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Background: Incorrect use of inhaler devices is associated with unfavorable outcomes Aim: To evaluate device use errors in asthma and COPD patients treated in outpatient clinics of 3 tertiary hospitals and one private practice office in Greece Methods: Demographics and medical history were recorded. Patients demonstrated the use of their prescribed device and use was evaluated according to predefined steps Results: 607 patients (50.2%male, mean age 60.2years) performed 663 demonstrations (56 patients were using 2 different types of devices). 49.8% were treated for asthma and 50.2% for COPD. 79.5% were using DPIs. Errors were documented in 41.2%, were associated with the type of device, p Conclusion: Device use errors are common and associated with unfavorable outcomes. Trained patients were more likely to use the device correctly. Patients should be encouraged to demonstrate the use of their devices during medical visits in everyday clinical practice

Introduction: Alpha1-antitrypsin (A1AT) deficiency is an autosomal co-dominant disease related to SERPINA-1 gene mutations predisposing to pulmonary emphysema and/or liver disease. Aim: to examine the genotype and phenotype of a Greek cohort of A1AT-deficiency patients. Methods: This multicenter study enrolled A1AT-deficiency patients under augmentation treatment from 8 centers in Greece. Results: 23 adult patients, 61% male, 17.4% non-smokers, diagnosed at a median age (IQR) of 47(42-58) years with A1AT levels of 0.24 (0.04-0.4) g/L were identified. Indications for A1AT measurement were severe obstructive pulmonary disease at the age Conclusion: In contrast with the literature, where Z and S are the most common A1AT-deficiency alleles, the present study reveals extremely rare deleterious variants in Greek A1AT-deficiency patients under augmentation treatment. Further examination of phenotype-genotype associations and outcome is expected to unveil their clinical significance in the future.

Introduction : Smoking has been associated with high serum levels of leptin, a pleiotropic hormone shown to up-regulate the expression of several pro-inflammatory cytokines. In contrast, it has been reported that smokers have lower levels of adiponectin. Objectives: The objective of this study was to assess the longterm effects of smoking cessation on plasma leptin and adiponectin levels. Methods: 45 apparently healthy smokers of both sexes were recruited. The subjects who successfully quit smoking constituted the sample group. 12 healthy non-smokers constituted the control group. Serum leptin and adiponectin levels were evaluated at the beginning of the study and at 3, 6 months after smoking cessation. Results : We report our preliminary results. Among the sample group, 17 subjects had quitted smoking at 3 months and 9 subjects at 6 months. Samples’ leptin was increased from baseline to three months (mean change 47.8 pg/ml [95% CI 2.016931 93.578481], p =0.042), whereas controls9 leptin did not change from baseline (p>0.05). Samples’ leptin was decreased from three to six months (mean change -68.95289 pg/ml [95% CI -111.20515 -26.70062], p Conclusions: Serum leptin levels appear to increase considerably within 3 months after smoking cessation and then decrease significantly from 3 to 6 months. This finding may provide further information on how long inflammation persists after smoking cessation and whether it is definitely irreversible.

Objectives: Polymorphisms in promoter region of TNF-α gene were shown to interfere with the transcriptional activity of the gene resulting in the production of different levels of TNF-α product suggesting their involvement in susceptibility or severity of many inflammatory diseases. We set up a case–control study consisting of 117 COPD (Chronic Obstructive Pulmonary Disease), 62 DB (bronchiectasis) patients and two control groups (109 smokers without COPD-healthy smokers control group and 212 general population subjects) to evaluate involvement of TNF-α gene polymorphisms in the abovementioned diseases in a homogeneous population. Methods: The novel methodology of the NanoChip™ Molecular Biology Workstation (MBW Nanogen http://www.nanogen.com ) was employed to genotype the 5 promoter SNPs. Results and conclusions: Genotype frequencies of the 5 SNPs showed no significant difference between the COPD and DB patient groups and the healthy smokers group. Statistical difference ( p = 0.043) was only revealed between the haplotype frequencies in COPD patients compared to the general population control group. The NanoChip™ MBW is an accurate method for SNP screening.

In order to investigate the incidence of cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations and unclassified variants in chronic pulmonary disease in children and adults, we studied 20 patients with asthma, 19 with disseminated bronchiectasis (DB) of unknown aetiology, and 12 patients with chronic obstructive pulmonary disease (COPD), and compared the results to 52 subjects from the general Greek population. Analysis of the whole coding region of the CFTR gene and its flanking intronic regions revealed that the proportion of CFTR mutations was 45% in asthma (P0.05), 26.3% in DB (P0.05), 16.7% in COPD (P0.05), compared to 15.4% in the general population. Seventeen different molecular defects involved in disease predisposition were identified in 16 patients. Three potentially disease-causing mutations, T388 M, M1R and V11I, are novel, found so far only in three asthma patients. The hyperactive M470 allele was found more frequently in COPD patients (frequency 70.8%, P0.01) than in the controls. The study of the TGmTnM470 V polyvariant CFTR allele revealed the presence of CFTR function-modulating haplotypes TG13/T5/M470, TG11/T5/M470, TG12/T5/V470 and TG12/T7, combined with M470 or V470, in six asthma patients, four DB patients (P0.01), and two COPD patients (P0.05). These results confirm the involvement of the CFTR gene in asthma, DB and possibly in COPD.