RESUMEN
OBJECTIVE: To evaluate the impact of highly active antiretroviral therapy (HAART) on the haemorrhage status, joint function, and physical ability of the patients of hemophilia combined with acquired immunodeficiency syndrome (AIDS). METHODS: Thirty-nine hemophilia A/AIDS patients, all male, aged (40+/-13), underwent HAART and followed up for 6 years from 2002 to 2008 to observe the yearly hospital visit time, bleeding time, transfusion times, amount of factor VIII transfusion, VIII: C level, physical ability, and joint function. Flow cytometry was used to count the CD4+ T cells, and bDNA assay was used to examine the HIV virus load. RESULTS: The average hospital visit time, bleeding time, transfusion time, and amount of factor VIII transfusion, hemoglobin, white blood cell count, and platelet count before HAART were not significantly different from those after treatment (all P>0.05); only one case showed moderate decrease in VIII: C level, and another one case showed slight decline in physical ability and joint function. The serum HIV RNA load decreased from (4.8+/-1.0) log copies/ml before HAART to (2.4+/-1.0) log copies/ml (P<0.05) and the CD4+ T cell count raised from 183+/-97/mm3 to 456+/-157/mm3 (P<0.05) after HAART. CONCLUSION: HAART has no obvious impact on the haemorrhage status, joint function, and physical ability in hemophilia A/AIDS patients, however, it is effective to inhibit HIV replication and raise CD4+ T cell number which indicates that HAART therapy is positive for immune recovery.
Asunto(s)
Síndrome de Inmunodeficiencia Adquirida/tratamiento farmacológico , Terapia Antirretroviral Altamente Activa , Hemofilia A/tratamiento farmacológico , Síndrome de Inmunodeficiencia Adquirida/complicaciones , Adulto , Estudios de Seguimiento , Hemofilia A/complicaciones , Humanos , Masculino , Persona de Mediana Edad , Resultado del TratamientoRESUMEN
Malignant monoclonal B cells of chronic B cell lymphocytic leukemia (B-CLL) usually fail to be cleared, which indicates important costimulatory molecules may be lacking. Among those costimulatory signals, B7-1/CD80 and B7-2/CD86 caused utmost attention. In this study, B7-1 and B7-2 expression on B cells in chronic B cell lymphocytic leukemia patients were detected. Data showed that B7-2 expression in chronic B cell lymphocytic leukemia patients is significantly lower than in normal people, which suggests defective B7-2 expression may be one of the pathogenic mechanisms of chronic B cell lymphocytic leukemia. Further, we confirmed interferon-gamma could induce B7-2 expression slightly and promote T-cell response against chronic B cell lymphocytic leukemia cells, indicating interferon-gamma has clinical value in chronic leukemia immunotherapy based on modulating B7-2 expression.