Clinical Journal of Gastroenterology最新文献

Pancreatic cancer is an aggressive malignancy with a poor prognosis. Although distant metastases are common at the time of diagnosis, metastatic spread to the rectum is rare. Furthermore, there have been no reports of acute rectal obstruction caused by a metastatic rectal tumor from pancreatic cancer. A 75-year-old man presented with lower gastrointestinal bleeding, abdominal pain, and distention. Colonoscopy and abdominal computed tomography confirmed acute rectal obstruction. Additionally, computed tomography identified a tumor in the pancreatic tail. An emergency loop colostomy on the transverse colon was performed. During preoperative assessment, the patient was initially considered to have synchronous primary cancers of the rectum and pancreas. However, microscopic examination confirmed that the rectal tumor was a metastasis from pancreatic cancer. Chemotherapy for pancreatic cancer was initiated immediately, and as of this writing, the patient has survived for more than 1 year. In summary, we herein report a rare case of pancreatic cancer metastasizing to the rectum. The prognosis of pancreatic cancer with distant metastases may be improved by enabling early initiation of chemotherapy. Minimally invasive surgery could be an effective approach for managing rectal obstruction due to metastasis.

Endoscopic step-up approach, which involves endoscopic ultrasound-guided drainage followed by necrosectomy, has been suggested as a potentially advantageous alternative to the surgical step-up approach for walled-off necrosis (WON) following acute pancreatitis. Recent studies indicate that although there is no significant difference in major complications or mortality between the two approaches, the endoscopic step-up approach is often preferred due to shorter hospital stays and lower re-intervention rates. However, a multidisciplinary approach should be considered for complex cases. Transgastric or transduodenal approaches can be challenging in cases of extensive intra-abdominal WON, whereas percutaneous endoscopic necrosectomy (PEN) has been reported as a safe and effective minimally invasive technique. We report the cases of two critically ill patients with extensive WON and uncontrolled sepsis who were successfully treated with simultaneous dual-endoscopic PEN. This approach may offer a promising strategy for enhancing treatment efficacy in extensive WON when performed appropriately.

Systemic therapy for advanced hepatocellular carcinoma (HCC) has progressed significantly, yet the management of immune-related adverse events (irAEs) remains a challenge, particularly with anti-CTLA-4 and anti-PD-L1 antibodies. We present two cases of severe irAEs during durvalumab plus tremelimumab (DT) therapy, demonstrating successful management and favorable outcomes. In Case 1, a 76-year-old male with metabolic-associated steatotic liver disease-related HCC experienced disease progression after lenvatinib and subsequently initiated DT therapy. He developed Grade 3 immune-related myositis at week 5, which was successfully managed with prednisolone. A partial response (PR) was achieved and maintained, with a 55% tumor reduction at 8 months. In Case 2, a 73-year-old male with alcoholic cirrhosis and a 16-cm HCC received DT therapy. On day 19, he developed Grade 3 immune-related hepatitis and thyroiditis, which were controlled with prednisolone. After steroid tapering, durvalumab was successfully rechallenged, maintaining a 38% tumor reduction at 6 months with a sustained PR. In the case series, lower baseline serum interleukin (IL)-6 levels were associated with the development of Grade ≥ 3 irAEs. These findings suggest that IL-6 may serve as a predictive biomarker, aiding in risk assessment and the optimization of individualized treatment strategies prior to anti-CTLA-4 therapy.

Portal hypertension typically occurs in cirrhosis but can rarely develop in the absence of hepatic fibrosis, particularly in hematologic malignancies such as chronic lymphocytic leukemia (CLL). We report a 70-year-old man with CLL who developed portal hypertension, presenting with massive splenomegaly, esophageal variceal rupture, and refractory ascites. He was initially diagnosed with alcohol-related cirrhosis based on a history of alcohol use and elevated liver stiffness on elastography. Chemotherapy had been discontinued due to cerebral hemorrhage and cytopenia. Ascites was refractory to and intolerant of diuretics and was worsened by renal dysfunction due to spontaneous bacterial peritonitis. After resolution of peritonitis, partial splenic artery embolization (PSE) was performed to relieve portal hypertension. Although ascites improved post-PSE, the patient developed a severe infection and died. Autopsy revealed no cirrhosis or hepatic fibrosis; instead, portal hypertension was attributed to CLL cell infiltration leading to splenomegaly and portal venous obstruction. This case underscores the need to consider hematologic malignancies as potential causes of non-cirrhotic portal hypertension. While PSE may offer symptomatic relief, the risk of fatal infection must be carefully weighed in patients with hematological malignancies. Histologic confirmation remains critical for accurate diagnosis in atypical presentations of portal hypertension.

A 67-year-old woman was diagnosed with pancreatic head cancer. Staging laparoscopy (SL) was performed, peritoneal cytology (CY) was positive (CY1), and a peritoneal access port was created. The patient was started on nab-paclitaxel plus gemcitabine therapy (GnP). After 6 courses of GnP therapy, computed tomography revealed a single metastatic tumour in the liver. The disease was considered advanced, and nal-IRI + 5-FU/LV therapy was initiated as second-line treatment. After 13 courses of treatment, both the liver nodule and the primary tumour decreased in size, and CY became negative (CY0). A second-look SL and partial resection of the metastatic liver were performed. Thereafter, after 7 additional courses of nal-IRI + 5-FU/LV therapy. A third-look SL revealed no distant metastasis, and CY0. Then, pancreatoduodenectomy was performed as the conversion surgery. Histological examination revealed Grade 1a disease. She resumed adjuvant chemotherapy and is alive 7 months postoperatively without any signs of recurrence. In our rare case, a patient with CY1 pancreatic cancer and liver metastasis was successfully treated with nal-IRI + 5-FU/LV and was able to undergo radical resection. To our knowledge, this is the first report on conversion surgery with this regimen, which is not considered to have a high response rate.

This study investigated histological liver-tissue changes before and after 1 year of pemafibrate treatment in two women with metabolic dysfunction-associated steatotic liver disease (MASLD) and hypertriglyceridemia who were refractory to ≥ 6 months of lifestyle intervention. The patients underwent paired liver biopsies before and after receiving pemafibrate (0.2 mg, once daily) for 52 weeks. Improvements in the non-alcoholic fatty liver disease activity score and fibrosis stage were examined. In Case 1, pre-treatment liver biopsy revealed 90% steatosis, ballooning, lobular inflammation, and fibrosis (Brunt grade 2, stage 3). Post-treatment, steatosis decreased to 50%, ballooning and inflammation resolved, and fibrosis improved (grade 1, stage 2). In Case 2, pre-treatment liver biopsy showed 70% steatosis, mild lobular inflammation, and fibrosis (grade, 1, stage 3). Post-treatment, steatosis increased to 90%, inflammation resolved, and fibrosis improved (grade 1, stage 1). The fibrosis-4 index improved in both cases; however, shear wave elastography showed no improvement. Pemafibrate may exert antifibrotic and anti-inflammatory effects in MASLD regardless of steatosis trends and that histological assessment remains crucial, especially when non-invasive markers provide inconsistent results. This is the first report to confirm histopathological improvement with pemafibrate via serial liver biopsy, offering important insights into its therapeutic potential for MASLD with dyslipidemia.

Patients with decompensated cirrhosis complicated by hepatocellular carcinoma (HCC) or those who have undergone liver transplantation following liver failure after HCC treatment should continue to receive post-transplant surveillance. Any new liver tumor must be carefully evaluated to determine whether it is a recurrence of HCC. Focal nodular hyperplasia (FNH), the second most common benign hepatic tumor, is believed to result from the hyperplastic response of hepatocytes to pre-existing vascular malformation. Here, we report a case of hepatic FNH two years after living-donor liver transplantation in a patient who experienced liver failure following treatment for HCC. Given the rarity of hepatic FNH after liver transplantation, we present this case along with a review of the literature.

Carbon dioxide (CO₂) embolism is an intraoperative complication during laparoscopic hepatectomy (Hx). Paradoxical CO₂ embolism with right-to-left systemic shunting can cause cerebral infarction. Iatrogenic atrial septal defect (IASD) can occur after catheter ablation (CA) for atrial fibrillation (AF), and patients with IASD are at risk of paradoxical CO₂ embolism. The present case report described two CO₂ embolism cases during laparoscopic Hx after CA for Af (one is a paradoxical CO₂ embolism). Intraoperative transesophageal echocardiography (TEE) is required for quick identification of CO₂ embolism, and the procedure should be converted to laparotomy when paradoxical CO₂ embolism occurs. Those patients were fortunately discharged without any postoperative morbidity. CA for AF may increase the risk of paradoxical CO₂ embolism. The indication for laparoscopic Hx should be carefully judged based on the surgical procedure and the findings of preoperative TEE. Intraoperative TEE may be beneficial for early detection for quick identification of CO₂ embolism, and the procedure should be converted to laparotomy when paradoxical CO₂ embolism occurs.

Although observation is the standard management strategy for hepatic hemangiomas (HHs), surgical intervention may be indicated in cases of progressive enlargement, lesions > 50 mm, those causing compressive symptoms, or those associated with Kasabach-Merritt syndrome. Here, we report the case of a 51-year-old woman with a giant HH occupying almost the entire liver with a volume of 6572.5 mL. The patient presented with severe compressive symptoms and coagulopathy; however, surgical resection was infeasible. Because she did not develop liver failure, transplantation was not indicated, and no effective treatment options were available. Sirolimus, a mammalian target of rapamycin inhibitor, has been used to treat intractable lymphatic disorders and congenital vascular malformations; however, there have been no previous reports on its use in adult giant HHs. Moreover, sirolimus was administered, which resulted in remarkable tumor shrinkage. This suggests that sirolimus may be a valuable therapeutic option for adult patients with giant HHs in whom conventional treatments are not applicable.

Clostridioides difficile infection is a prevalent healthcare-associated infection that can lead to severe gastrointestinal complications, including gastrointestinal bleeding. This case report presents a 77-year-old female with multiple comorbidities, including a history of cerebral infarction, who was on long-term aspirin therapy. She initially presented with melena, suggestive of upper gastrointestinal bleeding. Preliminary treatment with pantoprazole and somatostatin resolved the melena. However, she later developed dark red blood per rectum, indicating a shift to lower gastrointestinal bleeding. Further workup, including abdominal CT, colonoscopy, and fecal antigen testing, supported the diagnosis of C. difficile colitis. She was subsequently treated with vancomycin and metronidazole, which resulted in clinical improvement and ultimately led to her discharge from the hospital. This case emphasizes the importance of considering C. difficile infection in patients with gastrointestinal bleeding who are receiving proton pump inhibitors and somatostatin, particularly those with risk factors for the infection.