A 58-year-old man, who was under treatment for urticaria with emedastin fumarate for seven days, was admitted to our hospital because of jaundice. On admission, laboratory data showed the cholestatic type of liver dysfunction, AST 106 U/1, ALT 274 U/1, T-Bil 6.8 mg/dl, γ-GTP 857IU/1, and ALP 807IU/1. Anti-mitochondrial antibody (AMA) was positive with titer of 1: 80, whereas anti-pyruvate dehydrogenase (PDH) antibody was negative. Histologically, mild lymphocytic infiltration in portal area was noted. There was no fibrosis or cholangitis. A lymphocyte stimulation test for emedastin fumarate was positive and the diagnosis of drug-induced liver injury was established. Administration of the drug was immediately withheld followed by an immediate improvement in the most of the liver function tests, whereas both AMA and γ-GTP were constantly abnormal for the following two years. Anti-PDH antibody was still negative. The second biopsy of the liver showed minimal expansion of the portal area with fibrosis and mild lymphocytic infiltration. Pseudo-ductular formation and vanished bile ducts were also confirmed although no granulomas were found. These findings were atypical for primary biliary cirrhosis. This seems to be a rare case of drug-induced liver injury with long-standing anti-mitochondrial antibody without primary biliary cirrhosis as an underlying disease.

We encountered a case of far advanced hepatomas involving the lungs and portal veins. The patient was a 38-year-old woman. Chemoembolization had transient effects. Cachexia occurred. After repeated episodes of upper gastrointestinal bleeding, she died. An autopsy revealed a deep gastric ulcer to which a nodule of the hepatocellular carcinoma adhered. Histopathologically, the infiltration of the hepatoma was not evident. These findings suggested that circulatory distarbances of the gastric wall due to the adhesion of the growing hematoma had caused the ulceration.