A 32-year-old woman with asymptomatic primary biliary cirrhosis had autoimmune hemolytic anemia associated with reticulocytopenia and thrombocytopenia despite an intensely erythroid bone marrow. Her anemia was successfully treated with oral prednisolone and intravenous pulse methylprednisolone, with a rapid response of reticulocytosis and sustained erythrocytosis. Tiopronin therapy was later initiated and resulted in fever, rash, exacerbation of the liver disease, and positive direct and indirect antiglobulin tests.
Summary.-Lipids extracted from leucocyte pellets with chloroform-methanol were applied to a DEAE-Sephadex column and the gangliosides were eluted with 02M sodium acetate in methanol. The eluate was desalted by Sephadex G-50 column chromatography. The purified ganglioside was spotted on the high-performance thin-layer plate. The plate was developed and sprayed with resorcinol reagents and heated.Seventeen bands of gangliosides were demonstrated in normal human leucocytes. The composition of these gangliosides was different in the various kinds of leucocytes. Amounts of GM3 ganglioside were apparently greater in normal lymphocytes and leukaemic cells than in granulocytes. Among the acute-leukaemic cells, some kinds of complex gangliosides were much more abundant in myelogenous cells than in lymphocytic cells. These changes in ganglioside composition are suggested as new biochemical markers for leukaemic cells.
A 77-year-old female patients developed severe hepatic injury after the administration of UFTR, which contains tegafur and uracil, for postoperative chemotherapy of colon cancer. Liver damage was recognized 10 months after its administration. Serum markers for viral hepatitis and various autoantibodies were negative. The wedged biopsied liver specimen revealed advanced chronic active hepatitis with periportal confluent necrosis, marked intralobular spotty necrosis, and significant proliferation of pseudo-bile ductules. Although the cessation of the drug and conservative therapies improved hepatic function, an accidental readministration of UFTR caused her severe hepatic damage again. These findings suggest that liver injury in the present case was caused by UFTR. Histological findings were unique. Although tegafur is known to worsen hepatic function when given to patients with liver cirrhosis, UFTR may also cause severe hepatic injury in those without preexisting liver disease.
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