RESUMEN
Histologic studies of liver tissue from 27 patients given up to 395 mCi (cumulative) of intravenous colloidal 198Au showed no definite radiation injury and no correlation between hepatic abnormalities and dose. Demonstration of aggregates of colloidal gold in the Kupffer cells was inconsistent, suggesting slow removal or dispersion. Although the liver ordinarily receives the highest radiation dose, the critical organ is the marrow. Results support the recent introduction of 198Au to supplement teletherapy for certain neoplasms diffusely infiltrating the liver. Apparently the beta distribution minimizes endothelial injury in large vessels, which has been shown to be the cause of radiation hepatitis.
Asunto(s)
Oro Coloidal Radiactivo/uso terapéutico , Neoplasias Hepáticas/radioterapia , Hígado/patología , Adolescente , Adulto , Anciano , Autopsia , Autorradiografía , Niño , Femenino , Oro Coloidal Radiactivo/efectos adversos , Humanos , Hígado/efectos de la radiación , Neoplasias Hepáticas/patología , Masculino , Persona de Mediana Edad , Traumatismos por Radiación/etiologíaRESUMEN
Encephalitis developing after prolonged antineoplastic therapy in two patients with Hodgkin's disease and in one with multiple myeloma was found at autopsy to be caused by toxoplasmosis. To better understand the pathogenesis of the brain lesions, ranging from microscopic foci to some having a diameter of 6 cm. and characterized by proliferation of the organisms at the margins of expanding necrosis, an animal model was studied. Similar lesions were produced in hamsters by inducing relapse of chronic latent toxoplasmosis through administration of cortisone, cyclophosphamide, or whole body irradiation, but toxic doses of nitrogen mustard and urethane did not precipitate relapse. Notably, relapsing toxoplasmosis generally involves the brain exclusively, suggesting a special susceptibility related to immune mechanisms. The roles of cells and of antibodies in immune surveillance against this chronic infection in otherwise normal hosts are considered. In man the suppression of cellular immunities by certain antineoplastic agents would seem to be decisive in causing relapse of toxoplasmosis, rather than the replacement of immunologically active cells by neoplasm. Because the infection can be controlled with sulfadiazine and pyrimethamine, a high index of suspicion is essential to detect incipient cerebral toxoplasmosis. serial serologic testing is helpful by demonstrating titer elevations; however, poor antibody production or transferred antibody may be misleading clinically when single tests are evaluated. Similarly, a poor inflammatory cell response can make it difficult for the histopathologist to detect small lesions in these patients.