GSTM1, GSTP1, prenatal smoke exposure, and atopic dermatitis

I. Jen Wang, Yueliang Leon Guo, Tien Jen Lin, Pau Chung Chen, Yu Nian Wu

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Background: The increase in the prevalence of atopic dermatitis (AD) is likely to involve changes in specific environmental exposures among genetically susceptible individuals. Objective: To evaluate the effect of glutathione S-transferase (GST) genotype polymorphisms and prenatal smoke exposure on pediatric AD on the basis of the cord blood cotinine levels. Methods: We conducted a case-control study composed of 34 children with AD and 106 non-AD controls, all of whom were selected from 483 participants in the Taiwan Birth Panel cohort study. Cord blood samples and information on perinatal factors of children were gathered at birth. At 2 years of age, information about the development of AD and environmental exposures was 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 genotype polymorphisms and cotinine levels with AD. Results: GSTM1 null and GSTP1 Ile/Ile genotypes showed a significant increase in the risk of AD (odds ratio [OR], 3.61; 95% confidence interval [CI], 1.40-9.31; and OR, 3.11; 95% CI, 1.30-7.46; respectively). In children with a cotinine level less than 0.1 ng/mL, the risk of AD increased for those carrying 2 GSTP1 Ile-105 alleles (OR, 6.63; 95% CI, 1.46-30.18). In children a with cotinine level of 0.1 ng/mL or greater, the GSTM1 null genotype was significantly related to AD (OR, 5.21; 95% CI, 1.32-20.58). Conclusions: Within groups of children, genetic polymorphisms in GSTM1 and GSTP1 may be responsible for differences in susceptibility to AD with regard to prenatal smoke exposure.

Original languageEnglish
Pages (from-to)124-129
Number of pages6
JournalAnnals of Allergy, Asthma and Immunology
Volume105
Issue number2
DOIs
Publication statusPublished - Aug 2010
Externally publishedYes

Fingerprint

Atopic Dermatitis
Smoke
Cotinine
Odds Ratio
Genotype
Confidence Intervals
Environmental Exposure
Dermatitis
Fetal Blood
Parturition
Genetic Polymorphisms
Glutathione Transferase
Taiwan
Case-Control Studies
Cohort Studies
Logistic Models
Alleles
Pediatrics

ASJC Scopus subject areas

  • Immunology and Allergy
  • Pulmonary and Respiratory Medicine
  • Medicine(all)

Cite this

GSTM1, GSTP1, prenatal smoke exposure, and atopic dermatitis. / Wang, I. Jen; Guo, Yueliang Leon; Lin, Tien Jen; Chen, Pau Chung; Wu, Yu Nian.

In: Annals of Allergy, Asthma and Immunology, Vol. 105, No. 2, 08.2010, p. 124-129.

Research output: Contribution to journalArticle

Wang, I. Jen ; Guo, Yueliang Leon ; Lin, Tien Jen ; Chen, Pau Chung ; Wu, Yu Nian. / GSTM1, GSTP1, prenatal smoke exposure, and atopic dermatitis. In: Annals of Allergy, Asthma and Immunology. 2010 ; Vol. 105, No. 2. pp. 124-129.
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abstract = "Background: The increase in the prevalence of atopic dermatitis (AD) is likely to involve changes in specific environmental exposures among genetically susceptible individuals. Objective: To evaluate the effect of glutathione S-transferase (GST) genotype polymorphisms and prenatal smoke exposure on pediatric AD on the basis of the cord blood cotinine levels. Methods: We conducted a case-control study composed of 34 children with AD and 106 non-AD controls, all of whom were selected from 483 participants in the Taiwan Birth Panel cohort study. Cord blood samples and information on perinatal factors of children were gathered at birth. At 2 years of age, information about the development of AD and environmental exposures was 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 genotype polymorphisms and cotinine levels with AD. Results: GSTM1 null and GSTP1 Ile/Ile genotypes showed a significant increase in the risk of AD (odds ratio [OR], 3.61; 95{\%} confidence interval [CI], 1.40-9.31; and OR, 3.11; 95{\%} CI, 1.30-7.46; respectively). In children with a cotinine level less than 0.1 ng/mL, the risk of AD increased for those carrying 2 GSTP1 Ile-105 alleles (OR, 6.63; 95{\%} CI, 1.46-30.18). In children a with cotinine level of 0.1 ng/mL or greater, the GSTM1 null genotype was significantly related to AD (OR, 5.21; 95{\%} CI, 1.32-20.58). Conclusions: Within groups of children, genetic polymorphisms in GSTM1 and GSTP1 may be responsible for differences in susceptibility to AD with regard to prenatal smoke exposure.",
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AB - Background: The increase in the prevalence of atopic dermatitis (AD) is likely to involve changes in specific environmental exposures among genetically susceptible individuals. Objective: To evaluate the effect of glutathione S-transferase (GST) genotype polymorphisms and prenatal smoke exposure on pediatric AD on the basis of the cord blood cotinine levels. Methods: We conducted a case-control study composed of 34 children with AD and 106 non-AD controls, all of whom were selected from 483 participants in the Taiwan Birth Panel cohort study. Cord blood samples and information on perinatal factors of children were gathered at birth. At 2 years of age, information about the development of AD and environmental exposures was 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 genotype polymorphisms and cotinine levels with AD. Results: GSTM1 null and GSTP1 Ile/Ile genotypes showed a significant increase in the risk of AD (odds ratio [OR], 3.61; 95% confidence interval [CI], 1.40-9.31; and OR, 3.11; 95% CI, 1.30-7.46; respectively). In children with a cotinine level less than 0.1 ng/mL, the risk of AD increased for those carrying 2 GSTP1 Ile-105 alleles (OR, 6.63; 95% CI, 1.46-30.18). In children a with cotinine level of 0.1 ng/mL or greater, the GSTM1 null genotype was significantly related to AD (OR, 5.21; 95% CI, 1.32-20.58). Conclusions: Within groups of children, genetic polymorphisms in GSTM1 and GSTP1 may be responsible for differences in susceptibility to AD with regard to prenatal smoke exposure.

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