RESUMO
BACKGROUND: It is known that children with respiratory syncytial virus (RSV) infection frequently have complications of acute otitis media (AOM). METHODS: The hospital records of 148 inpatients aged 6-35 months who had RSV infection between January 2004 and December 2007, were retrospectively investigated. RESULTS: Forty-six out of 148 children (31%) had AOM. There was a significantly greater number of children with fever who had AOM (P = 0.005). The percentage of children with beta-lactamase-non-producing ampicillin-resistant (BLNAR) Haemophilus influenzae in nasopharyngeal culture who had AOM showed a tendency to be greater than that of those who did not have AOM, but this was not statistically significant (P = 0.068). Moreover, BLNAR H. influenzae was positive in middle ear fluid specimens from four of five children with AOM who underwent tympanocentesis. There were no significant differences in the incidence of lower airway infection, leukocytes counts, or serum C-reactive protein levels between children with and without AOM. CONCLUSIONS: Children who had RSV infection with AOM had a higher incidence of fever than those without AOM.
Assuntos
Otite Média/diagnóstico , Infecções por Vírus Respiratório Sincicial/diagnóstico , Doença Aguda , Proteína C-Reativa/análise , Pré-Escolar , Feminino , Humanos , Lactente , Contagem de Leucócitos , Masculino , Otite Média/virologia , Infecções por Vírus Respiratório Sincicial/complicações , Estudos RetrospectivosRESUMO
It is known that the use of adjunctive dexamethasone in bacterial meningitis reduces audiologic and neurologic sequelae. The cerebrospinal fluid (CSF) level of soluble tumor necrosis factor 1 (sTNFR1) is an important indicator of neurologic sequelae in bacterial meningitis. We measured the CSF levels of IL-6 and sTNFR1 before administration of antibiotics (CSF1) and 1-3 days after administration of antibiotics (CSF2) in nine patients with bacterial meningitis who received dexamethasone sodium and five without dexamethasone. The CSF2 IL-6 levels of patients with/without dexamethasone were significantly lower than for CSF1 IL-6 levels (p = 0.0077, and p = 0.0431, respectively). There were no significant differences of the ratio of CSF2/CSF1 IL-6 levels between patients with dexamethasone and those without dexamethasone. CSF2 sTNFR1 levels of patients with dexamethasone were significantly lower than for CSF1 sTNFR1 levels (p = 0.0208). However, CSF2 sTNFR1 levels of patients without dexamethasone were significantly higher than for CSF1 sTNFR1 levels (p = 0.0422). The ratio of CSF2/CSF1 sTNFR1 levels of patients with dexamethasone was significantly lower than that without dexamethasone (p = 0.0063). Our present study suggests that dexamethasone inhibits increase of CSF sTNFR1 levels after antibiotics therapy in bacterial meningitis.