台灣兒科醫學會第165屆學術演講會教育演講－環境生態和遺傳與兒童氣喘

The 165th Scientific Meeting of the Taiwan Pediatric Association and Continuing Medical Education-Childhood Asthma: Aspects of Global Environment, Genetics and Management

楊崑德(Kuender D. Yang)

《Acta Paediatrica Taiwanica》 42卷s期 (2001/11) Pp. 27-28

https://doi.org/10.7097/APT.200111.0027

摘要

兒童氣喘盛行率在過去二十年來已經急速增加5至10倍。在台灣的盛率由1970年代的1.3%增加到最近的10%左右。目前全球以紐西蘭和澳洲的盛行率最高，達15%c h ,亞非洲國家較低，但也有5至10%的盛行率。一般而言，在已開發國家盛行率比開發中國家高。除了工業化以外，其實地理位置和生態的分佈也影響其盛行率的多寡。溫帶亞熱帶的海岸國家有較高盛行率；寒帶和赤道國家其盛行率較少。在亞熱帶和溫帶地區其盛行率明顯增加者以塵蟎爲主要過敏原；在熱帶沙漠型氣候則以動物和草花爲主要過敏原；寒帶則以寵物和樹花爲主要過敏原。室內過敏原如塵蟎、蟑螂和寵物主要引起全年性氣喘；室外的過敏原如花粉，特定黴菌則引起季節性氣喘。近來有些氣喘基因已經被發現和重視，其中染色體11q13被認爲與母親傳遞氣喘有關，也和IgE抗體接受器基因型有關。另外染色體上5q31-33間的一些細胞素基因或腎上腺素接受器基因圓形也有關；我們則發現國人兒童氣喘與IL-4 promoter的基因多型性有關。
其他免疫基因和神經物質基因也受重視。顯然不是單基因疾病，證據顯示汙染如空氣如O3,NO2,SO2等的在在加上過敏基因和過敏原的互動才促動過敏抗體(IgE)産生和過敏反應。現行的氣喘治療方式多以免疫藥理的方式去阻斷IgE抗體媒介的早期氣管收縮反應和晚期的發炎反應；另外也因爲簡易最大吐氣流量(PEFR)測定，使得自我照顧與自我用藥，可以簡化爲四個步驟來調節。我們最近與婦産科的合作研究發現母親的過敏體質確實與嬰兒期溼疹和過敏抗體IgE增加有相關；父親則沒有相關。更進一步的防治方式是在胎幼兒期的避免過敏原，可以有效降低過敏盛行率；另外早期使用抗發炎治療也有保養肺功能的功效。若能兩者同時進行則效用會有加成效果。展望未來，隨著氣喘控制基因的了解和氣喘基因疫苗的關發，篩選高危險群進行早期過敏原避免和基因疫苗的使用，將對未來的兒童氣喘病的防治提供革命性的成效。

關鍵字

兒童氣喘 ； 生態環境 ； 過敏基因 ； 過敏原避免

並列摘要

The prevalence of asthma in children has been dramatically increasing in the past two decades. In Taiwan, the prevalence of childhood asthma has risen to around 10% in the 1990s, in contrast to a lower prevalence about 1% in the 1970s. Currently, Australia and New Zealand have the highest prevalence in the world (＞15%). African and Asian countries have a low prevalence about 5 to 10 %. In general, countries in the coast, temperate and subtropical zones have the highest mite-sensitive asthma prevalence. Countries in the subarctic or semiaridic areas have a lower prevalence. Indoor allergens such as house dust mites, cockroaches and fungi usually cause perennial asthma; and outdoor allergens such as grass and tree pollens as well as outdoor fungi induce seasonal asthma. The gene in chromosome 11q13 is significantly linked to maternal inheritance of asthma, and possibly involves polymorphisms in the, 5’ subunit of the high affinity IgE receptor. Cytokine genes in chromosome 5q3 1-33 are known to regulate IgE production resulting in various seventies of allergic diseases. Recent studies suggest that pollutants such as diesel exhaust, 03, NO2, and SO2, together with allergens and susceptible genes are likely to promote the development of IgE production and allergic reactions. As a result, asthma is apparently not a single gene disorder, but a disease determined by the interaction between gene and environment. In practice, immunopharmacological interventions to block IgE-mediated early bronchospasm and late inflammatory reactions are the major regimens for asthma treatments. It is made possible for a step-wide self-management based on the monitor of airway resistance by a portable peak expiratory flow rate (PEFR). Early avoidance of allergen exposure in utero as well as early anti-inflammatory therapy in infancy all showed effectiveness in decrease of the prevalence of allergic diseases. A combination of both strategies may benefit much more in prevention of childhood asthma. As progress in therapeutic gene vaccines as well as genetic immunoregulation, we would expect early environmental avoidance and genetic vaccines may be more promising in prevention of children from asthma in the near future.

並列關鍵字

Childhood asthma ； ecology ； allergic genes ； allergen avoidance