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The first case of hepatic injury induced by Venoplant, extracts of Aesculus Hippocastanum, having antiinflammatory activities, was described. A 37 yr-old man was admitted for treatment of pathological fracture of the left brachial bone. He had been received 65 mg Venoplant at another hospital several hours before admission. 17 days later, a liver function test showed mild abnormality and 60 days after injection, he complained of pruritus and jaundice. Laboratory studies revealed moderate elevation of total bilirubin, ALP, gamma-GTP and mild eosinophilia. CT studies and ERC showed no signs of extrahepatic obstructive jaundice. The lymphocyte stimulation test was positive. The liver biopsy demonstrated marked cholestasis with zonal necrosis in the centrilobular areas but showed little or no changes in the portal tracts. These features are consistent with drug-induced hepatic injury.

Orthotopic liver transplantation has been recommended for patients with disabling polycystic liver disease (PCLD). Because of the shortage of cadaveric donors, living donor liver transplantation (LDLT) has been developed as an alternative. We describe the case of a woman with PCLD as an extrarenal manifestation of autosomal-dominant polycystic kidney disease (ADPKD) who was successfully palliated by LDLT. The patient was a 48-year-old woman with abdominal distention. Computed tomography showed a massively enlarged liver containing innumerable cysts, as well as bilateral kidney cysts. Hepatic and renal functions were well preserved. Genetic analysis of the family did not exclude linkage to the PKD1 locus. Two and a half years after the first examination, the patient reported severely disabling symptoms caused by the PCLD. Living donor liver transplantation was performed using a right-lobe graft. The recipient and donor were both well 8 months after the transplantation. The excised liver weighed 7.4 kg, and the histopathology revealed multiple cysts and von Meyenburg complexes in the portal areas.

ABSTRACT— Intrahepatic cholestasis in paraquat poisoning in man has been thought to be secondary to extensive bile duct injuries, though its exact mechanism remains unsettled. We have examined liver biopsy specimens from two cases of paraquat poisoning. Case 1 (fatal) presented severe intrahepatic jaundice, and liver biopsy showed centrilobular cholestasis with extensive bile duct loss. Ultrastructurally, dilatation of bile canaliculi with decrease of microvilli and thickening of pericanalicular ectoplasm was found in the hepatocytes. Case 2 (alive) showed mild liver dysfunction without jaundice. While liver biopsy showed nonspecific reactive changes with intact bile ducts and ductules, electron microscopy disclosed dilatation of bile canaliculi with decrease of microvilli and thickening of pericanalicular ectoplasm in the hepatocytes, suggesting that damage to the bile secretory apparatus in the hepatocytes develops irrespective of extensive bile duct loss. These findings suggest that bile secretory apparatus in the hepatocytes as well as biliary epithelial cells could be a target of paraquat or its metabolites.