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  • 1
    Electronic Resource
    Electronic Resource
    A polymorphism in the coding region of interleukin-13 gene is associated with atopy but not asthma in Chinese children (2001)
    Oxford, UK : Blackwell Science, Ltd
    Clinical & experimental allergy 31 (2001), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Interleukin (IL)-13 is an important cytokine secreted from type 2 helper T lymphocytes. It is essential for modulating IgE synthesis by human B cells. Previous studies showed that polymorphisms in the IL-13 gene were associated with serum total IgE or allergic asthma. The relationship of this marker with sensitization to individual aeroallergens has not been evaluated.Objective We tested whether a polymorphism in the coding region of the IL-13 gene is associated with asthma and atopy in asthmatic children in Hong Kong.Methods We used restriction fragment length polymorphism to detect R130Q genotype in Chinese children with asthma and control subjects. Serum total IgE was measured by microparticle immunoassay and specific IgE to common aeroallergens was measured using fluorescent enzyme immunoassay. Pulmonary function studies were performed using spirometry.Results One hundred and fifty-seven patients and 54 control children were recruited. Their mean serum total IgE concentrations were 994 kIU/L and 473 kIU/L, respectively (P 〈 0.0001). Atopy as defined by ≥ 1 positive RAST was found in 141 patients and 32 control children. The GlnGln form of the R130Q polymorphism in the IL-13 gene was associated with serum total IgE (P = 0.005) as well as specific IgE to Der p 1 (P = 0.021), mixed cockroaches (P = 0.03) and dog (P = 0.003) but not with physician-diagnosed asthma (P = 0.621). In addition, the R130Q polymorphism did not correlate with subjective or objective indicators of asthma severity in our patients.Conclusion Our results suggest that the R130Q polymorphism of the IL-13 gene is associated with elevated serum total and allergen-specific IgE but not asthma in Chinese children.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2001.01212.x
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  • 2
    Electronic Resource
    Electronic Resource
    Urinary leukotriene E4 correlates with severity of atopic dermatitis in children (2004)
    Oxford, UK : Blackwell Science Ltd
    Clinical and experimental dermatology 29 (2004), S. 0 
    Details
    ISSN: 1365-2230
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Leukotriene E4 (LTE4) is elevated in adults with atopic dermatitis (AD). We evaluated whether urinary LTE4 as a noninvasive marker correlates with clinical indices of disease activity in children with AD. AD patients aged 18 years or younger were eligible for inclusion in the study. Disease severity over the preceding 3 days was evaluated by the SCORing Atopic Dermatitis (SCORAD) index. Severity of AD over the past 12 months was evaluated by the Nottingham Eczema Severity Score (NESS) in Chinese. Urinary LTE4 concentration was measured by competitive enzyme immunoassay. One hundred and twenty-six children with AD (82 boys and 44 girls) and 45 controls were recruited. The mean ± SD urinary log-transformed LTE4 concentration in AD patients and controls was 2.94 ± 0.32 and 2.62 ± 0.20 pg/mg creatinine, respectively (P 〈 0.0001). SCORAD significantly correlated with NESS (r = 0.681, P 〈 0.0001). There were significant correlations between urinary LTE4 concentration and overall SCORAD score (r = 0.270, P = 0.002) and its extent (r = 0.185, P = 0.038) and intensity components (r = 0.247, P = 0.005), but not with NESS. When compared with mild AD, urinary LTE4 concentrations were higher in patients with moderate-to-severe disease (P = 0.049). Urinary LTE4 measurement is noninvasive and may be useful in supplementing the SCORAD for following longitudinal changes in AD severity in children. However, the practical value of this assay in a clinical setting remains to be determined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2230.2004.01512.x
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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