Background and aims. Achromobacter spp., as causative agent of the nosocomial infections, has caught the eye last Decades. The growth of the infecting of the respiratory tract of the cystic fibrosis patients by this microorganism is formidable. The aim of this investigation was the Achromobacter spp. identification in expanded cohort of the Russian CF patients, genotyping of the microorganism according to the international standards and molecular epidemiological analysis of the situation with this opportunistic microorganism. Methods. Clinical samples from about 300 patients: sputum, tracheal aspirate, throat swabs and strains, isolated from the samples, were the material for the investigation. Method of the multilocus sequence typing (MLST), extended by the additional targets, was the base for the research. Results. 25 percents of the patients routinely hospitalized because of the severity of the disease, were infected by Achromobacter spp. of five species: A. xylosoxidans, A. ruhlandii, A. marplatensis, A. dolens, A. pulmonis, and one genogroup. The species A. ruhlandii has dominated (58.5%). One of the drug resistance indicator – oxacillinase gene blaOXA – helps in the differentiation of the genera Achromobacter and Burkholderia, and also some species in the genus Achromobacter. From 26 identified Achromobacter spp. genotypes (sequence type, ST) 16 STs relate to the species A. xylosoxidans, five – to A. ruhlandii. ST263 is specific to the patients from the Far Eastern Federal District. ST261 and 36 are the most numerous: the patients of all Federal Districts are infected by this ST. The chronological analysis allows suggesting the replacement of the genotype 261 by the genotype 36 in the end of the 1990s years and the A. ruhlandii ST36 nosocomial outbreak. At present 39% of the patients with Achromobacter spp. are infected by A. ruhlandii ST36, transmissivity of which is proved the coinfection cases of the siblings and simultaneously hospitalized patients. The influence on the respiratory function of the CF patients was the most expressed for the A. ruhlandii ST261strains. For the younger age group (1997 year of birth and younger), infected by A. ruhlandii ST36, the median of the FEV1 was slightly lower than in older age group, infected by those strain, that can indicate the accumulation of the pathogenic properties by the A. ruhlandii ST36 during the circulation between the patients. Conclusions. A. ruhlandii ST36 strain by the combination of the identified properties may be considered as the Russian epidemic strain.

Bronchiolitis obliterans syndrome (BOS) is a serious complication of lung transplantation that decreases the patients' survival. The International Society for Heart and Lung Transplantation, American Thoracic Society, and European Respiratory Society developed the current recommendations for better definition of BOS, describing risk factors for developing BOS, diagnosis, management and prevention of BOS. The recommendations were based on the evidenced data published from 1980 through to March, 2013 and were evaluated according to the GRADE system. The committee discussed the use of systemic corticosteroids, cyclosporine, tacrolimus, azithromycin and retransplantation in patients with BOS. The diagnosis of BOS should be made after exclusion of other post transplant complications that can cause persistent lung function decline. Currently, there is no therapy able to improve significantly or to prevent BOS development. Further randomised controlled trials are needed to search optimal therapies and preventive measures for BOS.

According to reports of World Health Organization, chronic obstructive pulmonary disease (COPD) is the 3rd leading cause of death worldwide. Near 2.8 million patients die from COPD yearly, this is 4.8% of all deaths in the world. Causes of death in COPD patients include respiratory causes, acute exacerbation of COPD in 50–80% of cases, lung carcinoma in 8.5 to 27% and other non respiratory causes. Key predictors of poor prognosis of COPD include age, severity of bronchial obstruction and of lung hyperinflation, hypoxemia and hypercapnia, frequent exacerbations, comorbidity, etc. Long term oxygen therapy (for hypoxemic patients), non invasive ventilation (for hypercapnic patients), lung transplantation (for patients with end stage of COPD), and novel bronchodilators (tiotropium bromide) are therapeutic modalities that could decrease mortality, improve lung function and reduce number of exacerbations.

This review includes history of development of devices for drug delivery to the airways. Currently, there is a large diversity of different drug delivery devices for inhalation therapy of chronic obstructive pulmonary disease (COPD): pressurized metered dosing aerosol inhalers (activated or not activated by breath), dry powder nhalers (single dose or multiple dose), jet nebulizers, ultrasound nebulizers and soft mist inhalers. This wide spectrum of different inhalation drug delivery devices provides an improvement in treatment of various respiratory diseases, primarily COPD, due to individual choice of an inhaler considering the patient's age, comorbidity and severity of the disease.

Functional interaction between parenchyma components, stroma, and hematopoietic cell populations of the alveoli under acute inflammation have been described in this review. Cells interact via cytokines and growth factors; a role of this interaction for the pathogenesis of pneumonia is also discussed. We suppose a need of omprehensive research of pneumonia pathogenesis in terms of all structural components of inflammation focus. Thereafter we introduced a concept of interaction systems. Parenchymal elements, such as type I and type II pneumocytes, brush cells, and stromal elements, such as interstitial tissue, fibers, cell populations, alveolar capillaries, and autonomic nerve terminals, are describes in the article. Certain aspects of pneumonia pathogenesis are poorly understood including mechanisms of neutrophil migration to the alveoli and a role of interaction systems in this process. We offer to apply the term of interaction systems relating to the lung tissue when investigating pneumonia.

Secretoglobin SCGB1A1 is a protein produced by airway epithelium secretory cells (club cells or Clara cells) and other epithelial cells of the respiratory and urogenital tracts. Secretoglobin family 1A member 1 (SCGB1A1) refers to as secretoglobin superfamily and participates in maintaining homeostasis under the oxidative stress, inflammation, autoimmune diseases and carcinogenesis. It is a multifunctional protein with antiinflammatory and immunomodulatory properties. It also has antichemotactic, antiallergic, antineoplastic, and grow thstimulatory embryonic activities. SCGB1A1 gene polymorphism appears to be associated with several inflammatory and autoimmune diseases. These properties could be useful for diagnosis and treatment of inflammatory, autoimmune and allergic diseases.

The aim of this study was to investigate polymorphisms of cytokine genes (TNF G308A, IL 10 C592A, IL 10 C819T, IL 10 G1082A), and molecular regulation of inflammation (CD14 C159T) and vascular tone (еNOS C786T) in patients with A / H1N1 flu complicated by pneumonia.

Methods. Patients hospitalized for pneumonia complicating influenza A / H1N1 / 09 were involved in the study: 37 patients with severe pneumonia, 74 patients with non severe pneumonia and 115 healthy subjects as controls. Polymerase chain reaction (PCR) was used for molecular investigations.

Results. Patients with influenza A / H1N1 complicated by pneumonia carried the homozygous G allele of TNF gene polymorphism (308 G/A) and the homozygous G allele of IL 10 gene polymorphism (1082 G/A) more often compared with controls. Patients with pneumonia more often carried IL 10 gene 592 C/A allele and largely as homozygous variant. Frequencies of homozygous IL 10 gene polymorphism (819 C/T) T/T and CD14 gene polymorphism (159 C/T) T/T were significantly lower compared with healthy subjects. On contrary, the homozygous T/T polymorphism (786 C/T) of еNOS gene was more common in patients with pneumonia. Prognostic risk factors for occurrence of pneumonia in patients with influenza А / H1N1 were IL 10 gene polymorphisms 592 CC, 819 CC, and 1082 GG. TNF (308 GG); IL 10 (819 CC) and (1082 GG) haplotypes had the highest prognostic value for severe pneumonia in patients with influenza A / H1N1. TNF (308 GG); IL 10 (819 CC); (1082 GG) and TNF (308 GG); IL 10 (819 CC); (1082 GG) and CD14 (159 CC) haplotypes predicted ARDS and death in patients with influenza A / H1N1 / 09, respectively.

Conclusion. Identifying genetic status in a patient with influenza A / H1N1 could predict severity and complications of the disease.

The objective of this study was to investigate structural changes of the lower respiratory tract using clinical and functional characteristics and biomarkers of inflammation in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD).

Methods. This observational cohort study involved 101 symptomatic patients with acute exacerbation of COPD who met 2 or 3 Anthonisen's criteria. According to high resolution computed tomography (HRCT) findings patients were divided into two groups: 57 patients with COPD and bronchiolitis and 44 people with COPD and no signs of bronchiole lesion. Clinical manifestation, lung function, respiratory failure, structural changes in the lung parenchyma and biomarkers of adaptive immune response were analyzed.

Results. Inflammatory changes in small bronchi and bronchioles in patients with acute COPD exacer bation was associated with more severe exacerbation, occurrence of the respiratory failure, need in respiratory support, lung parenchyma consolidation, increased sputum purulence, lower total serum immunoglobulin E as a marker of humoral immune response.

Conclusion. Inflammation in bronchioles in patients with acute exacerbation of COPD is associated with more severe respiratory failure and need in respiratory support. Consolidation of the lung parenchyma is noted more often in patients with COPD and co existing bronchiolitis. Exacerbation of COPD accompanied by bronchiolitis is characterized by less prominent humoral immune hypersensitivity response that could be diagnosed by the total serum

immunoglobulin E level.

The purpose of this study was to assess efficacy of a fixed combination of bisoprolol and amlodipine (Concor AM, Takeda) in patients with chronic obstructive pulmonary disease (COPD) and hypertension (H).

Methods. Thirty eight stable patients with stage 2 COPD and stage I–II H were treated with a fixed combination of bisoprolol and amlodipine. 24h ambulatory blood pressure monitoring (ABPM), electrocardiography, echocardiography, and lung function were performed at the baseline and in 12 weeks of therapy.

Results. Thirty four (89.5%) patients continued the treatment after 12 weeks. The therapy with the fixed combination of bisoprolol and amlodipine in average dose of 7.5 / 10 mg/day provided a target blood pressure (BP) level in 32 (84.2%) patients. ABPM analysis demonstrated stable significant improvement in BP parameters including the heart rate variability. A trend toward normalization of the left heart diastolic function was noted during treatment. Lung function did not differ significantly before and after 12 weeks of the treatment indicating that the fixed combination of bisoprolol and amlodipine did not impact negatively on bronchial obstruction.

Conclusion. The results confirm the rationale of therapy with the fixed combination of bisoprolol and amlodipine in patients COPD

and H.

Comorbidity of chronic obstructive pulmonary disease (COPD) and metabolic syndrome (MS) creates the need of comprehensive approach to treatment, and prevention and rehabilitation of the patients.

The aim. The objective of this study was to evaluate clinical efficacy of a comprehensive pulmonary rehabilitation program in patients with COPD and MS. This program was based on patient education, smoking cessation, physicaltraining, and nutritional correction in addition to the standard treatment of COPD.

Methods. The study involved 70 patients (27 women (38.6%)
and 43 men (61.4%) with stable moderate COPD and MS aged 18 to 60 years (mean age, 48.31±0.64 years). The patients were randomly divided
into two groups: 35 patients were involved in a pulmonary rehabilitation program in addition to the standard therapy of COPD; other 35 patients
were treated with the standard therapy. Clinical and laboratory parameters were assessed at baseline and in 12 months.

Results. To the end of the study the groups differed significant in number of COPD exacerbations, emergency calls, hospitalizations, clinical symptoms of COPD and impact of the disease on physical activity and health status of the patients, quality of life (QOL), and physical tolerance.

Conclusions: Management of patients with comorbid COPD and MS should include specific educational programs and physical training in order to improve treatment efficacy and quality of life of the patients.

The aim of this study was to investigate Fas (CD95) and Tumor necrosis factor
α (TNF α) expressions in patients with different manifestations of tuberculosis (TB).

Methods. The study involved 54 patients with active pulmonary TB of different severity and 22 healthy volunteers. CD95 cell number was counted by lymphocyte immunophenotyping. Spontaneous and stimulated TNF α production by Mycobacterium bovis (BCG) was assessed in the supernatant of 24h blood mononuclear cell culture using the ELISE method.

Results. Patients with severe and complicated TB had significantly increased both CD95 number and spontaneous TNF α production in comparison to patients with milder TB course and to healthy volunteers. CD95 cell number was associated with cavitation and positive culturing of Mycobacterium tuberculosis.

Conclusion. These results improve our knowledge of immunopathology of TB and facilitate further search for targeted immune rehabilitation.

The aim. The purpose of this study was to analyze causes of deaths of hospitalised HIV infected patients with tuberculosis.

Methods. Medical reports of patients with tuberculosis who died in a specialized hospital of Samara city in 2013 were analyzed using the total sampling method.

Results. Ninety per cent of deaths in hospitalised HIV infected TB patients were caused by end stage AIDS with the high proportion (82%) of miliary tuberculosis, involvement of multiple organs (53%) and drug dependence (88%).

Conclusion. Improving interaction of TB specialists and experts on HIV infec tion is needed to improve statistic analysis of morbidity of and mortality from tuberculosis and to reduce mortality from these comorbid diseases.

The aim of this study was to identify social risk factors of pulmonary tuberculosis.

Methods. We used a questionnaire to evaluate living conditions, number of subjects living together, including children; dwelling space, and family income.

Results. The study involved 342 patients with newly diagnosed pulmonary tuberculosis (56.4±5.26% were men) and 386 healthy individuals (54.7±4.97% were women). Poor living conditions (OR = 8.4 (5.25; 13.44); p < 0.001) and extremely low income (OR = 2.5 (2.17; 2.97); p < 0.001) were associated with the highest risk for pulmonary tuberculosis morbidity followed by living in an individual household, small dwelling space, low family income and less living rooms in a house. A relatively small proportion of TB foci involving children was found.

Conclusion. The results can facilitate targeted measures for active diagnosis of pulmonary tuberculosis in high risk cohorts. This could increase efficacy of preventive measures and reduce diagnostic costs per a patient.

Pulmonary complications in Stevens Johnson syndrome (SJS) or toxic epidermal  ecrolysis (TEN) are rare and mostly manifest as broncho bron chiolitis obliterans with poor prognosis. Recently, there is no effective therapy for this condition in patients with SJS / TEN. We described a case of SJS with progressive hypercapnic respiratory failure in 4.5 year boy who died despite an intensive treatment. herefore, lung transplantation should be considered at the early stage of this disease.

This article is a case report of a 45 year old male with severe primary lung emphysema. He underwent lung transplantation. In a year after the transplantation, the patient experienced exercise dyspnea again. Multiple soft tissue rounded foci were found in the lungs in CT scans. Thoracoscopic lung biopsy followed by histological examination of the bioptates allowed diagnosis of Kaposi's sarcoma. This case is of particular interest as Kaposi's sarcoma is extremely rarely seen in allograph.

α1 Antitripsin deficiency (AAT) is an orphan respiratory disease. Genetic risk factors of chronic obstructive pulmonary disease (COPD) can cause AAT and primary emphysema of the lungs. AAT genotyping plays the key role for diagnosis. Early detection of AAT deficient phenotypes is crucial for prevention and treatment of COPD and slowing emphysema progression. A case of inherited AAT deficiency in a patient with deficient phenotype PiZZ is described in this article. A diagnostic algorithm for AAT is proposed.