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Endoscopic ultrasound-guided hepaticogastrostomy (EUS-HGS) is a useful alternative treatment for endoscopic retrograde cholangiopancreatography (ERCP) failure. However, serious complications sometimes occur. Bleeding is an early complication that occurs during puncture; however, there have been some reports of late-onset rupture of a pseudoaneurysm. These reports describe cases of patients who underwent metal stent placement. Herein, we report the first case of pseudoaneurysm formation after plastic stent placement via EUS-HGS. The patient was a 75-year-old man with obstructive jaundice due to pancreatic head cancer. ERCP was unsuccessful, and EUS-HGS was performed with plastic stent placement from B3. The patient subsequently experienced repeated HGS stent failure within a short period, and the plastic stent was replaced each time. No metal stents were placed during treatment. 106 days after EUS-HGS, the patient presented with hematochezia and shock, and contrast-enhanced computed tomography suggested the rupture of a pseudoaneurysm in the left hepatic artery branch. Emergency angiography revealed that the pseudoaneurysm originated from the A2+3 branch of the left hepatic artery, and embolization was performed. Subsequently, there has been no recurrence of bleeding, and the patient was eligible for chemotherapy to treat pancreatic cancer.

Herein, we report a rare case of gastroduodenitis associated with ulcerative colitis (UC). A 42-year-old man was diagnosed with UC 1 year prior to admission to our hospital. The patient underwent a 3-stage total colectomy and ileal pouch-anal anastomosis for severe UC. Two months after the second surgery, the patient was admitted to our hospital with nausea, appetite loss, abdominal pain, and frequent bloody diarrhea. Blood analysis showed an increase in white blood cell count and C-reactive protein levels. Esophagogastroduodenoscopy (EGD) revealed diffuse UC-like inflammation from the stomach to the duodenum and ulcers in the descending and horizontal regions of the duodenum. Pouchoscopy revealed ulcers and friable mucosa within the pouch. The patient was diagnosed with gastroduodenitis associated with UC (GDUC) and diversion pouchitis based on endoscopic and pathological findings. Inflammation in the GDUC was resistant to oral crushed mesalazine and prednisolone (60 mg/day) infusion, resulting in arterial bleeding from the duodenal ulcer and bloody stool in the stoma. Endoscopic hemostasis was performed for the duodenal ulcer. Oral tacrolimus was initiated because the inflammation was steroid-resistant. Approximately 2 weeks after the initiation of tacrolimus, abdominal symptoms, including bloody diarrhea, disappeared, and EGD showed improvement in the GDUC.

Spontaneous regression of endoscopically invasive colorectal cancer (CRC) after biopsy has been rarely reported. We report three cases of endoscopically invasive CRC with spontaneous regression after biopsy and a review of the literature regarding spontaneous regression of CRC with somatic mismatch repair deficiency (MMR-d). Case 1 involved a 54-year-old man who underwent a colonoscopy (CS) after positive fecal immunohistochemical test. A 15-mm elevated lesion with a depression was detected in the transverse colon, and biopsy results indicated adenocarcinoma. When surgical resection was performed 8 weeks later, the lesion was no longer present. Case 2 involved a 75-year-old man with a 10-mm elevated lesion with a depression in the ascending colon during screening CS. Biopsy results indicated adenocarcinoma. CS was performed 9 weeks later to tattoo the lesion before surgery; however, it was no longer present at that time. Case 3 involved an 84-year-old man who underwent surveillance CS after polyp resection and a 12-mm elevated lesion with a depression was observed in the rectum. Biopsy results indicated adenocarcinoma; therefore, endoscopic resection was scheduled. CS performed 8 weeks later showed the disappearance of the lesion. Mismatch repair deficiency was detected in two of these three patients. The literature search identified 12 cases with the evaluation of MMR, including our three cases, which showed spontaneously regressing colorectal cancer. All 12 lesions had depression; 11 were located on the proximal colon, and 11 cases showed MMR-d.

Hypercontractile esophagus is a motility disorder characterized by excessive contractions in the esophageal body. Certain cases of hypercontractile esophagus exhibit eosinophilic infiltration in the muscle layer; however, its clinical significance is unclear. Here, we report a case of hypercontractile esophagus with possible eosinophilic inflammation despite the absence of eosinophilic infiltration on hematoxylin and eosin staining. A 75-year-old man presented with dysphagia, primarily triggered by the ingestion of meat. Esophagogastroduodenoscopy showed abnormal peristalsis of the esophageal body, while the lower esophageal sphincter function remained normal. High-resolution manometry confirmed hypercontractile esophagus, according to the Chicago Classification version 4.0. As symptoms persisted despite medical treatment, the patient underwent peroral endoscopic myotomy. Biopsies obtained from the inner circular muscle layer revealed no notable eosinophilic infiltration on hematoxylin and eosin staining. However, immunofluorescence staining for major basic protein (MBP), a cytotoxic eosinophil granule protein that persists in tissues, showed patchy depositions. Corresponding counterstaining revealed collapsed nuclei surrounded by eosinophilic material, suggesting MBP release via eosinophil cytolysis. This case demonstrated that immunostaining for eosinophil granule proteins may uncover eosinophilic activity in the esophageal muscle layer, even in the absence of eosinophils. While the precise pathogenic role of eosinophilic inflammation in hypercontractile esophagus remains unclear, MBP deposition could reflect a localized immune-mediated process contributing to motility disturbance. Further investigation is needed to determine the prevalence, mechanisms, and clinical implications of these findings in esophageal motor disorders.