RESUMO
We investigated the clinical symptoms of 206 pediatric patients with influenza virus infection and compared them among oseltamivir-treated, zanamivir-treated, and laninamivir-treated groups in 2013/2014 influenza season. The drug compliance of each neuraminidase inhibitor was good in all three groups. Although the duration of fever after administration of the first dose of each neuraminidase inhibitor were significantly prolonged in the patient with influenza B infection than in the patient with influenza A infection, no statistically significant difference in the clinical efficacy and the side effect among three groups were found. The number of biphasic fever episodes in patients treated with neuraminidase inhibitor was rare (two episodes of oseltamivir-treated group and one episode of zanamivir-treated group). In conclusion, under the good drug compliance, the efficacy of all three neuraminidase inhibitor was the same for the treatment of influenza virus infection in children.
Assuntos
Antivirais/uso terapêutico , Inibidores Enzimáticos/uso terapêutico , Influenza Humana/tratamento farmacológico , Neuraminidase/antagonistas & inibidores , Criança , Guanidinas , Humanos , Japão , Adesão à Medicação , Oseltamivir/uso terapêutico , Piranos , Ácidos Siálicos , Fatores de Tempo , Zanamivir/análogos & derivados , Zanamivir/uso terapêuticoAssuntos
Fíbula/anormalidades , Síndrome de Hajdu-Cheney/diagnóstico , Hidrocefalia/diagnóstico , Fenótipo , Idade de Início , Encéfalo/patologia , Criança , Pré-Escolar , Feminino , Fíbula/lesões , Seguimentos , Fraturas Espontâneas/diagnóstico , Humanos , Lactente , Recém-Nascido , Imageamento por Ressonância Magnética , Platibasia/diagnóstico , Tomografia Computadorizada por Raios XRESUMO
Casitas B-lineage lymphoma b (Cblb) is a negative regulator of T-cell activation and dysfunction of Cblb in rats and mice results in autoimmunity. In particular, a nonsense mutation in Cblb has been identified in a rat model of autoimmune type 1 diabetes. To clarify the possible involvement of CBLB mutation in type 1 diabetes in humans, we performed mutation screening of CBLB and characterized functional properties of the mutations in Japanese subjects. Six missense mutations (A155V, F328L, N466D, K837R, T882A, and R968L) were identified in one diabetic subject each, excepting N466D. Of these mutations, F328L showed impaired suppression of T-cell activation and was a loss-of-function mutation. These data suggest that the F328L mutation is involved in the development of autoimmune diseases including type 1 diabetes, and also provide insight into the structure-function relationship of CBLB protein.
