Clinical Journal of Gastroenterology最新文献

Intestinal fatty acid-binding protein (I-FABP) is a promising biomarker for small-bowel ischemia including non-occlusive mesenteric ischemia (NOMI). A 75-year-old woman with diabetic nephropathy sustained a distal radius fracture. Two days later, she underwent a brachial plexus block to facilitate orthopedic surgery, which resulted in hypotension. Despite prompt fluid resuscitation and ephedrine administration, the patient developed abdominal pain. Contrast-enhanced computed tomography revealed hepatic portal venous gas, but no direct evidence of small-bowel ischemia. The gastrointestinal surgery team opted for cautious in-hospital observation overnight. Unfortunately, the patient's condition significantly worsened the following day, prompting an urgent laparotomy. Surgery confirmed ileal segment necrosis, macroscopically characterized by a distinctive geographic pattern. Retrospective analysis of stored serum samples using a human enzyme-linked immunosorbent assay demonstrated that I-FABP levels were moderately elevated (7.2 ng/mL) at the initial outpatient visit for the fracture, peaked (17.9 ng/mL) at the clinical onset of NOMI, and returned to normal (0.7 ng/mL) by postoperative day 2. Serum I-FABP levels correlated with the progression of NOMI, showing potential as an early detection marker. However, the longitudinal analysis of serum I-FABP also highlighted significant challenges of this biomarker, including the influence of renal function and the importance of sampling timing.

Wandering spleen is a relatively rare condition and may be complicated by intestinal obstruction or abnormal intestinal rotation. Herein, we report a case where these three conditions appeared concomitantly. An 18-year-old woman with an intellectual disability was admitted to the hospital because of vomiting and fever. The patient's abdomen was distended. Computed tomography revealed a dilated small intestine, a swollen spleen located in the lower abdomen, as well as twisting and swirling of the splenic artery and vein. The patient was diagnosed with torsion of the wandering spleen and emergency surgery was performed. The vascular pedicle was found to be rotated 900° clockwise, and a markedly enlarged spleen was observed in the lower abdomen. When the splenic torsion was released, the pulsation of the splenic artery was well palpated, suggesting that the spleen could be preserved. Additionally, the sigmoid colon to the cecum was not fixed to the retroperitoneum. Dilatation of the small intestine was observed, but there were no findings of intestinal tract necrosis. Splenic torsion is part of the differential diagnosis for acute abdomen. Familiarity with embryology and anatomy is necessary to select the appropriate surgical technique.

Amoebic colitis is a parasitic gastrointestinal disease caused by Entamoeba histolytica (E. histolytica). In Japan, metronidazole (MNZ) monotherapy is often used and most cases are effective. However, we report a case of MNZ-insufficient amoebic colitis caused by residual cysts. A 73-year-old man had been staying in Southeast Asia for over a decade. He had undergone a screening colonoscopy and ulcerative lesions were observed in the cecum, and a biopsy confirmed amoeba parasites. The patient was treated with MNZ monotherapy. However, he forgot to take the medicine for several days, and the ulcerative lesions persisted. The patient was referred to our facility, and we performed a colonoscopy and confirmed trophozoites. Since we considered that previous treatment failure was due to the low oral dosage, we re-prescribed MNZ. A colonoscopy after 6 months showed that the ulcerative lesions persisted. We clinically diagnosed MNZ-insufficient amoebic colitis caused by residual cysts and prescribed MNZ and paromomycin (PRM) each for 10 days. One year later, no ulcerative lesions were observed. MNZ-insufficient amoebic colitis should be considered, when ulcerative lesions remain after MNZ administration and PRM is effective drug against cysts, and we propose a combination therapy of PRM to MNZ.

A 90 year-old man underwent endoscopic mucosal resection for lesions in the descending and sigmoid colons as well as endoscopic submucosal dissection (ESD) for a lesion in the rectal peritoneal reflection (Ra) 1 month before undergoing laparoscopic resection and D3 dissection for advanced cancer in the descending colon. One year later, he underwent a surveillance colonoscopy, and advanced colorectal cancer was detected on the ESD scar. The history suggested that this newly detected recurrent colorectal neoplasm on the ESD scar may have originated from cancer cells derived from the descending colon cancer that were implanted in the ESD ulcer, thereby initiating a new colorectal neoplasm. Cancer genomic testing further indicated that three of the four pathogenic variants detected in the recurrent colorectal neoplasm were consistent with pathogenic variants of descending colon cancer. This finding strongly supports our contention that cancer cells derived from the descending colon cancer were implanted in the post-ESD ulcer of the rectal Ra and proliferated, forming the recurrent colorectal neoplasm. This case report highlights the potential for tumor cell implantation on endoscopic resection ulcers and the utility of cancer genomic testing in validating this phenomenon.

Upper gastrointestinal tumors, including ampullary adenomas, occur frequently in patients with familial adenomatous polyposis (FAP). Guidelines recommend upper gastrointestinal endoscopy in FAP for surveillance of gastric and duodenal adenomas. However, adenomas can rarely arise from biliary epithelium in patients with FAP. Here, we describe a case of tubular adenoma at the hepatico-jejunal anastomosis with intraductal extension in a patient with FAP and previous pancreaticoduodenectomy. This report illustrates a unique case and emphasizes the need for data on postoperative surveillance in patients with FAP, particularly following pancreaticoduodenectomy.

Bleeding-related adverse events may occur due to anti-vascular endothelial growth factors. Here, we report two cases of variceal rupture during atezolizumab plus bevacizumab (ATZ/BV) treatment for unresectable hepatocellular carcinoma (u-HCC).Case 1 involved a man in his 60 s with alcoholic liver cirrhosis (LC) and u-HCC. Seventy-four days after ATZ/BV administration, the patient was admitted for hematemesis. Upper esophagogastroduodenoscopy (EGD) revealed worsening of the esophageal varices (EVs) to F2 grade with active bleeding. Endoscopic variceal ligation successfully achieved hemostasis.Case 2 involved a man in his 70 s with alcoholic LC and u-HCC. The patient was admitted with hematemesis 114 days after ATZ/BV administration. During EGD, the EVs deteriorated to F3 grade, although hemostasis had already been achieved. The evaluation was discontinued during the observation stage because of the worsening hepatic reserve.Neither patient had EVs warranting prophylactic treatment before ATZ/BV administration, showed a partial tumor response, or had portal vein tumor thrombus. Both patients demonstrated increased total diameters of the collateral veins and splenic volume compared to those before treatment. These findings suggest that ATZ/BV treatment may increase portal pressure. In conclusion, the administration of ATZ/BV to patients with LC and u-HCC necessitates careful management of EVs aggravation and rupture.

Acute liver failure secondary to metastatic melanoma is exceedingly rare with the literature limited to case reports. The disease itself presents with vague symptoms making diagnosis difficult without a high clinical suspicion. Further to this, the prognosis of acute liver failure secondary to metastatic melanoma is dismal. We present the case of a 59-year-old male with a distant history of previously excised cutaneous melanoma who presented to our institution with abdominal pain and liver enzyme derangement suggestive of acute hepatitis. Due to progressive derangement in liver function and cross-sectional imaging suggestive of an infiltrative cause, a left axillary lymph node was biopsied which demonstrated metastatic melanoma. The patient subsequently deteriorated into acute liver failure and despite acute treatment of his underlying metastatic melanoma died 17 days post initial presentation. This case highlights an uncommon cause of acute liver failure as well as the poor prognosis associated with acute liver failure secondary to metastatic melanoma.

We report a case of diffuse large B-cell lymphoma (DLBCL) of the gallbladder with extensive hepatoduodenal invasion, which was challenging to diagnose histologically due to a strong tendency to be necrotic. An 71 year-old man presented with upper abdominal pain and was referred to our hospital. Computed tomography revealed a distended gallbladder with air within the irregular gallbladder wall and an indistinct border with the hepatoduodenum, suggesting invasion. Esophagogastroduodenoscopy detected an ulceration in the duodenal bulb. However, histologic analysis failed to provide a definitive diagnosis due to the presence of necrotic tissue. Furthermore, direct biopsy from the gallbladder mucosa by endoscopic retrograde cholangiography revealed only necrotic tissue and no diagnosis. Contrast ultrasonography for the hepatic invasion revealed enhancement with blood flow, suggesting non-necrotic tissue. Subsequently, an ultrasound-guided core-needle biopsy was conducted to obtain tissue samples from the described lesion. The pathology showed atypical lymphocytes with irregular nuclei. Immunostaining indicated positive expression of CD10, CD20, Bcl-6, and C-Myc, consistent with a diagnosis of DLBCL. In our case, the lymphoma exhibited a strong tendency to be necrotic, making histologic diagnosis difficult. However, selective biopsy from the site of blood flow made the diagnosis possible and proved to be useful.

Perforated esophageal cancer rarely results in the formation of mediastinal abscess. Endoscopic ultrasound (EUS)-guided abscess drainage (AD) has increasingly been used in the management of abscesses in locations that are difficult to treat percutaneously. We describe a case of EUS-AD for mediastinal abscess due to perforating esophageal cancer and successful bridge to surgery. A 71-year-old man with suspected esophageal issues was referred to our hospital. Computed tomography showed an esophageal cancer perforating the mediastinum, forming a mediastinal abscess. EUS-AD was planned before curative resection, because there was little improvement in inflammatory response with antimicrobial therapy. The mediastinal abscess cavity was confirmed on EUS and punctured using a 19-G needle, and then, a 0.025-inch guidewire was placed in the abscess cavity. The fistula was dilated with a 7-Fr dilator and a 6-Fr, single-pigtail nasobiliary tube was placed in the abscess cavity. One month later, clinical signs had improved and curative surgery was performed. Postoperative adjuvant therapy was administered using fluorouracil/cisplatin therapy. As of 2 years postoperatively, the patient remains free of recurrence.

There is no established treatment for bleeding bile duct varices (BDVs). We report the first case of portal vein (PV) stenting completely eradicating bleeding BDVs. A 70-year-old male with malignant lymphoma developed BDVs due to PV obstruction, which had caused compression and stricture of the distal bile duct. Endoscopic retrograde cholangiography was performed to evaluate the stricture and bleeding from the ruptured BDV was observed. Endoscopic hemostasis was difficult, requiring reopening of the extra-hepatic PV and reducing the blood flow to the BDVs for hemostasis. Therefore, PV stenting was performed. During the procedure, portal angiography confirmed an inflow tract to the BDVs. Therefore, covered stents were placed in the PV and adjusted to block the inflow tract to the BDVs at the distal end. After stenting, the BDVs were successfully blocked and all PV blood flowed through the stent placed in the extra-hepatic PV. Two weeks after stenting, the BDVs had disappeared completely and the bleeding has not recurred for months. We experienced a case in which PV stenting not only reopened an obstructed PV but also successfully occluded the inflow tract. This case demonstrates the potential of PV stenting for the treatment of hemorrhagic BDVs.