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Objective: To investigate the rhinovirus infection and childhood asthma incidence relationship. Methods: 60 cases, 5 to 15-year-old children with asthma as the experimental group, including 30 cases of asthma in children with remission (remission group), acute exacerbation of asthma in children with 30 cases (asthma group). Select no allergic disease history and parasitic infections, the past six months is not systemic glucocorticoid steroids and immunomodulators 5 to 15 years old, 30 cases of normal children as a control group. Three groups of children were using the reverse transcription polymerase chain reaction (RT-PCR) assay nasopharyngeal secretions in rhinovirus (RV) gene; chemiluminescence detection of total serum IgE (T-IgE), pulmonary function first second forced expiratory volume percentage of predicted value percentage (FEV1% pre) and peripheral blood eosinophil percentage (E0S%). Results: 1, asthma group rhinovirus infection rate of 36.67%, the remission group rhinovirus infection rate was 3.33%, the control group was not detected rhinovirus; the asthma group rhinovirus infection rate mitigation and control groups, the difference was statistically significance (P <0.01), to ease the group rhinovirus infection control group comparison, the difference was not statistically significant, P gt; 0.05 asthma group rhinovirus-positive children with pulmonary function FEV1% pre (62.73 ± 13.54)% asthma group of children with rhinovirus-negative lung function FEV1% pre (86.42 ± 17.78)%, in comparison, the difference was statistically significant, P <0.01. 3, children with asthma group rhinovirus-positive T-IgE (836.32 ± 44.801) IU / ml, E0S% (10.63 ± 4.09)%, T-IgE in children with asthma group rhinovirus negative (439.10 ± 231.28) IU / ml, E0S% to (5.04 ± 2.64)%, in comparison, the difference was statistically significant, P <0.01; asthma group rhinovirus-positive children T-IgE E0S% of correlation (rs = 0.364, P gt; 0.05). 4, T-IgE asthma group (584.74 ± 374.59) IU / ml, E0S% to (7.09 ± 4.19)%, the remission group T-IgE for (316.90 ± 163.88) IU / ml E0S% to (4.45 ± 1.53) %, T-IgE control group (150.23 ± 81.83) IU / ml, E0S% (2.47 ± 0.90)%; asthma group T-IgE E0S% mitigation and control groups, the difference was statistically significant, P <0.05, the remission group T-IgE E0S% compared with the normal control group, the difference was statistically significant (P <0.01); and asthma group showed a positive correlation (rs = 0.763, rs = 0.607 remission group of T-IgE and E0S% , P lt; 0.01). Conclusion: 1, acute exacerbation of asthma in children with rhinovirus infection was significantly higher than the children with asthma in remission, suggesting that rhinovirus infection with acute exacerbation of asthma is closely related. 2, FEV1% pre acute exacerbation period rhinovirus-positive children with asthma lung function was significantly lower than the rhinovirus-negative children with asthma, suggesting that rhinovirus infection and asthma exacerbations relevant. 3, acute exacerbation of rhinovirus-positive children with asthma is higher than T-IgE rhinovirus-negative children with asthma, suggesting that rhinovirus may be a specific allergen, infection can lead to elevated T-IgE, which eventually lead to asthma episodes; children with high levels of serum T-IgE easier to rhinovirus infection induced asthma exacerbations. 4, T-IgE and EOS both to participate in the pathophysiology of bronchial asthma.
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