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OII‐C‐2
Author(s) -
Kennedy M. J.,
Sullivan J. E.,
Doll M. A.,
Griffin A.,
Hein D. W.
Publication year - 2006
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2005.12.019
Subject(s) - genotype , atopic dermatitis , arylamine n acetyltransferase , medicine , pathogenesis , atopy , odds ratio , asthma , allele , immunology , pharmacogenetics , genetics , biology , gene
BACKGROUND N ‐acetyltransferase 2 (NAT2) plays an important role in the inactivation of arylamines, some of which may be important biochemical mediators of atopic dermatitis (AD), a common pediatric condition. Given that genetic variability in NAT2 activity may contribute to the pathogenesis, severity and/or treatment response in children with AD, we investigated the association of NAT2 acetylation genotype with pediatric AD. METHODS A buccal swab was obtained from Caucasian, African‐American and Hispanic children (6 mo‐5 yr) with AD (n=245) and healthy pediatric controls (n=247) without a personal/family history of atopy/asthma. Genomic DNA was isolated and NAT2 acetylation genotype was determined using a Taqman allele discrimination assay. Analysis of the relationship between NAT2 acetylator genotype and AD was completed via chi‐square analysis. RESULTS Genotype frequencies in the Caucasian AD (n=119) and control (n=124) subjects were as follows: (Table)Acetylator Genotype Frequency (number of subjects)Rapid / Intermediate Slow Odds Ratio 95% CIControl (n=124) 0.52 (64) 0.48 (60)AD (n=119) 0.37 (44) 0.63 (75) χ 2 = 5.3 p = 0.02 1.9 (1.3, 2.6)CONCLUSION These preliminary data suggest an association between the slow acetylator NAT2 genotype and AD in infants and children. Altered (i.e., reduced) metabolism of arylamines in children with AD could influence disease pathogenesis and/or expression and studies to test this hypothesis are planned. Partially supported by NIH grant 5U10‐HD045934. Clinical Pharmacology & Therapeutics (2005) 79 , P6–P6; doi: 10.1016/j.clpt.2005.12.019