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Журнал «Здоровье ребенка» 3 (63) 2015

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Side effects of basic therapy in children with allergic asthma

Авторы: V.M.Dudnyk, K.V. Khromykh — Pirogov Vinnitsa National Medical University, Vinnitsa, Ukraine

Рубрики: Педиатрия/Неонатология

Разделы: Клинические исследования

Версия для печати

Purpose - to determine the presence of side effects of basic therapy , namely the development of endothelial dysfunction in children with allergic asthma.

Materials and methods.

The study involved 224 child with allergic asthma aged 6 to 17 yearsThe average age of the patients was 9,42 ± 3,43 years. The children were divided into two groups: the main group consisted of patients with asthma who received BAIT IGC (n = 92), comparison group consisted of patients who didn’t receive BAIT (n = 86), and both groups were randomized by the severity and duration of disease. In carrying out the basic treatment IGC also accounted for the duration of drugs BAIT: 1 year 1 to 5 years and over 5 years.Homocysteine was determined by liquid chromatography apparatus Hewlett Packard (USA) after sequential processing and working solution trybutylphosphynparahlormerkuribenzoat method by Pentyuk A.A. (2003). Vascular endothelial growth factor in serum were determined by enzyme-linked immunosorbent assay (ELISA) using standard sets the company IBL International (Germany). Ultrasonography (USG) carotid and brachial artery was made on the machine Philips HD11 XE, in B - mode with color Doppler flow mapping linear transducer in the range of 5 - 10 MHz, 7 MHz optimally. 40 healthy children were examined as a control group.

Results.

Observed that children with asthma had a number of adverse effects of treatment, including - oropharyngeal candidiasis, dysphonia, reflex cough and bronchospasm, growth inhibition and activation of herpes infection that occurred when using the IGC for 1 - 5 years (12.49 - 33.3) % more likely than children with treatment lasting up to a year. We found that significant differences between groups of children with asthma, with different duration of use IGC there. Comparing homocysteine and VEGF in children with asthma, depending on the availability BAІT, was found that their content are significantly lower in children who didn’t receive BAІT (p <0.05).
Treatment of medium and high doses IGC is a risk factor homocysteine increase above 17.36 [11.3 - 24.5]mmol/L (OR 1 504; 95% CI 1,141 - 7,519 and 2,456 OR, 95% CI 1,427 - 29,343, respectively). As for growth over the content VEGF 431.66 [238.04 - 658.09] pg/ml, it probably increases with the use of low (OR 1,385; 95% CI 1,117 - 4,602) and medium (OR 2,462; 95% CI 1,200 - 30.275) doses of IGC.
After analyzing the relationship between ultrasound indexes and groups of these enzymes, we have found that the application of patients had at IGC (3.05 - 7.01) % higher values than those used antileukotrien drugs. Thus, observed that TAV and SD was significantly (p <0.01) differed patients receiving IGC and those used antileukotrien drugs.
We have found that the likelihood of changes in ultrasound can trigger any - that dose IGC, including improving performance such as TAV (OR 1,714; 95% CI 1,214 - 4,118) and PI (OR 1,267; 95% CI 1,010 - 3,144) in the application only low doses of GCI and change TAV (OR 1,217; 95% CI 1,080 - 1,684), SD (OR 2,806; 95% CI 2,309 - 25,476) and RI (OR 1,041; 95% CI 1,015 - 2,406) using high doses of IGC.
After analyzing the dependency ultrasound indicators of brachial artery of homocysteine levels in children with asthma, we found that SD (32,89 ± 0,41), TAV (9,00 ± 0,24) and PI (10,87 ± 0, 22) more at 18.76%, 12.99% and 9.51% respectively in children with secondary form of hyperhomocysteinemia from those of healthy children (36,36 ± 0,83, 6,66 ± 0,38 and 6,82 ± 0,48 respectively).
Comparing the content of VEGF in the serum of children with asthma, with ultrasound indicators of brachial artery, we have observed that such indices as TAV (9,5 ± 0,39), SD (30,18 ± 0,62) and PI (10 42 ± 0,36) differed at 16.11%, 10.64% and 4.52% in children with asthma who were content VEGF level III - IV quartiles compared with healthy children (6,66 ± 0,38, 36,36 ± 0,83 and 6,82 ± 0,48 respectively).
It is established that the risk factors on the appearance of the manifestation of endothelial dysfunction as IM thickening in children with asthma were content increase in serum homocysteine levels above 17.36 (11.3 - 24.5) mmol/l (OR 1.253; 95% CI 1,005 - 1,562) and VEGF over 431.66 [238.04 - 658.09] pg/ml (OR - 2,211; 95% CI 1,484 - 10,092). Also noted that indicators such as the brachial artery ultrasound TAMX (OR 1,455; 95% CI 1,179 - 2,944) and RI (OR 2,100; 95% CI 1,879 - 5,019) change significantly with increasing content of VEGF than 431.66 [238.04 - 658.09] pg / ml.

Conclusions.

Conduct basic treatment of asthma in children has a number of undesirable outcomes such as displays oropharyngeal candidiasis, dysphonia, reflex cough and bronchospasm, growth inhibition and activation of herpes-virus infection. In addition, the use of antileukotrien drugs and long-acting b2-agonists enhances endothelial dysfunction inherent in this disease, which is accompanied by an increase in homocysteine and VEGF, but its severity significant the largest (higher to 15.09 - 15.14%) in using inhaled glucocorticoids and significantly different in children who didn’t receive basic treatment (p <0.05). The emergence of endothelial dysfunction in children with asthma by ultrasound parameters hadn’t dose-dependent effect by using IGC, namely, increased TAV (OR 1,714; 95% CI 1,214 - 4,118) and PI (OR 1,267; 95% CI 1,010 - 3,144) with 'is even at low doses their application.

Список литературы

1. Anty`pkinYu. G., Goncharenko N. I., Tarasyuk B. A. Lazernadopplerivs`kafloumetriya u doslidzhenniendotelial`noyifunkciyi u ditej z bronxial`noyuastmoyu.  Zhurnal AMN Ukrayiny`, 2010; 2(16); 307–312
2. Regeda M.S., Regeda M.M., Furdy`chko L.O., Kolishecz`ka M.A., My`ronenko S.I. Bronxial`naastma. L`viv, 2012; 147
3. Adams N, Bestall JM, Jones PW. Cochrane Database Syst Rev 2002;(1):CD002310.
4. O'Sullivan S, Akveld M, Burke CM, Poulter LW. Effect of Montelukast to Inhaled Fluticasone Propionate on Airway Inflammation. Am J RespirCrit Care Med 2003;167:745-50.
5. Pauwels R, Pedersen S, Busse W, et al. Early intervention with budesonide in mild persistent asthma: a randomized, double-blind trial. Lancet 2003;361:1071-76.
6. Tawakol, A., Omland, T., Gerhard, M. etal. Hyperhomocyst(e)inemiais as¬sociatewithimpaired endothelium-dependant vasodilatationinhumans. Circula¬tion 1997; 95: 1119-21. 
7. Wanner A., Mendes E. S. AirwayEndothelialDysfunctioninAsthmaandChronicObstructivePulmonaryDisease: A ChallengeforFutureResearch .Am. J. ofRespiratoryandCrit. CareMed. 2010; 182; 1344–1351.

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