Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Clin Exp Allergy. 2011 Jun;41(6):794-800. doi: 10.1111/j.1365-2222.2010.03679.x. Epub 2011 Jan 24.
Although asthma and allergic rhinitis (AR) are considered to be one syndrome, many questions remain unanswered. Why do some AR patients develop asthma but others do not, and which factors play a role in the development of asthma that have so far not been clearly elucidated.
We hypothesize that children with AR who have the Clara cell secretory protein (CC16, secretoglobin 1A1) 38A/38A genotype (rs3741240) have an increased likelihood of developing asthma.
The study sample included 117 children, with AR, but no asthma diagnosed within the following 5 years, as the control group. Cases group (n=202) included age- and gender-matched children with AR first, and asthma developed 3-5 years later, as the study group. The CC16 genotype was determined by PCR and Sau96I restriction digestion of PCR products. The serum CC16 levels were measured by ELISA. Total serum IgE, allergen specific IgE, eosinophil count and pulmonary function were also measured.
In children with rhinitis who develop asthma, the frequencies of the AA genotype were significantly higher than those who did not develop asthma [odds ratio (OR)=2.527; 95% confidence interval (CI)=1.571-4.065; P<0.01]. Serum CC16 levels in the children with rhinitis who develop asthma and carry the AA genotype were significantly lower than those who carry the non-AA genotype and those who did not develop asthma.
Results of this study suggest that CC16 38A/38A genotype plays a role in the development of early asthma in children with AR. Early identification of rhinitis children at risk may assist in designing preventative approach to asthma development.
虽然哮喘和过敏性鼻炎(AR)被认为是一种综合征,但仍有许多问题尚未得到解答。为什么有些 AR 患者会发展为哮喘,而有些则不会,以及哪些因素在尚未明确阐明的哮喘发展中起作用。
我们假设 AR 患者中具有 Clara 细胞分泌蛋白(CC16,分泌球蛋白 1A1)38A/38A 基因型(rs3741240)的患者发展为哮喘的可能性增加。
研究样本包括 117 名患有 AR 但在接下来的 5 年内未被诊断为哮喘的儿童作为对照组。病例组(n=202)包括年龄和性别匹配的首先患有 AR 的儿童,并且在 3-5 年内发展为哮喘。通过 PCR 和 Sau96I 限制性消化 PCR 产物来确定 CC16 基因型。通过 ELISA 测量血清 CC16 水平。还测量了总血清 IgE、过敏原特异性 IgE、嗜酸性粒细胞计数和肺功能。
在患有鼻炎的发展为哮喘的儿童中,AA 基因型的频率明显高于未发展为哮喘的儿童[比值比(OR)=2.527;95%置信区间(CI)=1.571-4.065;P<0.01]。患有鼻炎且携带 AA 基因型的发展为哮喘的儿童的血清 CC16 水平明显低于携带非-AA 基因型和未发展为哮喘的儿童。
这项研究的结果表明,CC16 38A/38A 基因型在 AR 儿童早期哮喘的发展中起作用。早期识别有风险的鼻炎儿童可能有助于设计预防哮喘发展的方法。