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By Silvio Garattini

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Mansoni in vitro (Archer and Yarinsky, 1972), it is also inactive in mice infected with Japanese and Philippine strains of S. , 1972). By administering tritium-labeled hycanthone to mice infected with S. , (1970) observed that peak concentrations of the drug in the blood plasma were reached within 30 minutes and that these concentrations were higher than those in the blood red cells. The drug detected in the worms was unchanged hycanthone. At the end of 24 hours the schistosomes contained more drug than was present in the blood.

Fatal cases after hycanthone administration were published by Cunha (1970), Mendonsa et al. (1970), Medeiros et al. (1972), Gane (1971, 1973), Lapierre et al. (1973), Andrade et al. (1974), Godoy et a/. (1974), Marinho et al. (1974a,b), Bina and Prata (1974). , 1970; Coutinho and Barreto, 1971; Cunha et a / . , 1972). From these reports, counterindications are well established in some cases, although in others they can only be presumed. ). Summing up, hycanthone is a hepatotoxic drug sometimes producing only elevation of transaminase levels, sometimes inducing jaundice and, in some patients causing, severe hepatic injury, such as yellow atrophy, with consequent death.

1971). Sherif et al. (1971) achieved 89% cure after treating 1095 bilharzial patients, infected with either S. haematobium o r S. 7 mg/kg to 4 mg. In one group, hycanthone was administered with the multidose gun. Farid et al. 0 mg/kg. haematobium patients and 1 out of 10 S . mansoni patients seemed to be cured. Serial liver biopsies confirmed the development of hepatic-cell injury in 1 out of 4 patients that presented increase bromsulphalein (BSP) retention and serum transaminase levels. In newly infected patients, hycanthone displays poor activity.

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