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“Malignancy and its treatment are major causes of secondary immunodeficiency in childhood. The authors investigated the effects of chemotherapy on humoral immunity against hepatitis B, tetanus, and diphtheria in children with hematologic malignancies. Daporinad ic50 The authors recruited 54
patients with hematologic malignancies after the completion of chemotherapy (group A), 25 patients with newly diagnosed hematologic malignancies before initiation of chemotherapy (group B), and 74 healthy controls (group C). All participants had been vaccinated against hepatitis B, tetanus, and diphtheria according to the Iranian national vaccination scheme. Patients in group A achieved protective levels of diphtheria and hepatitis B antibodies significantly less frequently than the other 2 groups and protective
levels of tetanus antibody significantly less frequently than group C (P<.05). After controlling for age, the association observed for tetanus lost its significance, but chemotherapy was a significant and independent predictor of failure to achieve protective levels of antibodies against diphtheria (odds ratio [OR] = 7.7, P<.001) and hepatitis B (OR=3.13, P=.008). These results indicate that chemotherapy has independent adverse effects on vaccine-induced antibody protection against diphtheria and hepatitis B.”
“BACKGROUND: Single-nucleotide polymorphisms selleck chemical (SNPs) associated with active cytomegalovirus (CMV) infections after lung transplantation have not been identified.
METHODS: SNPs associated with varying levels of interferon (IFN)-gamma (+874T/A), tumor necrosis factor-alpha (-308G/A), interleukin-10 (-1082G/A, 819C/T, 592C/A) and
interleukin-6 (-174G/C) were characterized for 170 Caucasian lung transplant recipients who received alemtuzumab induction and valganciclovir prophylaxis against CMV.
RESULTS: Patients were followed for a median SCH772984 inhibitor of 34 months post-transplant, and 66% (113 of 170), 24% (40 of 170) and 10% (17 of 170) had no CMV infection, CMV viremia and CMV disease, respectively. Median times to CMV viremia and disease were 7 and 10 months, respectively. For each gene, there was no significant deviation from Hardy-Weinberg equilibrium. Independent risk factors for the development of CMV disease were IFN-gamma +874 T/T genotype (associated with high levels of TFN-gamma production), CMV donor-positive/recipient-negative (D(+)/R(-)) serostatus and acute cellular rejection requiring augmented immunosuppression (p = 0.001, 0.003 and 0.049, respectively). The association between IFN-gamma +874 T/T genotype and CMV disease was most striking among R(+) patients (p = 0.02). D(+)/R(-) serostatus was also a significant risk factor for CMV viremia (p = 0.0005).