In:
Pediatric Allergy and Immunology, Wiley, Vol. 27, No. 5 ( 2016-08), p. 507-513
Kurzfassung:
Genetic associations of the response to inhaled corticosteroids ( ICS s) during an asthma exacerbation are unknown. Objective To evaluate the role of genetic variants in the therapeutic response to high‐dose ICS in children with moderate‐to‐severe asthma exacerbations. Methods Eighty‐two children (56 boys/26 girls, mean age 9.6 ± 3.2 years) with moderate–severe asthma exacerbation were genotyped for eight single‐nucleotide polymorphisms that were a priori associated with ICS response in chronic asthma treatment: glucocorticosteroid receptor ( NR 3C1) rs41423247; corticotrophin‐releasing hormone receptor1 ( CRHR 1) rs242939, rs242941, and rs1876828; T‐box 21 ( TBX 21) rs2240017; glucocorticoid‐induced transcript 1 ( GLCC l1) ; and T gene rs3099266 and rs2305089. Children were treated with a single high‐dose (4000 μg) fluticasone propionate given by a nebulizer followed by 1000 μg/day of inhaled fluticasone propionate for 6 days. Primary outcome measure was the improvement in FEV 1 at 4 h. Results Mean FEV 1 was 71.7 ± 14.2% at presentation. Overall, fluticasone treatment resulted in a significant improvement in asthma score and FEV 1 (p 〈 0.0001 for both). Children with the GG genotype at NR 3C1 rs41423247 (n = 26) had a higher improvement in FEV 1 [24.2% (interquartile range 11.5–36.3)] compared to those with CG + CC (n = 19), [7.9% (interquartile range 6.1–24.6) (p = 0.006)] . Conclusion Homozygosity for the G allele at rs41423247 of the glucocorticosteroid receptor ( NR 3C1 ) gene is associated with a higher improvement in FEV 1 at 4 h in children with moderate‐to‐severe asthma exacerbation treated with high‐dose ICS . This observation may have important clinical implications especially for children who use systemic steroids frequently for recurrent asthma exacerbations.
Materialart:
Online-Ressource
ISSN:
0905-6157
,
1399-3038
DOI:
10.1111/pai.2016.27.issue-5
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2016
ZDB Id:
2008584-9
