In an attempt to clarify the protective action of an antioxidant agent against acute toxicity of thioacetamide (TAA) and in order to throw some light on an satisfying concept of the mechanism of its action, a single dose of alphatocopherol (200 mg per kg) was given orally by stomch tube to male mice prior to the administration of thioacetamide in a dose of 200 mg per kg of body weight. Sections of liver samples, obtained from the mice which were sacrificed at intervals of 3, 6, 9, or 12 hours after TAA administration, were stained using the methyl green-pyronin technique. At 3 hours following TAA administration, the pretreatment with alpha-tocopherol inhibited almost completely such alterations of the hepatocytes in the animals given TAA alone, as revealed by loss and clumping of cytoplasmic pyroninophilic granules in the periportal zone of the lobule. At 6, 9, and l2 hours, the prevention of alpha-tocopherol was incomplete in degree and extent. The changes of the hepatocytes were more intense and extensive in the TAA-treated 6 to 12 hour-groups than in the 3 hour-group of TAA-treated ones. Some discussion is given of the mechanism of TAA toxicity, with respect to the microsoma1 lipid peroxidation.
Acetamides/poisoning* ; Animal ; Hepatitis, Toxic/pathology* ; Hepatitis, Toxic/prevention & control ; Liver/pathology* ; Male ; Mice ; Vitamin E/pharmacology* ; Vitamin E/therapeutic use

Ticlopidine inhibits platelet aggregation and provides beneficial secondary prevention of cerebrovascular and coronary artery disease. Frequently reported adverse effects of ticlopidine include diarrhea, nausea, and rash. However, to our knowledge, there are only a few published reports of the simultaneous occurrence of cholestatic hepatitis and pure red cell aplasia. Here we report a patient with simultaneous severe cholestatic hepatitis and pure red cell aplasia associated with ticlopidine. Although these adverse effects are rare, periodic hematological and liver function tests are recommended after starting ticlopidine.
Acute Disease ; Cholestasis/*chemically induced/diagnosis/etiology ; Female ; Hepatitis, Toxic/*diagnosis/pathology ; Humans ; Liver Function Tests ; Middle Aged ; Platelet Aggregation Inhibitors/*adverse effects ; Red-Cell Aplasia, Pure/*chemically induced/diagnosis/pathology ; Ticlopidine/*adverse effects

In attempting to ellucidate the mechanism of action of CCl4 toxicity on the liver, the histobgical and histochemical studies were carried out, at the cellular or ultrastructural level, rats were given a single oral dose of 1.25 ml/kg of CCl4 one hour after cervical spinal cordotomy. Hepatic lesions induced by CCl4 administration such as the fatty change of hepatic cells and the sinusoidal congestion were abolished by cordotomy. The decreased activities of adenosine triphosphatase and alkaline phosphatase in the hepatic cells and bile canaliculi of the poisoned animals were restored to a large extent by the operation. Cordotomy also prevented some liver cell changes as seen by the electron microscope in the CCl4-intoxicated rats. It is evident that the hepatotoxic effects of carbon tetrachloride can be inhibited or prevented by cervical cordotomy.
Acid Phosphatase/analysis ; Adenosinetriphosphatase/analysis ; Animal ; Carbon Tetrachloride Poisoning* ; Cordotomy* ; Hepatitis, Toxic/prevention & control* ; Histocytochemistry ; Liver/drug effects* ; Liver/enzymology ; Liver/pathology ; Male ; Microscopy, Electron ; Rats ; Rats, Inbred Strains

Allopurinol-induced hypersensitivity syndrome is characterized by an idiosyncratic reaction involving multiple-organs, which usually begins 2 to 6 weeks after starting allopurinol. In rare cases, the adverse reactions to allopurinol are accompanied by a variety of liver injury, such as reactive hepatitis, granulomatous hepatitis, vanishing bile duct syndrome, or fulminant hepatic failure. Here we report a case with granulomatous hepatitis and ductopenia. A 69-year-old man with chronic renal failure, hyperuricemia, and previously normal liver function presented with jaundice, skin rash, and fever 2 weeks after taking allopurinol (200 mg/day). In histopathology, a liver biopsy specimen showed mild spotty necrosis of hepatocytes, marked cholestasis in parenchyma, and some granulomas in the portal area. There were vacuolar degeneration in the interlobular bile ducts and ductopenia in the portal tracts. Pathologic criteria strongly suggested the presence of allopurinol-induced granulomatous hepatitis with ductopenia and cholestasis. The patient fully recovered following the early administration of systemic corticosteroid therapy.
Aged ; Allopurinol/*adverse effects/therapeutic use ; Antimetabolites/*adverse effects/therapeutic use ; Bile Duct Diseases/*chemically induced/diagnosis/pathology ; Bile Ducts, Intrahepatic/*drug effects/pathology ; Cholestasis/*chemically induced/diagnosis/pathology ; Drug Eruptions/pathology ; Granuloma/*chemically induced/pathology ; Hepatitis, Toxic/*pathology ; Humans ; Kidney Failure, Chronic/complications/drug therapy ; Male