Resume. Sarcoidosis is a systemic granulomatous disease of unknown etiology that primarily affects the lungs and lymphatic system of the body, although multiorgan involvement frequently occurs. Granulomas occur as a result of a helper T cell Type II, Type I protective immune response and are dynamic structures. Under certain known and unknown circumstances, the exuberance of the granulomatous response becomes deleterious, resulting in organ damage and scar formation. A diagnosis of the disorder usually requires the demonstration of typical lesions in more than one organ system and exclusion of other disorders known to cause granulomatous disease. For more than 125 years much progress has been made in terms of understanding the protean clinical and unique immunological features of the disorder. Less is known about the epidemiology and genetic factors that contribute to the development and expression of the disease. The appropriate therapy for the disorder also has not been well defined for all patients. Most importantly, the cause of the disorder is still unknown. The paper provides data on pathogenesis, classification, clinical manifestation, diagnosis, differential diagnosis and treatment of sarcoidosis.

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.

The DPLDs are important, accounting for about 15% of respiratory practice. They comprise a very wide spectrum of pathologies, presentations, and outcomes. There is a serious paucity of evidence about the management of DPLDs, but the morbidity of the DPLDs themselves and the treatments available may be high, with potentially serious consequences therefore for mismanagement. There is concern that DPLDs may be poorly recognized and managed by nonspecialists. Respiratory specialists are the only group with appropriate training and skills to deal with the complexity of the diagnosis and management of these conditions. British Thoracic Society (BTS) Standards of Care Committee set up a sub-committee to formulate recommendations on DPLD management. Purpose of the recommendations: to support improved recognition, diagnosis, assessment, and treatment of patients with DPLD, to raise awareness of the importance of DPLDs, to provide an authoritative current literature review of DPLDs management, to provide practical, evidence and consensus based recommendations that will aid the development of clinical services for patients with DPLD. This article contains the summary of diagnosis and assessment of diffuse parenchymal lung disease, based on BTS recommendations on DPLD management.

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.

Abstract. This article refers to the management of adults with community acquired pneumonia (CAP) of all ages in the community or in hospital. Details of general investigations for patients managed in the community and for patients admitted to hospital, treatment in community, hospitals and in intensive care unit, follow up planning, empirical antibiotic choice, duration of antibiotic administration, failure to improve, the level of evidence of recommendations are given in the text and are summarized in figures and tables. Severity assessment is recommended as the key to planning appropriate management both in the community and in hospital. Certain adverse prognostic features have been associated with an increased risk of death and should be assessed in all patients. Patients who have two or more “core” adverse prognostic features are at high risk of death and should be managed as having severe pneumonia. Patients who display no adverse prognostic features can be managed as having non-severe pneumonia and may be suitable for outpatient treatment or early hospital discharge.

Background: Interleukin-33 (IL-33) cytokine plays a crucial role in asthma pathogenesis. Recent studies have established that IL-33 activity was increased in serum, airway smooth muscle and epithelial cells from patients with asthma and this increase positively correlates with asthma severity. We hypothesized that several genetic variations that contributing IL-33 expression and activity, which may risk factor for susceptibility to asthma. In this study, we examined the association between rs16924159 single nucleotide polymorphism (SNP) of IL-33 gene and asthma susceptibility. Methods: 51 asthma patients and 54 healthy volunteers were involved in this case-control study. Blood sample was collected for genomic DNA extraction. rs16924159 SNP genotyping was performed by the allele specific-polymerase chain reaction (AS-PCR) method. Statistical analysis was performed using STATA 13.0 software. Results: The groups were matched for age, gender and body mass index (p>0.05). The distribution of rs16924159 allele and genotypes among patients and controls was found in accordance with those expected by the Hardy-Weinberg equilibrium (p=0.088). Adenine (A) allele frequency of rs16924159 was significantly different between case and control groups (OR = 1.91, 95% CI = 1.04- 3.51, p = 0.037). Also, homozygote A/A (OR=6.53, 95% CI 0.68-62.38, p=0.104) and heterozygote (OR=2.08, 95% CI 0.93-4.62, p=0.073) genotypes were more frequent among asthma patients than in controls. Conclusions From these findings, we conclude the A allele of rs16924159 SNP in IL-33 gene may be contributing to asthma susceptibility, increasing the carrier`s risk to the development of asthma.