferential superficial esophageal squamous cell carcinoma located on esophageal varices. To prevent post-ESD stricture, both oral prednisolone and local triamcinolone were administered. Ascites worsened significantly, and large-volume paracentesis was performed. Subsequently, the patient developed a mural thrombus in the superior mesenteric vein and non-occlusive mesenteric ischemia, leading to bowel perforation and death on day 51 post-ESD. In LC patients with refractory ascites, oral corticosteroids may exacerbate ascites and increase thrombotic risk, potentially leading to fatal complications. This case highlights the need for careful risk–benefit assessment of subcircumferential ESD in vulnerable cirrhotic patients.

A 49-year-old male developed liver dysfunction during chemotherapy for rectal cancer located in the rectosigmoid region. Although magnetic resonance cholangiopancreatography initially indicated sclerosing cholangitis, endoscopic retrograde cholangiopancreatography and intraductal ultrasonography revealed multiple non-contiguous intraductal masses. Histopathological analysis confirmed distal bile duct metastasis from rectal cancer, characterized by papillary intraductal lesions. The distribution and morphology of the tumors suggested implantation via bile flow or hematogenous dissemination through the peribiliary capillary plexus. Extrahepatic bile duct metastasis from colorectal cancer is exceptionally rare and poses significant diagnostic challenges. This report presents a rare case of distal bile duct metastasis detected during chemotherapy for rectal cancer, where endoscopic imaging was instrumental in establishing the diagnosis.

A 75-year-old man presented with an esophageal subepithelial lesion (SEL) measuring 2.5 cm, first identified over a decade ago. The patient was followed up regularly with computed tomography and endoscopy and remained asymptomatic since then. However, over the past year, the patient developed dysphagia, and endoscopic evaluation revealed that the tumor had enlarged to 6.0 cm. Although nine endoscopic examinations with biopsies were performed, no definitive histopathological diagnosis was established. Endoscopic ultrasonography revealed that the tumor originated primarily from the submucosa. Given the rapid growth of tumor size and progressive symptoms, the tumor was removed with endoscopic submucosal dissection (ESD) in an en bloc manner. Histopathological analysis revealed a SEL characterized by vascular proliferation, thickening of the lamina muscularis mucosa, and inflammatory changes. No evidence of neoplasm was identified, suggesting the presence of a reactive lesion. The patient's dysphagia improved following ESD, and no recurrence was observed during a 15-month follow-up period. To date, no reports have documented rapidly growing esophageal SELs with abundant vascularization during follow-up.