Assuntos
Transplante de Medula Óssea , Transtornos Linfoproliferativos/terapia , Ciclofosfamida/uso terapêutico , Ligação Genética , Rejeição de Enxerto/efeitos dos fármacos , Humanos , Imunossupressores/uso terapêutico , Transtornos Linfoproliferativos/genética , Masculino , Transplante Homólogo , Irradiação Corporal Total , Cromossomo XAssuntos
Neoplasias/terapia , Equipe de Assistência ao Paciente , Encaminhamento e Consulta , Neoplasias da Mama/terapia , Carcinoma de Células Pequenas/terapia , Neoplasias do Colo/terapia , Terapia Combinada , Feminino , Doença de Hodgkin/terapia , Hospitais Comunitários , Humanos , Neoplasias Pulmonares/terapia , Masculino , Neoplasias Ovarianas/terapia , Prognóstico , Neoplasias da Próstata/terapia , Neoplasias Retais/terapia , Neoplasias Testiculares/terapiaRESUMO
In 1974, an 11-year-old white boy with the X-linked lymphoproliferative syndrome developed hyper-IgM after becoming infected with Epstein-Barr virus. However, he failed to develop normal immune responses against the virus. In December 1981, when red cell aplasia occurred, he was given packed erythrocytes and gammaglobulin. Nine weeks later, acute infectious mononucleosis developed. Concurrently, his T4/T8 helper/suppressor ratio decreased from 2.7 to 0.2, and IgM antibodies to Epstein-Barr virus appeared. Subsequently, circulating B cells became undetectable in his blood, and agammaglobulinemia appeared. Red cell aplasia abated transiently. This patient's course was complicated by Haemophilus influenzae and Mycobacterium tuberculosis pneumonias, and red cell aplasia and agammaglobulinemia have persisted. Epstein-Barr virus acting as a slow virus probably induced the red cell aplasia and agammaglobulinemia because of the aberrant immune responses to Epstein-Barr virus. Immunodeficient responses to Epstein-Barr virus should be sought in other patients with the diseases documented in our patient.
Assuntos
Agamaglobulinemia/complicações , Anemia Aplástica/complicações , Mononucleose Infecciosa/etiologia , Agamaglobulinemia/genética , Agamaglobulinemia/imunologia , Anemia Aplástica/genética , Anemia Aplástica/imunologia , Linfócitos B/imunologia , Criança , Feminino , Infecções por Haemophilus/etiologia , Haemophilus influenzae , Herpesvirus Humano 4/imunologia , Humanos , Deficiência de IgG , Mononucleose Infecciosa/genética , Mononucleose Infecciosa/imunologia , Masculino , Pneumonia/etiologia , Linfócitos T/imunologia , Fatores de Tempo , Cromossomo XRESUMO
Improved tolerance of splenectomized patients with Hodgkin's disease (HD) to radiotherapy and chemotherapy has been reported. The present study was undertaken to determine the effects of splenectomy and nitrogen mustard (NM) on colony-forming cells (CFC's) of bone marrow cells obtained from CF1 male mice by in bitro agar-gel technique. Splenectomized mice were given NM intraperitoneally on day 11. On day 15, they were sacrificed and the bone marrow was cultured with a source of colony-stimulating factor (CSF). Spleen extract was prepared by grinding spleens from CF1 mice. On the eighth day of incubation, significantly higher numbers of CFC's were found in splenectomized animals at 1% confidence level (F Test) compared with the nonsplenectomized animals. Both splenectomized and non-splenectomized mice had a greater colony response after NM (at 5% confidence level) than saline-treated controls. Maximum numbers of colonies were obtained in the nustard-treated asplenic animals. Splenic extract, as well as extracts from other organs, when added to the culture plates resulted in inhibition of colony formation. The significance of in vitro inhibition after addition of organ extract is uncertain.
