Clinical Journal of Gastroenterology最新文献

Portopulmonary hypertension (POPH), a subtype of pulmonary arterial hypertension (PAH), develops with portal hypertension and may persist after liver transplantation. While there have been successes using balloon-occluded retrograde transvenous obliteration (BRTO) for POPH, no reports exist on long-term follow-up. A 60-year-old man with hepatitis C cirrhosis developed POPH. At the time POPH was diagnosed, the mean pulmonary artery pressure (mPAP) was 31 mmHg. After medical management, mPAP improved to 20 mmHg, and he underwent living-donor liver transplantation. Three years post-transplant, he presented with severe dyspnea and elevated mPAP of 67 mmHg. Despite pharmacological treatment for PAH, his symptoms and pulmonary pressures remained uncontrolled. After transplantation, the pre-existing splenorenal shunt expanded, suggesting that increased shunt blood flow contributed to worsening POPH. BRTO was performed after confirming that shunt occlusion did not elevate portal pressure. Post-procedure, his pulmonary pressures improved (mPAP, 25 mmHg), and symptoms resolved. Over 5 years, no recurrence of POPH, portal hypertension, or liver dysfunction occurred. This case demonstrates the long-term effectiveness of BRTO in treating POPH exacerbation post-liver transplantation. In cases of POPH following liver transplantation, portosystemic shunt occlusion via BRTO may be an effective strategy to improve POPH.

A 45-year-old healthy woman presented with peritonitis and septic shock, necessitating emergency surgery. Intraoperative findings did not definitively rule out secondary peritonitis, leading to a colon resection and ileostomy. However, the patient was later diagnosed with primary peritonitis caused by Group A streptococcus and complicated by streptococcal toxic shock syndrome (STSS). Given the poor prognosis and diagnostic challenges associated with STSS, surgeons should remain vigilant to the possibility of STSS in cases of peritonitis and ensure appropriate measures, including culture testing, are undertaken and provide aggressive systemic treatment alongside targeted therapy for the underlying condition.

A 36-year-old woman with an unremarkable medical history was admitted to our hospital owing to hematemesis. Upper gastrointestinal endoscopy revealed F3 esophageal varices and F3 gastric varices with erosions, which were treated with endoscopic injection sclerotherapy with histoacryl. Contrast-enhanced computed tomography showed that the superior mesenteric vein and splenic vein converged and drained into the inferior vena cava, with no identifiable intrahepatic portal vein branches. Additionally, collateral circulation and thrombosis in the superior mesenteric vein were identified. On the basis of these findings, we diagnosed congenital absence of the portal vein and associated portal hypertension. After treatment for various complications, the patient underwent living donor liver transplantation as a curative treatment. Surgical pathology also supported the diagnosis of portal vein agenesis. Congenital absence of the portal vein is a rare congenital condition, and only one case involving variceal rupture has been reported. There are no established treatment protocols; however, given the pathophysiology, the development of varices is certainly possible. Effective bridging therapy followed by living donor liver transplantation is expected to result in a favorable prognosis. Although the patient remained free from rebleeding for seven months after initial treatment, the absence of portal flow and progression of SMV thrombosis indicated a high risk of recurrence and other complications. After multidisciplinary discussion, living donor liver transplantation was chosen as the most reliable curative treatment compared with endoscopic therapy or shunt surgery.

A 48-mm splenic mass was incidentally discovered in a 78-year-old man upon computed tomography. Follow-up imaging at 12 months revealed enlargement to 60 mm, prompting endoscopic ultrasound-guided tissue acquisition with a 22-gauge needle. Histopathological analysis confirmed that it was a sclerosing angiomatoid nodular transformation. The patient was asymptomatic and had no hematologic abnormalities; therefore, splenectomy was not performed. After biopsy, the lesion regressed from 60 mm to 46 mm, possibly owing to hematoma formation or vascular disruption, and remained stable during 36 months of follow-up. Although splenectomy has been performed in most reported cases of sclerosing angiomatoid nodular transformation because of diagnostic uncertainty, a few recent reports have demonstrated that sclerosing angiomatoid nodular transformation can be diagnosed by endoscopic ultrasound-guided tissue acquisition, thereby avoiding splenectomy. This case highlights the diagnostic utility of endoscopic ultrasound-guided tissue acquisition and supports spleen-preserving management for biopsy-proven sclerosing angiomatoid nodular transformation.

Delayed anastomotic leakage (DAL), defined as occurring > 30 days postoperatively, poses diagnostic and therapeutic challenging. Radiotherapy is a recognized risk factor for DAL, but most studies focused on conventional radiotherapy rather than short-course radiotherapy (SCRT). We describe a case of DAL following SCRT in a very elderly patient to emphasize late presentation and diagnostic considerations. A 91-year-old man with rectal cancer underwent preoperative SCRT (25 Gy/5 fractions) without chemotherapy because of advanced age and low performance status. Twelve weeks later, he underwent robot-assisted low anterior resection with diverting ileostomy. Seventeen months postoperatively, he presented with general malaise and hematochezia. C-reactive protein was elevated to a higher level than postoperative, and colonoscopy identified an anastomotic posterior fistula, leading to DAL diagnosis. Transverse colostomy was subsequently performed, after which he remains asymptomatic, and C-reactive protein levels has returned to initial postoperative levels. This case highlights DAL occurring 17 months after low anterior resection with SRCT alone in a nonagenarian. DAL should be considered a potential late complication following both conventional radiotherapy and SCRT. Careful monitoring of C-reactive protein may provide a valuable diagnostic trigger for earlier detection, particularly in posterior site leakage where symptoms may be subtle or delayed.

We report a rare case of spontaneous regression of primary hepatic diffuse large B-cell lymphoma (DLBCL) in an 89-year-old man. A 12 cm solitary hepatic mass was found in the anterior and medial segments. Contrast-enhanced CT showed a hypovascular solid tumor. Serologic markers including hepatitis B virus, hepatitis C virus, human immunodeficiency virus, alpha-fetoprotein, protein induced by vitamin K absence or antagonist-II, carbohydrate antigen 19-9, and carcinoembryonic antigen were negative, but soluble interleukin-2 receptor was elevated. Ultrasound-guided liver biopsy confirmed DLBCL, and the diagnosis of primary hepatic lymphoma was established based on Caccamo's criteria. The patient declined chemotherapy or radiotherapy due to age and preference, and was observed without treatment. Initially, the tumor grew slightly, but later imaging showed spontaneous regression without intervention. No recurrence or progression was observed during 15 months of follow-up. The regression may have been triggered by an immune response, possibly induced by biopsy-related stimulation. Primary hepatic lymphoma is extremely rare, accounting for 0.07% of malignant liver tumors, and spontaneous regression of untreated DLBCL is exceedingly uncommon. This case highlights the potential role of immune-mediated mechanisms in spontaneous tumor regression and supports careful observation as a possible management strategy in select elderly patients with primary hepatic lymphoma.

Clonorchiasis, caused by Clonorchis sinensis, is a parasitic liver disease endemic in East Asia, primarily transmitted by consuming raw or undercooked freshwater fish. While clonorchiasis is often asymptomatic, chronic infection may lead to serious complications, including cholangiocarcinoma. In Japan, the prevalence has markedly declined, yet sporadic cases persist, especially in regions with traditional dietary practices. We report a rare suspected case of hepatic clonorchiasis in a Japanese woman in her 70s. She presented with mild liver dysfunction and no overseas travel history. Routine ultrasonography revealed a 12-mm hypoechoic hepatic lesion. Further imaging studies, including contrast-enhanced ultrasound (CEUS), CT, and MRI, revealed no contrast enhancement within the lesion. Tumor markers for hepatocellular carcinoma were also negative; however, these findings were insufficient to establish a definitive diagnosis. Serologic testing revealed weakly positive clonorchiasis antibodies. A liver biopsy identified a cystic lesion with eosinophilic infiltration and necrosis, consistent with a parasitic infection. Given the patient's dietary history and serologic/pathologic evidence, clonorchiasis was considered the most likely diagnosis. This case emphasizes the diagnostic challenges of hypovascular hepatic lesions and the limitations of imaging alone. This report highlights the importance of considering parasitic infections in the differential diagnosis of hypovascular hepatic lesions, even in non-endemic settings. Ultrasonography may facilitate the early detection of liver parasites.

Double gallbladder is a rare congenital anomaly of the biliary system. In this study, we present an extremely rare case of a double gallbladder with an accessory cystic duct draining into the main pancreatic duct. The patient was a 14-year-old boy with recurrent acute pancreatitis. Endoscopic retrograde cholangiopancreatography revealed an accessory gallbladder draining into the main pancreatic duct, along with a filling defect suggestive of a stone within the accessory cystic duct. These findings did not suggest pancreaticobiliary maljunction. We safely performed laparoscopic resection of the gallbladder and accessory gallbladder, as well as accessory cystic duct stone removal, using intraoperative cholangiography. Biochemical analysis revealed elevated amylase levels in the gallbladder bile and elevated bilirubin levels in the accessory gallbladder fluid, suggesting bidirectional reflux of pancreatic juice and bile. Given the potential risk of malignancy, careful long-term follow-up is required. In this case report, we reviewed existing classifications of multiple gallbladders and reorganized them based on previously reported cases.

We report a case of encapsulating peritoneal sclerosis (EPS) associated with tuberculous peritonitis. A man in his 50s presented with fever, anorexia, and abdominal distension and was urgently hospitalized because computed tomography (CT) revealed ascites. Despite hospitalization for 1 month, the diagnosis remained unclear and his condition worsened; therefore, the patient was transferred to our hospital. At our hospital, his fever reached approximately 38 °C and an upper abdominal mass was palpable. Contrast-enhanced CT revealed encapsulated ascites and extensive peritoneal thickening with adhesions, resulting in a diagnosis of EPS. Mycobacterium tuberculosis complex was detected in the ascitic fluid culture, thus confirming EPS secondary to tuberculous peritonitis. CT revealed rapid bowel dilatation, suggesting a high risk of ileus. We initiated treatment comprising four antituberculosis drugs (isoniazid, rifampicin, pyrazinamide, and ethambutol) and prednisolone (60 mg/day). The fever resolved rapidly and inflammatory markers improved. CT revealed resolution of ascites and bowel dilation. Therefore, the steroid dose was tapered. On day 28, the patient was discharged. This case highlights that tuberculosis should be considered as a cause of EPS in patients without a history of peritoneal dialysis, and that early steroid therapy is necessary to prevent EPS progression to ileus.