- Peculiarities of the basic anti-inflammatory therapy of non-atopic bronchial asthma phenotype in children depending on the acetylation status
Peculiarities of the basic anti-inflammatory therapy of non-atopic bronchial asthma phenotype in children depending on the acetylation status
SOVREMENNAYA PEDIATRIYA.2017.2(82):92-96; doi 10.15574/SP.2017.82.92
Bezrukov L. O., Tarnavska S. I., Shahova O. O.
Higher State Educational Institution of Ukraine «Bukovinian State Medical University», Chernivtsi, Ukraine
Objective: to assess the effectiveness of anti-inflammatory therapy in children suffering from non-atopic bronchial asthma (BA) depending on acetylation polmorphism.
Materials and methods. The 1st and 2nd degree comprehensive clinical and immunological examination of 45 children with non-atopic asthma has been held. The genetic marker, namely the acetylation type, on the method of W.M. Proebsting — V.I. Gavrilova, modified by Tymofeeva, was determined. According to the acetylation type two clinical groups were formed: the first group included 22 patients with non-atopic type of disease and slow acetylation phenotype, the second one comprised 23 patients suffering from non-atopic BA with fast acetylation phenotype.
Results. The conducted investigations revealed the distinct controlling effect of inhaled corticosteroids in the patients with slow acetylation type, as evidenced by an increase of relative risk by 57.6% and absolute risk by 45.0% of retention control non-atopic BA phenotype, with a minimum number of patients that need to be treated to achieve at least one positive result (NNT) — 1.7.
Conclusions. The slow acetylation status in patients with non-atopic BA increased the chances of disease control with using inhaled corticosteroids by 4.9–6.9 times.
Key words: asthma, children, acetylation status, anti%inflammatory therapy.
1. Koloskova OK, Іvanova LA. 2012. Phenotypic features of asthma in school-age children. Perinatologiya i pediatriya. 3(51): 96-98.
2. Umanets TR, Lapshin VF. 2014. The modern concept of asthma phenotyping. Zdorov’ya Ukraїni. 1(28): 52-54.
3. Batra J, Sharma SK, Ghosh Batra J. 2006. Arylamine N-acetyltransferase gene polymorphisms: markers for atopic asthma, serum IgE and blood eosinophil counts. Pharmacogenomics. 7(5): 673-682. https://doi.org/10.2217/146224126.96.36.1993; PMid:16886893
4. Jackson DJ. 2014. Inhaled Interferon: A Novel Treatment for Virus-induced Asthma? Am J Respir Crit Care Med. 190(2): 123–134. https://doi.org/10.1164/rccm.201406-1131ED; PMid:25025347 PMCid:PMC4226059
5. Anvari S, Vyhlidal CA, Dai H, Bridgette LJ. 2015. Genetic Variation along the Histamine Pathway in Children with Allergic versus Nonallergic Asthma. American J of Respir Cell and Mol Biol. 53(6): 802-809. https://doi.org/10.1165/rcmb.2014-0493OC; PMid:25909280 PMCid:PMC4742940
6. Faria da Silva-Martins CL, Couto SC, Muniz-Junqueira MI. 2013. Inhaled corticosteroid treatment for 6 months was not sufficient to normalize phagocytosis in asthmatic children. Clin Transl Allergy. – 30; 3(1): 28-36.
7. Pawlik A, Juzyszyn Z, Gawronska-Szklarz B. 2009. N-acetyltransferase 2 (NAT2) polymorphism in patients with atopic asthma. 40(4): 264-267.
8. Pocket Guide for Asthma Management and Prevention (updated 2015). http://ginasthma.org/wp-content/uploads/2016/01/GINA_Pocket_2015.pdf
9. Tamer L, Calikoğlu M, Aras Ateş N. et al. 2006. Relationship between N-acetyl transferase-2 gene polymorphism and risk of bronchial asthma. Tuberk Toraks. 54(2): 137-143. PMid:16924569
10. Thomson N.C. 2016. Novel approaches to the management of noneosinophilic asthma. Ther Adv Respir Dis. 10(3): 211-234. https://doi.org/10.1177/1753465816632638; PMid:26929306