Clinical Journal of Gastroenterology最新文献

Reactivation of cytomegalovirus (CMV) remains a significant concern in patients receiving immunosuppressive therapy. Although CMV infection and reactivation is associated with intrahepatic cholestasis in infants and immunosuppressive adults, intrahepatic cholestasis caused by CMV infection is rare in immunocompetent adults. Here, we report a case with CMV-induced intrahepatic cholestasis in an immunocompetent adult complicated by hemophagocytic syndrome (HPS). We excluded CMV infection from differential diagnosis of intrahepatic cholestasis based on serum CMV antibody profiles and immunocompetency at the initial assessment and then started oral administration of prednisolone (PSL). The development of CMV-induced lethal HPS after the treatment with PSL led us to reconsider the possibility of CMV infection as an etiology of cholestasis. Frozen serum before PSL administration exhibited a high copy number of CMV DNA and thus we reached the final diagnosis of CMV-induced intrahepatic cholestasis complicated by HPS. Resolution of cholestasis and HPS was achieved by ganciclovir. The patient exhibited elevated serum levels of IL-18, C-C motif chemokine ligand 2, and IL-13 with no alterations in serum levels of IFN-γ or TNF-α. This case underscores the importance of consideration of CMV reactivation as a differential diagnosis for intrahepatic cholestasis even in immunocompetent patients.

Background: Atezolizumab plus bevacizumab (ATZ + BV) is the standard first-line therapy for unresectable hepatocellular carcinoma (HCC). However, long-term treatment is frequently limited by adverse events such as proteinuria and hypertension, often resulting in treatment interruption or discontinuation. Evidence regarding the feasibility of dose modification, particularly half-dose BV, remains limited.

Case presentation: We report a patient with unresectable HCC who responded favorably to ATZ + BV but developed significant proteinuria (> 2 g/day) after several cycles. To manage this toxicity, BV was reduced to half the standard dose while continuing full-dose ATZ. Following dose modification, proteinuria stabilized, and systemic therapy was maintained for more than 3 years. During follow-up, the patient underwent gastrectomy for gastric cancer, at which time a peritoneal metastatic lesion of HCC was also resected. Histopathological examination revealed complete absence of viable tumor cells, confirming a pathological complete response (pCR). Of note, in our institutional experience with more than 70 patients treated with ATZ + BV, several also required BV half-dose, and long-term disease control was observed, supporting the reproducibility of this approach.

Conclusion: This case suggests that reducing the BV dose to half of the standard level may allow continued ATZ + BV therapy without loss of efficacy. Furthermore, the achievement of pCR in a resected peritoneal metastasis underscores the potential of this management strategy for durable disease control in unresectable HCC.

We present a case of mismatch repair deficient (dMMR) descending colon cancer complicated by peritoneal dissemination and adjacent organ invasion, initially considered unresectable. The patient, a 68-year-old male, experienced acute intra-abdominal hemorrhage due to spontaneous rupture of a pseudoaneurysm from segmental arterial mediolysis (SAM). Emergency surgery confirmed unresectability, prompting immunotherapy with pembrolizumab. Remarkably, after four cycles, significant tumor regression allowed for curative resection, with complete pathological response. Immunohistochemistry revealed a high density of tumor-infiltrating CD8 + T cells and PD-L1-positive stromal cells, indicating robust immune activation. This case underscores immunotherapy's emerging role in converting unresectable dMMR colorectal cancer into resectable disease. This highlights the significance of multidisciplinary management, incorporating immunotherapy, surgical interventions, and vascular assessment to optimize clinical outcomes in dMMR colorectal cancer complicated by vascular pathologies such as SAM. Further investigation into the relationship between vascular pathologies, such as SAM, and malignancy is warranted.

Hepatic hemangiomas, the most common benign liver masses, are often asymptomatic and do not require treatment; however, some subtypes develop complications, including diffuse hepatic hemangiomatosis, a rare disease in which hemangiomas replace the liver parenchyma. We describe a case in which the patient presented with esophageal varices. Upon admission, computed tomography showed a normal liver volume of 829 mL, 69% lower than the standard liver volume. Our findings suggest that in cases of large hepatic hemangiomas, regular imaging is necessary, especially if the liver volume falls below 70% of the standard volume; moreover, the possibility of complications should be considered.

Hereditary haemorrhagic telangiectasia (HHT) is a rare autosomal dominant disorder characterised by epistaxis, mucocutaneous telangiectasia, and arteriovenous malformations (AVMs) in various organs. When linked to mutations in the SMAD4 gene, it also involves multiple hamartomatous polyps; this condition is known as juvenile polyposis syndrome-HHT (JP-HHT) overlap syndrome. Typically considered a bleeding disorder, HHT is associated with an increased risk of vascular thrombosis. Early diagnosis and genotyping can significantly reduce morbidity and mortality in patients with JP-HHT overlap by allowing appropriate screening for complications. Treatment mainly aims to manage symptoms and complications. We present the case of a 32-year-old man exhibiting features of extrahepatic portal venous obstruction with portal hypertension and JP-HHT overlap, along with a review of the literature.

Eosinophilic infiltration of the esophageal muscular layer, known as eosinophilic esophageal myositis (EoEM), is an exceptionally rare condition that can mimic primary motility disorders such as achalasia. We present the case of a 72-year-old male with progressive dysphagia and significant weight loss, whose high-resolution manometry revealed findings consistent with achalasia, but with unusually elevated lower esophageal sphincter pressures. Surgical myotomy was performed and histopathological analysis unexpectedly revealed intense eosinophilic infiltration of the muscularis propria. The patient was treated with systemic corticosteroids, followed by topical budesonide, leading to partial and temporary clinical improvement. This case highlights eosinophilic esophageal myositis as a potential, but underrecognized differential diagnosis in patients with atypical achalasia features and treatment-refractory dysphagia.

This report describes a rare case of anorectal malignant melanoma with metastasis to the pancreas, liver, and small bowel. The patient presented with lower gastrointestinal bleeding and an anal mass. Computed tomography (CT) showed a 4.7 × 6.2 cm mass in the lower rectum. The patient underwent surgery and radiotherapy, achieving a two-year recurrence-free period. However, subsequent CT surveillance revealed a 1.6 cm hypo-dense mass at the head of the pancreas and small liver lesions. An endoscopic ultrasound (EUS)-guided fine-needle biopsy of the pancreatic mass was performed, showing a 2.7 × 1.4 cm hypoechoic lesion and pancreatic duct dilation at the pancreatic head region. The pathological diagnosis confirmed metastatic malignant melanoma. She underwent pancreaticoduodenectomy with liver wedge resection. Following surgery, she remained in remission for another two years before developing liver and jejunal metastases, ultimately succumbing to peritoneal carcinomatosis. This case highlights the diagnostic value of EUS in detecting pancreatic metastasis from anorectal melanoma and illustrates the complexities of managing this aggressive disease. The management of pancreatic metastasis from anorectal melanoma requires careful consideration of surgical resection and systemic therapy.