Aim : To assess the association between ERCP-related periampullary-biliary-retroperitoneal perforation and the local anatomy of the intrapancreatic portion of the common bile duct (CBD).
Method : Included in this study were 321 consecutive patients who underwent ERCP. The relationship between periampullary-biliary-retroperitoneal perforation and local anatomy of the intrapancreatic portion of the CBD was retrospectively investigated.
Results : We experienced two cases of periampullary-biliary-retroperitoneal perforation during ERCP procedures : endoscopic sphincterotomy and stone removal using a biliary balloon catheter in both cases. We performed diagnostic imaging with CT and MRI to study the local anatomy of the intrapancreatic portion of the CBD in the 321 patients. The following types of anatomy were observed. Type A : the CBD was covered other than the small portion of its posterior surface by the pancreatic parenchyma (PC), 76%. Type B : the CBD was completely surrounded by the PC, 8%. Type A/B : difficulty in distinguishing between types A and B, 8%. Type C : the CBD lay freely behind the pancreas, 3%. Type C/A ; difficulty in distinguishing between types C and A, 5%. Our two perforated cases were type C and C/A, respectively. Perforation occurred significantly more frequently in types C and C/A than in types A, A/B and B. One perforated case healed by endoscopic nasobiliary drainage, and the other case required surgery. The perforation site could be found in the surgical case, but could not be found endoscopically in the conservatively-treated case.
Conclusion : Types C and C/A may be anatomically associated with increased risk for perforation. It was thought that awareness of the lower biliary anatomy was important.

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A 44-year-old woman had a two-year history of food impaction. Esophago-gastro-duodenoscopy showed white exudates with fine furrows localized at the esophago-gastric junction. Examination of biopsy specimens showed marked intraepithelial infiltration of eosinophils (50 per high power field) in the esophageal mucosa. She was diagnosed as having localized eosinophilic esophagitis and received rabeprazole for 8 weeks. After treatment, her symptoms as well as endoscopic images and esophageal eosinophil infiltration improved. Here, we presented a patient with localized eosinophilic esophagitis that was successfully treated with a proton pump inhibitor.

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A 70-year-old man was referred to our hospital to treat a polyp in the duodenal bulb. Endoscopic examination showed that the polyp was composed of Yamada type IV lesions with thick stems and a head that was reddish. Magnifying endoscopy revealed a small opening and gastric epithelial metaplasia in the head of the polyp. We performed polypectomy for therapeutic diagnosis. Histologically, the lesion was a duodenal Brunner's gland hamartoma with abundant mature adipose tissue and gastric metaplasia. Brunner's gland hamartoma is composed of hyperplastic Brunner's glands mixed with elements such as adipose tissue, and is often accompanied by gastric epithelial metaplasia. Because diagnosis by biopsy is not possible, preoperative diagnosis of the disease is difficult. However, magnifying endoscopy enabled us to detect some characteristic findings of the disease, such as a small opening and gastric epithelial metaplasia. As a result, preoperative diagnosis might be possible by magnifying endoscopy. This case suggested that magnifying endoscopy is useful for the diagnosis of Brunner's gland hamartoma.

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A 92-year-old woman was admitted to our hospital with exertional dyspnea due to anemia. Gastrointestinal bleeding was suspected. Enhanced computed tomography revealed a small lesion in the upper jejunum, which was stained at the arterial phase, and video capsule endoscopy showed bloody fluid in the same region. Double-balloon enteroscopy revealed a reddish protruding lesion of 5 mm in size with blood oozing, which was suspected of being a hemangioma. Endoscopic mucosal resection resulted in arterial hemorrhage from the cut end, but endoscopic hemostasis was successfully performed. After discharge, the patient's anemia improved and there was no evidence of gastrointestinal bleeding. Histopathological examination showed that the lesion was an arteriovenous malformation, differing from the original diagnosis, but endoscopic treatment was successful.

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We describe a rare case of stricture-type ischemic enteritis, wherein hepatic portal venous gas (HPVG) and pneumatosis cystoides intestinalis (PCI) were observed at onset, followed by the subsequent development of small intestine stenosis.
An 82-year-old man presented with severe vomiting and was admitted to our hospital. Abdominal CT indicated the presence of HPVG and PCI, along with edema of the wall of the small intestine. Although the findings of HPVG and PCI suggested the presence of intestinal necrosis, signs of peritoneal irritation were not observed. Hence, conservative treatment was preferred over surgical intervention. Fasting and intravenous infusion led to gradual improvement of his symptoms, and the patient was able to follow the diet provided. However, after approximately 5 months, the patient developed abdominal distension. Abdominal CT indicated intestinal obstruction caused by wall thickening and stenosis of a part of the small intestine. Transanal single-balloon enteroscopy, performed 177 days following the onset of symptoms, revealed a circumferential ulcer and narrowing of the small intestine, which prevented further insertion of the endoscope. Partial resection of the small intestine was performed and pathological examination of the resected specimen showed the characteristic feature of ischemic stricture of the small intestine. Based on the clinical presentation and the results of pathological examination, the patient was diagnosed with stricture-type ischemic enteritis. Following surgery, the patient was discharged from the hospital in good health.
The findings of the present case suggest that the appearance of HPVG and PCI does not necessarily indicate the presence of intestinal necrosis. Furthermore, in patients with stricture-type ischemic enteritis, although the acute phase of the disease may be improved by conservative treatment, small intestine stenosis may still develop at a later stage. Therefore, in cases with a presentation similar to the current case, careful long-term follow-up should be considered.

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A 27-year-old man was admitted to our hospital complaining of large amounts of bloody stools without abdominal pain or diarrhea. Emergent colonoscopy revealed an ulcer with an exposed blood vessel on the ileocecal valve. Endoscopic hemostasis was attempted three times, but hemorrhage occurred again. A diagnosis of Campylobacter enterocolitis was made by bacterial culture test of the stool sample obtained on admission, and oral administration of levofloxacin was started. Despite administration of levofloxacin, he continued to have bloody stools. Then, we changed the antibiotic to azithromycin according to the drug susceptibility test on the 9th hospital day, and the bloody stools stopped in a few days. When physicians encounter an ulcer on the ileocecal valve without manifestations of infectious enterocolitis, bacterial culture tests of the stool and a detailed interview should be performed while keeping Campylobacter enterocolitis in mind.

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A 30-year-old man was admitted to our hospital with hematochezia and mucous stool. We performed total colonoscopy, and found a submucosal-tumor-like elevated lesion of 30mm in size in the lower rectum. The biopsy specimens showed nonspecific pathologic findings ; therefore, we were not able to make a qualitative diagnosis. Endoscopic ultrasonography (EUS) revealed a low echoic lesion of 25mm in diameter in the second and third layers of the lower rectum. The lesion had several small anechoic areas. EUS revealed that a submucosal layer was present between the lesion and the muscularis propria without invasion by the lesion into the intestinal tract. As a result of the EUS study, we assessed that the lesion could be excised via en bloc resection by endoscopic submucosal dissection (ESD). After obtaining informed consent, we performed ESD for both diagnosis and treatment. Pathological examination of the resected lesion led to the definitive diagnosis of mucosal prolapse syndrome with colitis cystica profunda. We report a case of colitis cystica profunda that was treated by ESD.

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Duodenal epithelial tumors are rare, and gastroenterologists have had little interest in the tumors. However, the incidence of duodenal carcinoma has been increasing over the past decade due to the widespread use of esophagogastroduodenoscopy and the advancement of an aging society in Japan. Accordingly, accurate diagnosis, characterization and determination of tumor extent by magnification endoscopy are sought for epithelial tumors in the duodenum as they are with tumors of the stomach and colorectum. Combining novel image-enhanced techniques (e.g., narrow-band imaging) with magnifying endoscopy allows us to visualize the microstructure of the mucosal surface including microvessels. It is important not to overlook small lesions that would be a good candidate for magnifying endoscopic diagnosis. This paper describes our original procedure of routine duodenoscopy as well as optimal techniques and key diagnostic points of magnifying endoscopy in the duodenum.

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