背景: 近年來異位性皮膚炎盛行率的增加可能和基因易感族群之特殊暴露有關。這項研究的目的將依據臍帶血cotinine值來評估Glutathione S - transferase (GST)基因多形性和懷孕期香煙暴露對小孩異位性皮膚炎之影響。 方法: 在2004年我們收集了261對母親和新生兒。臍帶血和孩子的資料在出生時即被取得。在2歲時收集後天環境暴露資料及判定小孩是否得過異位性皮膚炎。我們將cotinine濃度分層，比較得病與沒得病小孩之GTM1和GSTP1多形性。多重邏輯氏迴歸被用來評估基因多形性和cotinine濃度對異位性皮膚炎之影響。 結果:我們發現當臍帶血cotinine值上升時，異位性皮膚炎之風險便會增加，且以劑量趨勢反應方式增加。GSTM1 null及GSTP1 Ile/Ile基因型被發現會增加異位性皮膚炎之風險。對於臍帶血cotinine值小於0.1 ng/ml的小孩, GSTP1 Ile/Ile基因型會增加異位性皮膚炎之風險。對於大於等於0.1 ng/ml的，GSTM1 null基因型與異位性皮膚炎風險有顯著相關。 結論: GSTM1和GSTP1基因多形性可解釋懷孕期香煙暴露對小孩異位性皮膚炎易感性的不同。
Background: The evidence that both gene and environment play etiologic roles implicates that the increase in atopic dermatitis (AD) prevalence is likely to involve changes in specific exposures among genetically susceptible individuals. The purpose of this study was to evaluate the effect of Glutathione S -transferase (GST) genotypes polymorphisms and prenatal smoke exposure on pediatric AD on the basis of the cord blood cotinine levels. Method: We conducted a case-control study comprised of 34 AD children and 106 non-AD controls, all of whom were selected from 483 cases in Taiwan Birth Panel cohort study. Cord blood and information on perinatal factors of children were gathered at birth. At 2 years of age, information about development of AD and environmental exposures were collected. We compared AD with non-AD children for GTM1 and GSTP1 polymorphisms stratified by the cotinine level. Multiple logistic regressions were performed to estimate the association of genotypes polymorphisms and cotinine levels with AD. Results: GSTM1 null and GSTP1 Ile/Ile genotypes showed a significant increase in the risk of AD with OR (95% CI) of 3.61 (1.40–9.31) and 3.11 (1.30–7.46) respectively. In children with cotinine level < 0.1 ng/ml, the risk of AD increased for those carrying two GSTP1 Ile-105 alleles (OR = 6.63, 95% CI 1.46-30.18). In children with cotinine level ≧ 0.1 ng/ml, GSTM1 null genotype was significantly related to AD (OR = 5.21, 95% CI 1.32–20.58). Conclusion: Genetic polymorphism in GSTM1 and GSTP1 may be responsible for children differences in susceptibility to AD with regard to prenatal smoke exposure.
