Respiratory syncytial virus (RSV) bronchiolitis is the most common lower respiratory tract infection in infancy. To date, there is no effective therapy for RSV bronchiolitis.In order to investigate the efficacy of clarithromycin in the treatment of RSV bronchiolitis, the present authors conducted a randomised, double-blind, placebo-controlled trial comparing clarithromycin with placebo in 21 infants with a diagnosis of RSV bronchiolitis. The infants were randomised to receive clarithromycin or placebo daily for 3 weeks. Levels of interleukin (IL)-4, IL-8, eotaxin, and interferon-c were determined in plasma, before and after treatment, using ELISA. Six months after treatment, parents were surveyed as to whether their child had experienced wheezing within the previous 6 months.Treatment with clarithromycin was associated with a statistically significant reduction in the length of hospital stay, the duration of need for supplemental oxygen and the need for b 2 -agonist treatment. There were significant decreases in plasma IL-4, IL-8 and eotaxin levels after 3 weeks of treatment with clarithromycin. Readmission to the hospital within 6 months after discharge was significantly lower in the clarithromycin group.In conclusion, clarithromycin has statistically significant effects on the clinical and laboratory findings in respiratory syncytial virus bronchiolitis. Therefore, clarithromycin treatment may be helpful in reducing the short-term effects of respiratory syncytial virus bronchiolitis.

Anaphylaxis was seen significantly more in boys. Most of the reactions occurred at home. Foods were the most frequent cause. Epinephrine, the first-line treatment of anaphylaxis, was administered in only a third of the children.

Our study demonstrates that the CD14-C159T promoter variant influences total IgE levels and also indicates that the T allele has a more profound effect on total IgE in children with atopic asthma. Polymorphisms in the TLR4 gene may be associated with milder forms of disease in atopic asthmatics in the population studied.

Montelukast inhibits TNF-alpha-stimulated IL-8 expression through changes in NF-kappaB p65-associated HAT activity. Drugs targeting these enzymes may enhance the anti-inflammatory actions of montelukast.

Background: Human leukocyte antigen G (HLA-G) is a nonclassical major histocompatibility complex class I gene. HLA-G stimulates Th2 cytokine secretion by peripheral blood mononuclear cells. The role of soluble HLA-G (sHLA-G) in bronchial asthma is incompletely understood and the plasma level of sHLA-G in asthmatic children has not been investigated. Objective: It was the aim of this study to investigate the plasma level of sHLA-G in asthmatic children. Methods: Asthmatic (n = 53) and healthy children (n = 16) were included in the study. Levels of sHLA-G were determined in plasma using ELISA. Spirometry, total immunoglobulin E and eosinophil counts were obtained and skin testing done with a battery of 25 antigens with appropriate positive and negative controls. Results: No significant difference was observed in the plasma level of sHLA-G between the asthmatic and healthy children (p > 0.05). When we compared atopic asthmatics with healthy controls, we found significantly higher levels of sHLA-G in atopic asthmatics (p < 0.05). There was a significant difference in the peripheral blood eosinophil counts and total immunoglobulin E levels among the groups (p < 0.001). Conclusion: Our study shows that plasma sHLA-G levels do not differ between asthmatic children and healthy controls. However, higher plasma levels of sHLA-G in atopic asthmatics may suggest a role for sHLA-G in atopy. Further investigations are required to better define the mechanism of the production and the role of sHLA-G molecules observed in patients with asthma.

Turkish version of C-ACT is an accurate and reliable tool to evaluate asthma control in children aged 4-11 years. Its widespread use may facilitate appropriate assessment of asthma control and may lead to decrease the number of uncontrolled patients.

Our results suggest that children who express the asthma phenotype despite having a genetic variant that impairs their ability to express ALOX5 have more severe disease and thus are more likely to have asthma symptoms.

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