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.

A 67-year-old female patient, with a chief complaint of melena, was referred to our hospital because of a pancreatic tumor. A blood assessment revealed anemia with a hemoglobin (Hb) level of 7.7g/dL. Contrast-enhanced computed tomography (CT) detected a large pancreatic tail tumor and liver metastasis. Upper endoscopy demonstrated bile juice containing a blood-like red in the duodenum. We confirmed the pancreatic cancer diagnosis via endoscopic ultrasound-guided fine needle aspiration (EUS-FNA). CT after the procedure indicated a hematoma in the pancreatic tumor. The patient required frequent blood transfusions due to severe anemia. The second upper endoscopy demonstrated bleeding from the papilla of Vater. We diagnosed the patient with hemosuccus pancreaticus (HP). Pancreatic cancer, not hematoma, was considered to cause HP because we detected blood, such as red bile juice, before EUS-FNA. Her Hb levels decreased although she underwent coil embolization of the left gastric artery and splenic artery branches. We considered surgical treatment to stop the bleeding, but we abandoned surgery because of the pancreatic cancer invasion of the surrounding organs. We then attempted radiation therapy. Her Hb level stopped decreasing following treatment. She did not need frequent blood transfusions until she received radiation therapy and died 3 months later. The autopsy revealed a final diagnosis of anaplastic carcinoma. HP is an uncommon disease caused by bleeding from the papilla of Vater. HP is frequently caused by chronic pancreatitis, but it is also induced by a pancreatic tumor. Most HP cases received interventional radiology and surgical treatment. Here, we describe a case of HP caused by pancreatic cancer in which radiation therapy was effective for hemostasis.

Atezolizumab and bevacizumab combination therapy was initiated in a 71-year-old female patient with unresectable hepatocellular carcinoma. Severe anemia, which was managed with blood transfusion and demonstrated improvement, was observed after the treatment. However, anemia subsequently reoccurred, accompanied by signs of hemolysis. The condition was diagnosed as autoimmune hemolytic anemia due to atezolizumab. Steroid therapy exhibited improvement, and second-line treatment with lenvatinib was successfully initiated. The possibility of autoimmune hemolytic anemia should be considered when anemia is observed during immunotherapy for hepatocellular carcinoma.