Prevalence of chronic obstructive pulmonary disease in Korea: the fourth Korean National Health and Nutrition Examination Survey, 2008.

BACKGROUND AND OBJECTIVE: Because the mortality and social burden associated with COPD is increasing, repeated surveys of the prevalence of COPD have been used to assess risk factors, detect potential patients, and establish early diagnoses and management protocols. We report the prevalence of spirometrically detected COPD in Korea in 2008, using data from the fourth Korean National Health and Nutrition Survey. METHODS: Using nationwide stratified random sampling, based on the Korean Statistical Office census, 6840 subjects aged ≥19years underwent spirometry, which was performed by four trained technicians, during 2008. The place of residence, levels of education and income and smoking status, as well as other results from a COPD survey questionnaire were also assessed. RESULTS: Airflow obstruction (FEV(1) /FVC<0.7) was detected in 8.8% of subjects aged ≥19years (11.6% of men and 5.9% of women) and COPD was detected in 13.4% of subjects aged ≥40years (19.4% of men and 7.9% of women). Of the 6840 subjects, 27.3% were current smokers and 17.2% were former smokers, and the prevalence of COPD was higher in current and former smokers than in never smokers. Approximately 94% of patients with COPD had mild-to-moderate disease, without apparent symptoms; only 2.4% had been diagnosed by a physician and only 2.1% of patients had been treated. The independent risk factors for COPD were smoking, advanced age and male gender. CONCLUSIONS: Although the prevalence of COPD in Korea is high, the disease is underdiagnosed and most COPD patients are under-treated.

Phosphoinositide 3-kinase delta inhibitor as a novel therapeutic agent in asthma.

Multiple signal transduction pathways are involved in airway inflammation with one of the key signalling pathways being phosphoinositide 3-kinase (PI3K). Numerous components of the PI3K pathway play an important role in the expression and activation of inflammatory mediators, inflammatory cell recruitment, immune cell function, airway remodelling and corticosteroid insensitivity in asthma. More recently studies exploring the specific roles of different PI3K catalytic subunit isoforms in asthma have been initiated. Several of these have highlighted the importance of p110delta isoform as a novel target for therapeutic intervention in asthma. In this review the biological role of PI3Ks, especially PI3Kdelta, are highlighted and the therapeutic potential of selective PI3Kdelta inhibitor in asthma discussed.

PPAR-gamma modulates allergic inflammation through up-regulation of PTEN.

The ligand-activated nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) has been shown to regulate cell activation, differentiation, proliferation, and/or apoptosis. PPARgamma is also associated with anti-inflammatory responses. However, the signaling mechanism remains elusive. We have used a mouse model for asthma to determine the effect of PPARgamma agonists, rosiglitazone or pioglitazone, and PPARgamma on allergen-induced bronchial inflammation and airway hyperresponsiveness. Administration of PPARgamma agonists or adenovirus carrying PPARgamma cDNA (AdPPARgamma) reduced bronchial inflammation and airway hyperresponsiveness. Expression of PPARgamma was increased by ovalbumin (OVA) inhalation, and the increase was further enhanced by the administration of the PPARgamma agonists or AdPPARgamma. Levels of IL-4, IL-5, IL-13, and eosinophil cationic protein were increased after OVA inhalation, and the increased levels were significantly reduced by the administration of PPARgamma agonists or AdPPARgamma. The results also showed that the administration of PPARgamma agonists or AdPPARgamma up-regulated phosphatase and tensin homologue deleted on chromosome ten (PTEN) expression in allergen-induced asthmatic lungs. This up-regulation correlated with decreased phosphatidylinositol 3-kinase activity as measured by reduced phosphorylation of Akt. These findings demonstrate a protective role of PPARgamma in the pathogenesis of the asthma phenotype through regulation of PTEN expression.