RESUMEN
ABSTRACT The addition of the new protease inhibitors (PIs) to peg-interferon (IFN) and ribavirin (RBV), approved for chronic hepatitis C, has clearly improved sustained virological response (SVR) rates although several adverse events have been reported with this regimens, including mild hematological toxicity. Moreover, severe pancytopenia and aplastic anemia during triple therapy with telaprevir has recently been described in seven patients. We report here two cases of severe agranulocytosis/aplastic anemia using boceprevir or simeprevir in interferon-based combination and 2 additional cases of severe myelosupression in IFN-free therapy with sofosbuvir and simeprevir plus RBV. Our observations suggest that PIs could have a sort of class-effect in developing severe hematologic toxicity or, at least, an additive interaction with other potentially myelotoxic agents such as IFN or RBV that are used in the classical regimens against HCV. Unfortunately, the mechanisms behind this phenomenon are currently unknown. In conclusion, given the lifethreatening character of these complications, close monitoring is mandatory in patients under PIs based therapy to promptly detect serious hematological toxicities and to carefully evaluate treatment discontinuation. Prospective studies assessing the usefulness of RBV in the era of new IFN-free combinations are needed.
Asunto(s)
Humanos , Inhibidores de Proteasas/efectos adversos , Enfermedades de la Médula Ósea/inducido químicamente , Enfermedades de la Médula Ósea/terapia , Prolina/análogos & derivados , Hepatitis C/tratamiento farmacológico , Simeprevir/efectos adversos , Anemia Aplásica/inducido químicamente , Anemia Aplásica/terapia , Índice de Severidad de la Enfermedad , Examen de la Médula Ósea , Prolina/efectos adversos , Valor Predictivo de las Pruebas , Factores de Riesgo , Resultado del Tratamiento , Hepatitis C/diagnóstico , Resultado Fatal , Quimioterapia CombinadaRESUMEN
Background. We analysed the results of allogeneic haematopoietic stem cell transplantation (HSCT) in various genetic disorders, bone marrow failures and haematological malignancies done from 2002 to 2010 at the Army Hospital, Research and Referral, Delhi. Methods. A total of 119 matched-related allogeneic- HSCTs (allo-HSCTs) were done in 114 patients (men 76, women 38) aged between 2 and 60 years. Peripheral blood stem cells (n=75) and bone marrow (n=43) were used as the source of stem cells. Results. The overall survival was 62.3% (71/114) at a median follow-up of 34 months. Graft versus host disease (GVHD) was seen in 42 (36.8%) patients; grade III/IV acute GVHD in 17 (15%) and chronic GVHD in 24 (21%) patients. There were 4 (3.5%) graft rejections and one nonengraftment. The overall mortality was 37.7% (n=43) and the main causes of death were GVHD (32%), infections (26%), relapse (23%) and regimen-related toxicity (11%). Conclusion. Our results are comparable to published data in most disease conditions. With improvements in GVHD prophylaxis and better supportive care, we need to further reduce our mortality and morbidity.
Asunto(s)
Adolescente , Adulto , Enfermedades de la Médula Ósea/terapia , Niño , Preescolar , Femenino , Enfermedades Genéticas Congénitas/terapia , Rechazo de Injerto/etiología , Enfermedad Injerto contra Huésped/etiología , Neoplasias Hematológicas/terapia , Hospitales Militares , Humanos , India , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Tasa de Supervivencia , Trasplante Homólogo , Adulto JovenRESUMEN
La insuficiencia medular es un síndrome hematológico; de pronóstico siempre reservado; que reconoce dos mecanismos etiopatogénicos: la aplasia medular y la mieloptisis. La primera es de naturaleza benigna y recuperable (50 por ciento) y la segunda maligna. Ambas se manifiestan clínicamente por una pancitopenia de la sangre periférica, la que se traduce por la asociación de un síndrome anémico normocítico y normocrómico arregenerativo, uno infeccioso febril y uno purpúrico. El diagnóstico clínico de insuficiencia medular es fácil, no así su tratamiento, especialmente en las mieloptisis.
Asunto(s)
Humanos , Enfermedades de la Médula Ósea/diagnóstico , Enfermedades de la Médula Ósea/terapia , Leucopenia/terapia , Neutropenia/terapia , Enfermedades Hematológicas/diagnóstico , Enfermedades Hematológicas/terapia , Hematopoyesis , Mielopoyesis , PancitopeniaAsunto(s)
Humanos , Masculino , Femenino , Recién Nacido , Lactante , Anemia Aplásica/genética , Trasplante de Médula Ósea , Enfermedades de la Médula Ósea/fisiopatología , Enfermedades de la Médula Ósea/terapia , Factores de Crecimiento de Célula Hematopoyética/uso terapéutico , Anemia de Fanconi , Anemia de Fanconi/genética , Anemia de Fanconi/fisiopatología , Anemia de Fanconi/terapiaRESUMEN
Se reportan dos casos de aplasia medular jsevera adquirida, evaluados en el servicio de Pediatría que respondieron satisfactoriamente a la terapia con dosis altas de metilprednisolona, administrado en bolos intravenosos, iniciándose con 25 mg/kg/día disminuyéndolo en un período de cinco semanas. El tratamiento fue bien tolerado por ambos pacientes y no presentaron efectos adversos significativos. En nuestro medio que no contamos con la posibilidad del transplante de médula ósea y de la globulina antilinfocítica, debe considerarse la metilprednisolona como una alternativa terapéutica en los casos de aplasia medular severa.