• Clinical and genetic parallels of bronchial asthma in children

Clinical and genetic parallels of bronchial asthma in children

SOVREMENNAYA PEDIATRIYA.2017.4(84):72-76; doi 10.15574/SP.2017.84.72

Banadyha N. V., Voloshyn S. B.
Higher State Educational Establishment of Ukraine «Ivan Horbachevsky Ternopil State Medical University»

Objective — to follow up the impact of certain genetic markers of atopy on the clinical course of bronchial asthma (BA) in children.

Materials and methods. The in-depth clinical and laboratory examination of 101 inpatients with bronchial asthma (BA) was performed. Genotyping Arg16Gly of gene ADR β2-receptors rs1042713 and G308A of gene TNFα rs1800629 was performed by the polymerase chain reaction.

Results. Intermittent asthma was diagnosed in 29 (28,71%) of examined patients and 72 (71.29%) patients had persistent asthma. The detailed study of anamnesis revealed that 73 (72.28%) children required the administration of basic therapy to achieve asthma control. Analyzing the composition of basic therapy in hospitalized patients with acute exacerbation, it was found that 10 (16.13%) patients were treated with antileukotrienes, 29 (46.77%) patients were administrated inhaled glucocorticosteroids, and 23 (37.10%) children needed to combine inhaled glucocorticosteroids and antileukotrienes. The basic therapy in the majority of patients with the controlled asthma included the antileukotrienes (63.64%) and in limited cases (36.36%) inhaled glucocorticosteroids in accordance with the severity of clinical course. Attention was drawn to the study of polymorphism genotypes of Arg16Gly of ADRβ2-receptors gene and TNFα G308A gene replacement, depending on the drug sensitivity of basic therapy. The obtained data of diagnosed genotypes in inpatients showed a prevalence of Gly/Gly variant in patients who were administrated antileukotrienes and the combination of antileukotrienes with inhaled glucocorticosteroids. However, in patients who were assigned inhaled glucocorticosteroids alone, the heterozygous variant of Arg/Gly ADRβ2-receptors gene was more common. As for the replacement of TNFα G308A, regardless of the basic therapy composition, the genotype GG prevailed.

Conclusions. 1). It is possible to achieve proper control of BA in children with genotype Gly/Gly of ADRβ2-receptor, whereas the heterozygous genotype Arg/Gly and homozygous Arg/ Arg allele accompanied partially controlled and uncontrolled disease course. 2). The dependence between the basic therapy composition and the genotype of the ADRβ2-receptors was established. Homozygous genotype Gly/Gly by the minor allele was diagnosed in patients who were treated only with antileukotriens. However, in the case of Arg/Gly genotype to achieve asthma control was possible only by using inhaled corticosteroids (54.55%). 3). Diagnosed TNFα genotype in children with BA established a dominant influence of the main G allele, which was confirmed by the significant prevalence of the homozygous variant GG, regardless of the BA control level. 4). The basic therapy of BA demanded the revision of the inhaled glucocorticosteroids dose or the administration of combined therapy in patients with heterozygous genotype GA TNFα.

Key words: bronchial asthma, genetic polymorphism, β2-adrenergic receptors, tumour necrosis factor alpha, children.


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