Tranilast, an anti-allergic drug, was originally made in Japan, and is now being frequently used. Though ill effects of Tranilast in urology have been known widely, the adverse effect of Tranilast on liver function has been scarcely reported. Having experienced 7 cases of liver disease due to cholestasis by the drug, we summarized these cases and reported the characteristics of liver injury induced by the drug.
All the patients, who had took Tranilast orally and developed liver injury, first manifested hematuria and micturition pain, and then developed jaundice. Though the degree of liver injury was various depending on individuals, the clinical course turned better about 27 days after cessation of Tranilast.

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.

Eosinophilic gastroenteritis (EG) is characterized by infiltration of eosinophils into the wall of the digestive tract, and the clinical spectrum seems to depend on the predominant site of eosinophilic infiltration of the wall.
We experienced four cases of EG, and two of them (Cases, 1 and 2) manifested massive ascites, suggesting the principal lesion is located on the serous coat. Case 3 manifested abdominal pain and vomiting, and muscle layer involvement of the duodenum was detected by ultrasonography and CT scan. In case 4, epigastralgia was a main symptom. An endoscopic examination revealed marked redness and erosion of the gastric mucosa associated with massive infiltration of eosinophils. In this case, mucosal involvement seemed to be the main lesion because hypertrophy of the gut wall thickness was not found by ultrasonography and CT scan.
Although the pathogenesis of this disease is obscure, allergic mechanism may play an important role. Three cases had histories of allergic diseases, and steroid therapy resulted in prompt disappearance of symptoms.