Clinical Journal of Gastroenterology最新文献

A 23-year-old man with a history of anemia of unknown cause was referred to our hospital. He had experienced melena three times: at 6 months, 10 years, and 20 years of age. He underwent upper and lower gastrointestinal endoscopy at 10 and 20 years of age, and small intestinal capsule endoscopy twice at 20 years of age, but the site of bleeding could not be identified. At first, a transabdominal ultrasound was performed for suspected Meckel's diverticulum. A cystic diverticulum was found in the ileum, with an apertural diameter of 5 mm and a total size of 4 cm. The cyst showed an area of loss of wall stratification, which appeared to be an ulcer scar. Based on these observations, we diagnosed anemia resulting from a hemorrhagic Meckel's diverticulum and performed laparoscopic resection. Postoperative histopathology revealed ectopic gastric mucosa and ulcer formation within the Meckel's diverticulum, which was thought to be the cause of the bleeding. Meckel's diverticulum should be considered in cases of hemorrhage in young patients. A transabdominal ultrasound as a screening test detected a diverticulum with an ulcer scar in the ileum, which led to the identification of the underlying disease.

It is estimated that 153,020 cases of CRC per year, with an increase in diagnoses in younger patients. We present a case of a female with an early presentation of Lynch Syndrome and CRC, who, on her third malignant presentation, was re-diagnosed as a constitutional mismatch repair deficiency.

Rectal implantation cysts can occur at anastomotic sites after low anterior resection (LAR) for rectal cancer. Herein, we report a case of primary adenocarcinoma arising from a rectal implantation cyst after LAR for rectal cancer. A 70-year-old woman was referred to our hospital for diagnosis and treatment of a growing cystic lesion. She had LAR performed for rectal cancer 29 years previously and had a rectal implantation cyst detected 13 years previously. On the first visit to our hospital, serum CEA and CA19-9 levels were elevated, and computed tomography (CT) scans revealed a cystic lesion near the anastomosis. CT-guided biopsy revealed no cancer tissue in the cystic lesion. After that, the cystic lesion naturally shrank, and serum CEA and CA19-9 levels became normal. Follow-up included 3 monthly serum CEA and CA19-9 testing and 6 monthly CT scans. Two years later, serum CEA and CA19-9 levels were elevated again. Colonoscopy revealed an ulcerative lesion at the anastomotic site, in which adenocarcinoma was confirmed. Abdominoperineal resection with sacral resection was performed, and postoperative histopathological examination revealed a primary adenocarcinoma with mucinous component at the implantation cyst. Since rectal implantation cysts can become malignant after extended periods, clinicians need to be aware of this disease.

Eosinophilic gastritis (EoG) is defined as the presence of upper gastrointestinal symptoms combined with histologic findings of > 30 eosinophils/high-power field (eos/hpf) in 5 hpf in any part of the gastric mucosa, except for the secondary causes of gastric eosinophilia. This is the first case report of a serial change in gastric motility in EoG with pyloric stenosis using abdominal ultrasonography. A 56-year-old woman was diagnosed with pyloric stenosis by upper gastrointestinal radiographic examination during a medical checkup. She had nausea and loss of appetite, her gastrointestinal symptom rating scale (GSRS) score was 20, and her F scale score was 20. Esophagogastroduodenoscopy (EGD) demonstrated pyloric stenosis and multiple superficial ulcerations in the antrum. Histopathological findings of gastric biopsy specimens revealed severe eosinophilic infiltration (100 eos/HPF), and the diagnosis was EoG with pyloric stenosis. Before treatment, the gastric anterior wall thickness was 6.3 mm. The gastric motility in EoG was evaluated by intra-abdominal ultrasonography. Ultrasonography showed low motility in the antrum, especially the amplitude and motility index. After 6 months of steroid treatment, her symptoms improved. Her GSRS score was 13, and her F scale score was 19. Histological eosinophilic infiltration decreased to 50 eos/HPF, showing improvement. On ultrasonography, gastric motility also improved and recovered to normal. After 12 months, several examinations confirmed improvement, including gastric motility by ultrasonography.

We report a very rare case of delayed necrosis of the reconstructed colon 6 months after esophagectomy.A 67-year-old male patient had undergone esophagectomy with gastric tube reconstruction for esophageal cancer in 2014. Subsequently, total gastrectomy and ileo-colon reconstruction via a retrosternal route was performed for gastric tube cancer in 2022. Six months later, he suffered acute chest pain and came to our hospital. Contrast-enhanced CT showed severe dilation of the reconstructed colon with poor enhancement of the wall opposite mesentery, without arterial obstruction. Endoscopy showed no ischemic changes in the esophago-ileum anastomosis; however, mucosal color change to black was observed in the reconstructed colon. We diagnosed ischemic colitis of the reconstructed colon and started conservative treatment; however, 18 days later, he developed a right pyothorax due to perforation of the reconstructed colon. We performed necrosed colectomy with right chest drainage and cervical esophageal fistula was made. Histopathological examination revealed mucosal detachment, thinning of the muscularis propria, and ghost-like appearance of crypt. If necrosis of the reconstructed colon is suspected in the late postoperative period, endoscopic findings of the colonic mucosa may be useful in determining surgical treatment, even in the absence of arterial blood flow obstruction.

Transmesenteric internal hernia is an uncommon cause of small bowel obstruction that occurs when small bowel loops protrude through a mesenteric defect into the abdominal cavity. Herein, we present an unexpected case of colonoscopy-induced transmesenteric internal hernia. An 81-year-old male patient presenting with intermittent hematochezia and constipation had undergone a laparoscopic left nephrectomy for ureteral cancer. A colonoscopy was performed to identify the etiology of his symptoms. He complained of severe abdominal pain 2 h after the examination despite uneventful endoscopic procedures, including cold snare polypectomy. Contrast-enhanced computed tomography revealed a strangulated small bowel obstruction with a closed-loop formation outside the descending colon. The small bowel loop was incarcerated into the left retroperitoneal space. Emergency laparotomy detected small bowel loops that prolapsed into the nephrectomy pedicle via a descending mesenteric defect, developed during the laparoscopic left nephrectomy. The incarcerated small bowel was detached from the hernia and returned to its normal position, and the mesenteric defect was closed. He demonstrated an uneventful postoperative course, with no internal hernia recurrence after discharge. This case indicates the risk of transmesenteric internal hernia through inadvertently created mesenteric defects should be borne in mind, especially when performing colonoscopies in patients who underwent laparoscopic nephrectomies.

Recent studies have reported the occurrence of upper gastrointestinal (UGI) inflammation in patients with ulcerative colitis (UC). However, whether UC-associated UGI and colorectal lesions share pathogenic cytokine profiles and responses to biologics remains unknown. Herein, we report a case of concurrent UC and ulcerative duodenitis (UD) that displayed unique responses to biologic treatment. Although treatment with prednisolone (PSL) failed to induce remission in both disorders, golimumab (GLM) and ustekinumab (UST) were effective against UD and UC, respectively, and remission of both disorders was achieved using UST. Immunofluorescence analyses revealed that numbers of immune cells expressing TNF-α were comparable in both duodenal and rectal mucosa before the treatment. GLM or UST treatment markedly decreased numbers of TNF-α-expressing duodenal immune cells, suggesting the presence of correlation between TNF-α expression and disease activity of UD. In contrast, TNF-α expression was not parallel to disease activity of UC because GLM or PSL failed to induce remission despite a marked reduction in TNF-α expression. Responsiveness to GLM or UST together with immunofluorescence studies suggests that TNF-α and IL-12/23p40 are pathogenic cytokines causing UD and UC, respectively, in the present case.

A 62-year-old male with a history of stent graft replacement for an infectious aortic aneurysm, followed by multiple interventions for postoperative complications, was admitted with melena and anemia. Enhanced computed tomography (eCT) demonstrated fluffing and hyperdensities surrounding the graft, despite no evidence of an aortoenteric fistula (AEF). Emergency esophagogastroduodenoscopy (EGD) showed a massive bleeding in the reconstructed tract and the protruding lesion of postoperative granulation tissue with clots at the end of the blind pouch. Thereafter, hemorrhage temporarily reoccurred several times; however, the source could not be identified using eCT or EGD. Finally, on the third attempt, we performed gel immersion endoscopy (GIE) with manual injection of VISCOCLEAR^Ⓡ, and it showed purulent blood flowing from one side of the protruding lesion in the pouch. Based on the eCT findings showing exudation of the contrast agent from the graft into the pouch, we made a diagnosis of an AEF. However, radical surgery was not performed because of the patient's poor general condition. During conservative management, he died of uncontrolled bleeding from the AEF on the 5th day of hospitalization. This is the first case in which the GIE might provide tips to identify herald bleeding from a lethal AEF.

Ulcerative colitis (UC), a subtype of inflammatory bowel disease, occasionally manifests with extraintestinal manifestations. We present a 51-year-old male with refractory UC and immune thrombocytopenia (ITP) resistant to conventional treatments. The introduction of biologics, ustekinumab or adalimumab, resulted in clinical remission of colitis and improvements in platelet count. This case underscores the efficacy of biologics in managing refractory UC associated with ITP, emphasizing their potential to control intestinal inflammation and address concurrent thrombocytopenia, potentially avoiding surgical intervention.

Herein, we describe a case of olmesartan-associated sprue-like enteropathy, in which improvement in villous atrophy was confirmed using small bowel capsule endoscopy. The patient was a 69-year-old woman who had persistent watery diarrhea (20 bowel movements/day) for 1 year and experienced a weight loss of 10 kg in the same period. Abdominal computed tomography revealed no abnormalities, and blood test results revealed no inflammatory reactions. Upper endoscopy and colonoscopy revealed villous atrophy in the duodenum and terminal ileum. As the patient was administered olmesartan for a long time and capsule endoscopy showed villous atrophy throughout the small bowel, she was diagnosed with olmesartan-associated sprue-like disease. Following the discontinuation of the medication, symptoms of diarrhea soon improved, and repeat capsule endoscopy indicated improvement in small intestinal villous atrophy. Olmesartan-associated sprue-like enteropathy should be considered a differential diagnosis in patients with severe chronic watery diarrhea. Our report is the first in which capsule endoscopy was performed multiple times over a long period for follow-up observation of improvements in the small intestine. In addition, our literature review regarding capsule endoscopy for olmesartan-associated enteritis might aid clinicians in the early diagnosis of the condition and the assessment of treatment efficacy.