Bronchial asthma (BA) has a polygenic nature, and the onset of its manifestation and features course is realized due to the influence of genetic factors. This study aimed to investigate the effect of polymorphisms of the genes of the phase II detoxification system and genes of the cardiovascular tone on the severity of asthma in children. The study included 163 children aged 5-18 years: 38 with severe asthma, 69 with moderate asthma, and 56 with mild asthma. A molecular genetic study was conducted to determine the frequency of gene propagation and gen-gene interaction by GSTT1, GSTM1, GSTP1, ACE, eNOS, AT2R1, NAT2 genes at different severity of bronchial asthma. Found that in the prediction of the severity of asthma special place belongs to the analysis of the combination of genotypes. Independent effects were found for AT2R1 and ACE gene polymorphisms. The ACE (I / D) / AT2R1 (A1166C) / eNOS (T786C) / eNOS (4b / 4a) four-locus model was developed to predict the severe BA course and the need for additional analysis of the interaction of AT2R1 (A1166C) and eNOS (T786C), eNOS (T786C) genes was demonstrated (4b4a) and GSTT1. The risk of developing severe BA has been demonstrated for the combination of 1166SS + 786TT, 1166CC + 786TC genotypes by AT2R1 (A1166C) and eNOS (T786C) genes, and the reduction of this risk for combinations of eNOS (4b4a) 4b4b + GSTT1 genotypes. In moderate asthma, combinations of ACE genotypes DD + AT2R1 1166SS and AT2R1 313AA + GSTP1 1166SS were reliable risk markers for severe asthma. AT2R1 gene polymorphism was the leading marker in more severe asthma. A marker of severe BA was also found for the heterozygous 857GA polymorphism of the NAT2 gene (G857A). Conclusions. The influence of ACE (I / D), AT2R1 (A1166C), eNOS (T-786C), NAT2 (G857A), GSTT1, and GSTP1 gene polymorphisms on the severity of asthma in children has been established.
Проанализировали влияние полиморфизма гена L-myc (T3109G) на развитие токсичности у пациентов с неходжкинскими лимфомами. Выявлено ассоциацию генотипов 3109ТG и 3109GG с повышением риска развития нефрологической токсичности. Наличие генотипа 3109GG было ассоциировано с потерей массы тела и повышенным количеством лейкоцитов в период манифестации заболевания. Необходимы дальнейшие исследования для разработки лечебно-профилактических мероприятий Ключевые слова: неходжкинские лимфомы, токсичность химиотерапии, полиморфизм гена L-myc (T3109G) Aim of research. To define the influence of polymorphic variants of L-myc (T3109G) gene on the risk of development of hematological and non-hematological toxicity at polychemotharapy in patients with the different forms of non-hodgkin's lymphomas. Methods. Patients with diffuse-macrocellular and microcellular lymphomas underwent 4 courses of polychemotherapy according to the nosologic forms of disease and treatment protocol. The clinical course of disease was assessed paying attention to the toxic effects and response on the therapy. The clinical-laboratory parameters in the period of disease manifestation were analyzed in details. All patients underwent the molecular-genetic examination of polymorphic variants of L-myc (T3109G) gene. Using the statistical analysis was assessed the influence of polymorphic variants of gene on the risk of development of toxic effects and the interconnection with clinic-laboratory parameters.. Results. The studies of the influence of polymorphic variants of L-myc (T3109G) gene on the risk of development of hematological and non-hematological toxicity at PCT at the different forms of NHL proved that the summary frequency of detection of the clinical cases of hematological and non-hematological toxicity did not differ in patients with DMCL and MCL and was not associated with polymorphism of the studied gene. Polymorphism of L-myc (T3109G) gene determined the spread of the tumor process, the risk of development of II-IV stages of disease that were detected more frequently at 3109ТG and 3109GG genotypes; and the 3109GG genotype was associated with the loss of body weight and the rise of the number of erythrocytes in the period of disease manifestation before the beginning of PCT courses. The risk of development of nephrological toxicity at chemotherapy in patients with NHL was associated with 3109ТG and 3109GG genotypes on L-myc gene. The number of toxic effects and the features of their combination in examined patients were not connected with polymorphism of L-myc (T3109G) gene. Conclusions. The further studies are needed for elaboration of the therapeutic-preventive arrangements on the decrease of risk of nephrological toxicity in patients with non-hodgkin's lymphomas at polychemotherapy courses
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