Japanese Journal of Gastroenterology最新文献

A 71-year-old male patient with multiple liver and lymph node metastases of gallbladder cancer was diagnosed with gallbladder neuroendocrine carcinoma based on liver tumor biopsy. He received chemotherapy with attention to the medical history of interstitial pneumonia and achieved a partial response. The patient died of acute exacerbation of interstitial pneumonia 12 months after diagnosis. A pathological autopsy was performed which confirmed the diagnosis of primary neuroendocrine carcinoma of the gallbladder. The autopsy revealed no adenocarcinoma component, indicating the possibility of transformation from adenocarcinoma to neuroendocrine carcinoma or that the carcinoma originated from a small number of neuroendocrine cells that were originally present in the gallbladder. Gallbladder neuroendocrine carcinoma is very rare, and this case is valuable in that it was diagnosed medically and connected to treatment, and the diagnosis was corroborated with a general autopsy.

A 59-year-old woman presented with frequent episodes of hepatic encephalopathy due to cirrhosis caused by primary biliary cholangitis and a large splenorenal shunt, leading to repeated hospital admissions. We administered maximal medical therapy and enemas to prevent constipation, but her situation did not improve. Subsequently, balloon-occluded retrograde transvenous obliteration (BRTO) was considered;however, because the splenorenal shunt was large and liver function was poor (Child-Pugh C), BRTO might have caused a sudden rise in portal venous pressure and uncontrolled ascites. Therefore, we performed partial splenic artery embolization (PSE), embolizing 43% of the splenic volume, mainly in the lower portion. After PSE, her blood-ammonia level fell and consciousness improved. Since then, she has been hospitalized only once for recurrent encephalopathy. PSE-commonly used for hypersplenism or portal hypertension-decreases splenic venous return and portal pressure, thereby reducing splenorenal-shunt flow and directing ammonia-laden blood to the liver. Thus, PSE is a useful treatment option for hepatic encephalopathy, particularly in patients with large portosystemic shunts.

A 78-year-old male patient came to our hospital with a chief complaint of fever. Computed tomography revealed an indistinct tumor in the pancreatic head, along with dilatation of the bile duct and main pancreatic duct. An endoscopic transpapillary biopsy demonstrated adenocarcinoma in the glandular epithelium and a dense formation of quasi-round cells. Pathology results indicated positive CK AE1/AE3 and INSM-1, negative CD45, and a Ki67 index of about 80%, leading to a diagnosis of neuroendocrine carcinoma (NEC) Grade 3 of the pancreatic head. Consequently, a pancreatoduodenectomy was performed. Postoperative pathology revealed small cell NEC (SCNEC) at the pancreatic head, with infiltrative growth of atypical gland ducts around the bile ducts, indicating the presence of a well-differentiated adenocarcinoma. The adenocarcinoma contained in situ lesions and biliary intraepithelial neoplasia (BilIN), with SCNEC being contiguous. Therefore, the diagnosis was NEC originating from the extrahepatic bile duct, which invaded the pancreatic head. NEC of the extrahepatic bile duct is rare, accounting for approximately 0.2-2% of gastrointestinal neuroendocrine tumors, and it has a poor prognosis, similar to other gastrointestinal NECs, even when surgical treatment is performed. The patient remained an outpatient without recurrence 17 months postoperatively.

Reactivation of resolved hepatitis B virus (HBV) infection without any immunosuppressants has rarely been reported. Here, we describe the spontaneous HBV reactivation in a 78-year-old male patient with resolved HBV infection. Twenty-five years ago, he received interferon treatment for chronic hepatitis C. Concurrently, he was negative for HBsAg and positive for anti-HBcAb, and he achieved a sustained virological response (SVR). He developed hepatitis B infection without any cause at the age of 78 years. His serum was positive for HBsAg, HBeAg, and HBV DNA (4.9logIU/ml;genotype B), but negative for anti-HBc IgM and HCV RNA. A liver biopsy revealed A2F1. His serum HBsAg and HBV DNA levels became negative 2 months and 6 months after entecavir treatment, respectively. HBcrAg, the last remaining HBV marker, became negative after 2 years, and ETV treatment was completed after 27 months. No HBV reactivation was observed 4 years after the end of treatment. Full-genome HBV sequence analysis indicated that the patient was infected with HBV of subgenotype B1 and had no mutations in the S, the core promoter, and pre-core regions. This case developed de novo hepatitis B without any immunosuppressants, indicating that aging may have been responsible for the spontaneous HBV reactivation. Additionally, in this report, we summarized the reported cases of reactivation of resolved hepatitis B in elderly patients with no previous triggers.