Objective: To compare the efficacy of systemic and inhaled corticostcroid in patients with acute exacerbation of COPD.Methods: In this randomized, parallel-group study 80 patients (average age 59,7±7.7) were randomized to receive inhaled corticosteroid (fluticasone propionate 1000-1200 meg/daily, n -40) or systemic corticosteroid (intravenous dcxamethasone 4-8 mg every 24 hours, n-40). Outcome variables included the lung function tests (FEV1, FVC, FEV1/FVC), 6MWT, and 1 Symptoms. 2. Activity and 3. Impact components of St George's Respiratory Questionnaire for t OPD patients (SGRQ-C).Results: In group with systemic corticosteroid increased the FF.V1 from 63.5±9 to 68.118.1, FVC from 78.7±11.8 to 86.6±11, FEV1/FVC from 64.918.7 to 69.917.3; score of SGRQ-C improved I.from 58.5114.3 to 31 5ÈË 2. from 60.6116.7 to 37.7117.2, 3.1'rom 44.9+14.5 to 21.5113. In group wi«fi fluticasone propionate increased the FEV1 improved from 64.719 to 68.718.5, FVC from 79.7111.3 to 88.1110.7, and FEV1/FVC from 64.9+8.6 to 69.517.5; score of SGRQ-C I .from 58.5111.1 to 36.4113,0. 2.from 59.9117.2 to 39.1 + 16.8. 3.from 45.7114.7 to 23.5+13.8. The difference in efficacy of treatment in two groups was not significant.Conclusion:I fioth inhaled and systemic GSs improve airflow and lung function test in C'OPI) patients with ^cute exacerbation.2.1 ligh dose of ICSs may be an alternative to systemic corticosteroid in the treatment of non-severe acute exacerbation of COPD.3. Using of systemic and inhaled corticosteroids improve quality of life in COPD patients with acute exacerbation.

Introduction:Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease characterized by airflow limitation that is not fully reversible. The prevalence and burden Of COPD are projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population. COPD is one of the most important causes of death in most countries. The Global Burden of Disease Study has projected that COPD, which ranked sixth as the cause of death in 2000, will become the third leading cause of death worldwide by 2020. The chronic airflow limitation characteristic of COPD is caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). Airflow limitation is best measured by spirometry, as this the most widely available, reproducible test of lung function. COPD itself also has significant extrapulmonary (systemic) effects that lead to comorbid conditions. The goals of treatment of patients with stable chronic obstructive pulmonary disease (COPD) include: maintaining optimal health, symptom relief, preventing progression of disease, increase exercise tolerance, preventing complications and exacerbations, improving control of symptoms, enabling the patient to function to the greatest extent possible, improving quality of life. Home treatment usually works well for most people, but others with very severe disease may need hospitalisation. With early diagnosis, lifestyle changes (e.g., smoking cessation), and appropriate treatment, many people can lead normal and productive lives.

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Pathological changes characteristic COPD are found in the proximal airways, peripheral airways, lung parenchyma, and pulmonary vasculature.GoalTo evaluate corticosteroid therapy effects in patients with acute exacerbation of COPDMaterial and MethodsWe examined the efficacy of corticosteroid (CS) therapy in 45 patients who admitted to Department of Pulmonology at Shastin`s Central Hospital during 2011-2012 and met GOLD criteria of COPD exacerbation. All patients randomly divided into two groups. Patients received from randomization inhaled corticosteroids (flixotide 1000 mcg/daily or frenolyn 800-1200 mcg/daily), systemic corticosteroid (intravenous prednisone 30- 60 mg every 24 hours). In evaluation of efficacy of treatment we use lung function tests and St George`s Respiratory Questionnaire for COPD patients (SGRQ-C).Results45 patients (average age 59, 6±7.9) were enrolled in our study. 23 patients were randomly assigned to high dose of inhaled corticosteroids (ICS), 22 to intravenous prednisone. Outcomes of treatment were evaluated by 1. Symptoms, 2. Activity and 3. Impact components of SGRQ-C and FEV1, FVC, FEV1/FVC. The difference in quality of life and lung functional tests between ICS and prednisone was not significant. Score of SGRQC in two groups improved with CS therapy from 1. 50,8±1,7 2. 63,9 ±10,7 3. 45.2±15,0 to 1. 27,3±4,2 2. 40,8±9.5 3. 22,7±9,7 The changes of lung functional tests were 1.FEV1 65,7±10,7 2.FVC 80,5±12,0 3.FEV1/ FVC 65,1±8,7 before and 1.FEV1 69,4±9,2 2.FVC 88,3±11,1 3.FEV1/FVC 69,5±7,8 after treatment. Incidence of hyperglycemia and hypertension observed with prednisone. In some patients who used ICSs we detect throat hoarse.Conclusions:1. Both inhaled and systemic GSs improve airflow and lung function test in COPD patients with acute exacerbation.2. After treatment improve quality of life in COPD patients with acute exacerbation.3. High dose of ICSs may be an alternative to systemic prednisone in the treatment of no severe acute exacerbation of COPD.

IntroductionMany factors can contribute to the occurrence of COPD. Recent studies have pointed to the notion thatpolymorphism of candidate genes may also play a signifi cant role in COPD pathogenesis.GoalTo investigate the association of polymorphisms in ADRB2 and TNF-α genes with COPD.Materials and MethodsWe genotyped three SNPs included rs1042713 and rs1042714 in ADRB2, rs1800629 in TNF-α gene,using PCR-RFLP method.ResultsThere is no statistically signifi cant difference was observed for TNF-α rs1800629 between case andcontrol groups. Genotype frequency of the homozygote Gly16 (rs1042713) was more frequent in COPDpatients than controls (OR=3.25; 95%CI, 1.58–6.66, p=0.0037). Also, haplotype frequency of Gly/Gly16+Gln/Glu27 was signifi cant difference among cases and controls (OR=5.03; 95%CI, 1.8–14.2,p<0.01).Conclusion:Overall, ADRB2 rs1042713 and rs1042714 polymorphisms are associated with increased susceptibilityto the development of COPD. Further studies in large groups of patients with COPD are needed toaddress other genetic risk factors.