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Background and Objective. Asthma is an example of a chronic disease for which there are evidence-based guidelines for primary care. The authors undertook this study to demonstrate that physicians’ use and adherence to asthma management guidelines are improved when the guidelines are furnished in a computer-based format. Methods. Based on established guidelines, the authors devised a practical and simple computer-assisted program focused on asthma treatment and monitoring. They then undertook a preliminary investigation, “Easy Asthma Management (EAM)” study, using this program. Finally, the authors evaluated the program's effectiveness by measuring clinical outcomes and changes in prescription patterns before and after the study. Results. A total of 4682 asthma patients followed by 377 physicians were recruited, and 2187 completed the study (46.7%). The means of diurnal and nocturnal symptom scores were significantly reduced after a 3-month enrollment in the EAM study. Interestingly, the fraction of prescriptions for oral β2-agonists, oral methylxanthines, and systemic steroids (oral or injection) significantly decreased after the EAM study ( p = .02, p <.001, p <.001, respectively), whereas the fraction of prescriptions for inhaled forms of steroids combined with β2-agonists increased significantly ( p <.001). Conclusions. These findings suggest that a computer-assisted asthma management program can be used to improve the clinical outcomes of patients with asthma, and increase physician adherence to established guidelines. [ABSTRACT FROM AUTHOR]

Background: Although respiratory viral infections in early childhood can enhance the development of airway allergen sensitization, the exact mechanisms of the effects of viral infections on the adaptive immune response to inhaled allergens are controversial. Objective: We sought to evaluate the effects of double-stranded RNA (dsRNA) on airway sensitization to inhaled allergens. Methods: Novel mouse models were created through simultaneous airway sensitization to an allergen and low or high doses of dsRNA. The mouse models were applied to Toll-like receptor 3–, IL-13–, IL-4–, signal transducer and activator of transcription (STAT) 6–, IFN-γ–, and T-box expressed in T cells (T-bet)–deficient mice to evaluate underlying pathophysiologic mechanisms in the development of allergic lung inflammation. Results: We found that airway allergen sensitization with dsRNA induced lung inflammation that was not present in Toll-like receptor 3–deficient mice. Moreover, lung inflammation enhanced by low-dose dsRNA was impaired in IL-13–deficient mice, whereas lung inflammation by high-dose dsRNA was impaired in IFN-γ–deficient mice. The models also demonstrated that low-dose dsRNA enhanced IL-4 expression during allergen sensitization and that inflammation enhanced by low-dose dsRNA was not present in IL-4– or STAT6-deficient mice. In contrast, the present study showed that high-dose dsRNA enhanced IFN-γ expression during allergen sensitization and that the development of lung inflammation enhanced by high-dose dsRNA was impaired in T-bet–deficient mice. Conclusion: These findings suggest that airway allergen exposure during respiratory viral infections might induce asthma induced by both TH1 and TH2 immune responses to inhaled allergens. Clinical implications: Targeting both TH1 and TH2 lung inflammation might be important in the treatment of virus-associated asthma. [Copyright &y& Elsevier]

Background: Vascular endothelial growth factor (VEGF) has been suggested to be a key mediator in the development of atopy and TH2 inflammation. Objective: We sought to evaluate the effects of variations in the gene coding VEGF receptor (VEGFR) 2 on intermediate phenotypes of asthma in the Korean population. Methods: A cohort of 2055 children and adolescents responded to a questionnaire concerning asthma symptoms and risk factors and underwent methacholine bronchial challenge and skin tests. The VEGFR2 gene, including the promoter area, was sequenced on 24 healthy subjects to discover informative single nucleotide polymorphisms (SNPs; minor allele frequency >2%). After haplotype reconstruction, 4 tagging SNPs (IVS6+54A>G, +889G>A, +1416T>A, and IVS25-92G>A) were scored. These SNPs were also scored in 480 adult asthmatic patients to verify the above genetic association study. Results: The prevalence of atopy was associated with a single SNP (+889G>A) of VEGFR2 with borderline significance (P = .048; relative risk, 1.13; 95% CI, 1.00-1.28). However, haplotype analysis showed that the atopy prevalence was strongly associated with a haplotype (AGAG) of VEGFR2 (P = .002; relative risk, 1.25; 95% CI, 1.09-1.42). As for airway hyperresponsiveness, neither individual SNPs nor haplotypes were found to be associated. Interestingly, the significant association was also found between atopy and the AGAG haplotype among adult asthmatic patients (P = .008; odds ratio, 1.66; 95% CI, 1.14-2.44). Conclusions: The present study demonstrated that genetic variations of VEGFR2 are significantly associated with atopy in the Korean population. [Copyright &y& Elsevier]