A 74-year-old man was hospitalized due to hematemesis. Upper gastrointestinal endoscopy revealed a very large and dark red mass in the cardiac region of the stomach that extended from the upper esophagus. A biopsy specimen showed hemorrhagic tissue and no malignant cells. The tumor-like region ulcerated at 5 days after the administration of intravenous lansoprazole at a dose of 30 mg twice a day and resolved with scar formation at 2 months after a change to oral rabeprazole at a dose of 10 mg/day.We diagnosed the patient with gastroesophageal submucosal hematoma. Gastroesophageal submucosal hematoma is a rare complication. In this case, we could follow the process of its disappearance by endoscopy.

A 37-year-old man was diagnosed with Wilson disease at the age of 14. His first manifestations were neurological. He was treated with trientine for more than 10 years and suffered from anemia and liver dysfunction. Wilson disease is a genetic disorder characterized by accumulation of copper in the body. Excess copper is toxic, but copper is an essential trace element. Copper-binding ceruloplasmin is important for iron metabolism. Excess copper chelating treatment-induced anemia and iron deposition in the liver was suspected. Proper monitoring of copper status is important for the management of Wilson disease.

A 56-year-old woman with rheumatoid arthritis treated with methotrexate (MTX) was admitted to our hospital due to multiple liver tumors. Contrast-enhanced computed tomography (CT) revealed multiple hypovascular masses, and 18F-fluorodeoxyglucose positron emission tomography CT showed diffuse abnormal accumulation in the liver only. We therefore made a diagnosis of MTX-related primary hepatic lymphoma (MTX-PHL) exhibiting features of diffuse large B-cell lymphoma. Although MTX has been reported to increase the risk of lymphoproliferative disorders, MTX-PHL has not been reported previously. The present case is the first case in which MTX appears to have been involved in the development of PHL.

Background & Aims Hepatitis C virus (HCV) infection has been known to cause various extrahepatic autoimmune disorders. The prevalence of platelet‐associated immunoglobulin G (PA‐IgG) has been high in patients with HCV infection. Because thrombocytopenia in HCV‐related liver diseases is a notable problem, we performed prospective study on the effect of direct‐acting antivirals (DAAs) treatment on PA‐IgG and platelet count. Methods A total of 215 patients with HCV‐related liver disease were enrolled in this study. The patients who discontinued DAAs or did not undergo adequate laboratory examinations and who did not achieve sustained virologic response were excluded and finally a total of 187 patients were investigated. Results A total of 171 patients (91.4%) were PA‐IgG positive (>46 ng/107 cells) before starting DAAs (baseline). The PA‐IgG level elevation was significantly correlated with higher liver inflammation and fibrosis markers (P < 0.05) and lower platelet count (P = 0.000019). The platelet count of the patients with low PA‐IgG titer tended to be higher at baseline, end of treatment (EOT), and at 12 and 24 weeks after EOT. The platelet count increased at EOT (P < 0.05) and 24 weeks after EOT (P < 0.01). The PA‐IgG levels were significantly decreased at EOT, 12 and 24 weeks after EOT (P < 0.01). Multiple regression analysis found that only platelet count at baseline was closely associated with negative conversion of PA‐IgG at 24 weeks after EOT (P = 0.004). Conclusions Eradication of HCV by DAAs treatment successfully decreased PA‐IgG level and increased platelet count.

A 71-year-old male patient was diagnosed with rheumatoid arthritis (RA) in 2000. Various disease-modifying anti-rheumatic drugs (DMARDs) and an anti-tumor necrosis factor biologic etanercept were administrated, but were unable to control the disease activity of RA. He was then diagnosed with rheumatoid vasculitis and received a total of 3 courses of an anti-interleukin-6 receptor antibody, tocilizumab. After the 3 courses of tocilizumab therapy, ascites and renal dysfunction gradually appeared and he was admitted to our hospital. Biochemical data suggested that he had developed decompensated liver cirrhosis. His renal function deteriorated rapidly, and he died 9 days after the admission. Serum aminotransferase levels had been relatively low during the treatment with tocilizumab, however, autopsy showed marked atrophy of the liver. Immunohistochemical analysis revealed that the hepatocytes had fallen into apoptosis and that hepatic regeneration had been extremely suppressed. Although molecular target drugs such as tocilizumab are being widely used and are important emerging treatment options in adult patients with moderate to severe RA, these drugs could induce liver failure by inhibiting liver regeneration as in this case. Physicians need to stay alert to the impact of these drugs on liver regeneration and should follow up with ultrasonography or computed tomography.