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Patients with a combination of bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD) crossed phenotype (CP) BA and COPD are a separate nosological group. CP BA and COPD is a multifactorial disease. There is a hypothesis that genetic control of CP BA and COPD development at the posttranscriptional level is carried out by regulation of gene expression involving microRNA (miR) miR-21 and miR-146a; these molecules can be considered as potential diagnostic markers of CP BA and COPD. The purpose of this study was to evaluate the expression of miR-21, miR-146a in male with a combination of BA and COPD compared to those with isolated BA and COPD. Materials . We examined male patients (n = 65) (n = 48: 19 patients with CP BA and COPD; 14 patients with BA and COPD) and control group (n = 17). All the patients underwent a comprehensive clinical-laboratory and instrumental examination. The expression of miR-21, miR-146a was estimated in peripheral blood by a real-time polymerase chain reaction. Results . CP BA and COPD have lower levels of miR-21 and miR-146a than the BA, COPD, and control groups. CP BA and COPD patients have low levels of miR-21 and miR-146a associated with shorter duration of the disease and the presence of comorbid pathology (hypertension, angina pectoris), revealed in patients with the disease debut at an older age. Low miR-21 was associated with lower reversibility of bronchial obstruction in these patients, despite eosinophilic inflammation in the bronchi. Conclusion . It has been demonstrated that within the framework of complex diagnostics of CP BA and COPD in males it is reasonable to evaluate miR-146a and miR-21 expression in peripheral blood. MicroRNA miR-146a and miR-21 are promising molecular targets for phenotype-specific therapy in males with CP BA and COPD.

BACKGROUND: a comparative analysis of laboratory and instrumental tests at patients with bronchial obstructive diseases seems very actual due to the wide prevalence of these diseases. THE AIM: to evaluate characteristics of spirometry as well as allergic (total IgE, sputum eosinophils) and infectious (blood and sputum leucocytes, ESR, CRP, fibrinogen) inflammation markers at patients with bronchial obstructive diseases. PATIENTS AND METHODS: 104 case histories of patients with bronchial asthma, chronic obstructive pulmonary disease and overlap were analyzed including age, duration of smoking (pack-years), laboratory (clinical blood test, biochemical blood test, general sputum analysis, sputum culture) and instrumental (spirometry, body plethysmography, echocardiography) tests. Data were processed statistically with non-parametric methods. RESULTS: COPD patients were older than other groups’ patients, had the highest pack-years index. ACO patients were marked with maximal TLC and Raw, minimal FEV1, FEF25-75, FEV1/FVC. Patients with COPD had the highest inflammation markers (leucocyte count, CRP, fibrinogen). CONCLUSION: high active inflammation may cause severe lower airways possibility disorders at patients with COPD. Data related to a possible role of K. pneumoniaе in the pathogenesis of eosinophilic inflammation in lower airways are of significant interest. Patients with ACO occupy an intermediate position between asthma and COPD patients based on clinical and functional features.

217 people were examined including BA patients (n=78), patients with COPD (n=38), patients with combined asthma and COPD (n=39), and community-acquired pneumonia patients (n=17). The control group represented patients with essential hypertension and coronary heart disease (n=25) and 20 healthy persons. NE, AAT, phagocytic activity of neutrophils (FGC), oxygen blast, respiratory function and FeNO, serum IgE and IgG antibodies to Strept. pneumoniae, Neisseria perflava, Haemofil. influenzae and Staph. aigai were determined in all patients. The indicators of the functional state of neutrophils reflected the degree and severity of bronchopulmonary inflammation. Patients with bronchial asthma in combination with COPD had bacterial inflammation, manifested by bronchial obstruction with increasing level of AAT. These features were absent in patients with BA and COPD.

Thirty-five patients with non-allergic bronchial asthma (NABA), 22 patients with NABA and diabetes mellitus type 2 (DT2), 23 subjects with DT2, and 31 healthy controls were enrolled into the study. ELISA assays for IL-4, IL-10, IL-6, IFNγ were performed by means of a standardized protocol using immunoassay kits purchased from VectorBest, and Cytokine. In asthma patients complicated by DT2, the pattern of bronchial asthma was ascribed to NABA. This finding may be consistent with a theory of specific insulin-receptor interactions in asthma. The NABA patients with type 2 diabetes mellitus exhibited a significant increase in IL-6, IFNγ, and decrease of IL-4, as compared with healthy controls and NABA. Moreover, we have revealed an increase of IL-4, IL-6, IFNγ, when compared with DT2. Hence, the patients with coexistence of non-allergic bronchial asthma and DT2 were characterized by a specific cytokine profile of pro- and anti-inflammatory cytokines, which may correlate with increased glycation and deterioration of lung function.

Relevance. The use of inhaled glucocorticosteroids (IHCs) is one of the main basic treatment options forbroncho-obstructive diseases. IHCs suppress chronic inflammation in the bronchial tree, but can be associated with the risk of pneumonia due to impairment of bronchus mucosal immunity and increased microbial colonization in the mucosa. Aim . The aim of this study was to evaluate the incidence and risk factors of pneumonia during the IHCs therapy in patients with chronic obstructive pulmonary disease (COPD), bronchial asthma (BA), and with combination of COPD and asthma. Materials and methods . The retrospective study included patients with confirmed COPD, BA and combined COPD and asthma. The endpoint of this analysis was the incidence of pneumonia. Potential additional risk factors (age, gender, smoking, diagnosis, duration of the disease) were analyzed. Results. A total of 220 patients with broncho-obstructive pathology were included in the retrospective analysis. 184 patients received IHCs. 34 patients obtaining the basic therapy with IHCs developed pneumonia with a cumulative incidence of 36 % after 10 years. The primary diagnosis, gender, age and smoking did not significantly impact the risk of pneumonia. Conclusions. IHCs therapy is associated with a risk of pneumonia, which should be taken into account when planning long-term control of broncho-obstructive pathology.

Severe bronchial asthma is a serious healthcare and social challenge. Severe asthma in both in children and adults may have an unfavorable course, has heterogeneous clinical phenotypes and is very difficult to treat. Treatment of patients with inadequately controlled severe asthma requires significant resources from the healthcare system. At the same time, severe asthma in children, adolescents and adults has a number of specific features making it a separate phenotype. These groups of patients are at high risk of hospitalization and mortality.

The study was conducted to evaluate the activity parameters of local and systemic inflammation in women suffering from bronchial asthma (BA). 119 women with asthma were studied, and 48 with a regular menstrual cycle and 71 in menopause; 38,7% of BA was mild, 61,3% – moderate severity. All patients were examined in the remission phase of the disease. On the background of normal values of conventional indicators of inflammation it was showed a significant increase of IL 1 alpha and IL 8 more in the group of women with regular menstrual cycles and normal body weight, IL1 alpha amounted to 489±80 pg/ml and IL8 – 631±122 pg/ml (p

Forty-two patients with allergic bronchial asthma (ABA) forty persons with non-allergic bronchial asthma (NABA), and 47 healthy controls were involved into the study. Expression of FoxP3 mRNA was analyzed by RT-PCR. In patients with bronchial asthma (ABA and NABA) we have revealed a significant decrease in FoxP3 mRNA expression levels, in comparison with control group. The patients with severe BA exhibited lowest levels of the FoxP3 mRNA expression as compared with other groups. We revealed a decreased FoxP3 mRNA expression in mononuclear cells from peripheral blood, and an increased IL-17 level in blood serum of patients with bronchial asthma. These results may be considered a manifestation of serious inflammatory process. Probably, the data may reflect a disregulated expression of FoxP3 transcription factor. Therefore, we may assume a key role of FoxP3 for regulation of inflammatory activity in bronchial asthma.

Sixty patients with allergic bronchial asthma (ABA) and forty-one, with non-allergic bronchial asthma (NABA), as well as 23 healthy controls were under study. Expression of the SOCS5 mRNA from mononuclear blood cells was analyzed by RT-PCR. In patients with bronchial asthma, (ABA and NABA) we determined a significant increase of mRNA expression levels for a SOCS5 negative transcription regulator in peripheral blood mononuclears, in comparison with control group. Thus, an increase of SOCS5-expression, and of the SOCS3 mRNA expression in patients with BA may be associated with protective anti-inflammatory response.

Background. The aim of the study was to investigate cellular phenotypes of the spontaneous sputum, estimate possibilities of cytological sputum analysis in evaluation of airways inflammation peculiarities in comparison with the expired nitric oxide level and respiratory function tests. Materials and methods. functional properties of neutrophils were evaluated by respiratory burst intensity. 72 patients were included, 23 - with moderate bronchial asthma course and chronic bronchitis, 18 - with moderate bronchial asthma and COPD, 31 patient had COPD only. All patients were examined in the exacerbation period, all of them had productive cough. Results. Cytological phenotypes were stated as well as the links between different sputum cells presence and between cytological peculiarities, inflammation and functional state of the respiratory system. Functional defects of neutrophils were found in COPD patients.

The investigation concerned the diagnostic value of following inflammation markers in patients with mild or moderate bronchial asthma (BA), chronic obstructive pulmonary disease (COPD), chronic bronchitis and pneumonia: expired air nitric oxide (Feno) and serum levels of α 1-antitripsin and neutrophilic elastase. 93 patients were included: 6 with mild BA, 11 - with moderate BA, 17 - with mild BA and chronic bronchitis, 25 - with moderate BA and COPD, 25 - with COPD, 9 - with pneumonia. The control group consisted of 21 healthy donors. We revealed that Feno, α 1-antitripsin and neutrophilic elasthase indicate the presence of the inflammation: Feno elevation mostly related to allelrgic one, α 1-antitripsin and neutrophilic elasthase - to infection-dependent inflammation. Treatmentinduced remission of the disease leads to the decrease of α 1-antitripsin and neutrophilic elasthase, but levels are not reaching the normal values. This confirms the presence of airways inflammation during clinical remission of the disease. Elevated levels of α 1-antitripsin and neutrophilic elasthase are associated with the decreased forced expiratory volume during the first second (FEV 1 - % to the predicted values).

We observed sixty patients with allergic bronchial asthma (ABA) and 54 with non-allergic bronchial asthma (NABA). Quantitative SOCS3 and SOCS5 mRNA expression was evaluated by means of real-time PCR. Eighteen healthy persons served as a control group. In patients with bronchial asthma (irrespectively of pathogenetic form), a significant increase of SOCS3 transcription factor expression was detected in peripheral blood mononuclears, as compared with control group. This increase was more pronounced in NABA group. The mRNA SOCS5 level was significantly decreased in bronchial asthma patients, as compared to control group, especially, in ABA subgroup rather than in NABA patients. Thus, an increased expression of SOCS3 mRNA in BA patients could be regarded as a protective antiinflammatory response Decrease of SOCS5 mRNA expression in patients with bronchial asthma (being more pronounced in ABA), may be indicative for a deficiency in negative feedback regulation of gene transcription in allergic bronchial asthma.

Background. Early detection and treatment of severe forms of bronchial asthma (BA) is one of serious problems in clinical practice. BA is a multifactorial disease, so its progression is a result of both environmental factors and genetic predisposition. Aim of the study. To determine frequencies of genetic variants resulted from the mutation C3435T (rs1045642) in MDR1 gene among patients with different BA severity and in healthy controls. Methods. The trial included 122 patients with different severity of BA course and 103 healthy controls. Genomic DNA was extracted from peripheral blood leucocytes by routine phenol-chloroform protocol. Allelic variants were determined by polymerase chain reaction with subsequent restriction analysis with MboI restriction endonuclease. Results. For the first time association of allelic variant 3435C of MDR1 gene with BA was revealed. Differences between MDR1 genotypes distributions persisted in case of stratification BA patients according their severity courses. Severity of BA course was found to be strongly associated with 3435C allele. Conclusion. Allele 3435C and genotype 3435CC of gene MDR1 are markers of increased risk of BA progression. In patients with BA these alleles are associated with unfavorable severe course of the disease. Genotype 3435TT of gene MDR1 is a protective marker associated with favorable and well-controlled BA course.

The article concerns the role of respiratory tract bacterial infections in development of bronchial asthma and COPD. Analysis is based on current publications and results of clinical investigations. Ability of neutrophils to protect the respiratory system from bacterial agents is underlined. The results obtained during investigation of 132 bronchial asthma and 33 COPD patients showed that in allergic asthma patients high percentage of sputum neutrophils is associated with normal FEV1% and mild course of the disease. In COPD patients high percentage of sputum neutrophils is usually associated with low FEV1%. It is proposed, that in these patients functional activity of neutrophils is associated with predominant injury of respiratory structures.

The analysis of publications and results of original investigations concerning the pathogenesis and clinical course of bronchial asthma is performed. B ronchial asthma is a markedly heterogeneous disease, the heterogeneity is due to the differences in severity cause, phases, clinical pathogenetic variants, associations with the other allergic diseases, COP D, diseases of other organs, influence of different allergens and infectious agents. T hus, the effective treatment plan should be based also on attention to individual features of the patient and include both drugs and methods of non-drug treatment.

Article is devoted to the role of psychosomatic disorders in onset and development of bronchial asthma, to the diagnostics and treatment of neuropsychical variant of the disease course and possibilities of psychotherapeutic correction.

This work was aimed at estimating the role of special therapy of patients with bronchial asthma, COPD and hyperoxaluria designed to restrict the delivery or eliminate excess of oxalates and producing well apparent beneficial effect confirmed by the disappearance or decrease of clinical and functional manifestations of obstruction, reduction of requirements for broncholytic and anti-inflammatory agents.

We studied the role of oxalate release through the airways as a potential injurious factor in the development of inflammation, bronchial obstruction and cough syndrome (respiratory oxalosis). Detection of oxalates in bronhcoalveolar lavage fluid and daily urine is the most valuable method for diagnostics of oxalates. Systemic effects, such as cholelithiasis, urolithiasis, and spinal osteochondrosis are characteristic clinical signs of respiratory oxalosis, besides purely respiratory symptoms.

The prevalence of bronchial asthma and obesity has grown in the recent decades. The mechanisms of these pathologies remain unclear despite a number of publications on the relationship between the two diseases. Analysis of the association of BA with obesity should take into account that both diseases develop in young children undergoing effects of breast milk and specific nutrients, intestinal colonization pattern (neonatal and early childhood), body mass at birth and it growth rate, sedentary lifestyle, and adipokine level in early ontogenesis. The available data suggest that the phenotype of BA associated with obesity is characterized by a number of clear-cut peculiarities (more severe clinical manifestations with frequent exacerbaions and impaired control of the disease). Moreover; such patients show no signs of cellular inflammation. There are several distinct mechanisms characterizing obesity-associated BA, viz. co-morbid conditions such as gastroduodenal reflux disease, sleep apnea, obesity-associated systemic inflammation (elevated cytokine (IL-6, TNF-alpha) levels), oxidative stress, production of obesity hormones (leptin. adiponektin, resistin). Thus, BA and obesity have some common potential mechanisms, including genetic factors, systemic inflammation, mechanical factors, and concomitant diseases. Understanding the common mechanisms of these diseases will promote the development of new therapeutic strategies.

The specific features of bronchial epithelial cell apoptosis in asthma were studied, by evaluating the activity of the apoptosis-regulating genes Bcl-2, Bax, and caspase-3. Fibrobronchoscopy with target biopsy of the bronchial mucosa was carried out in 21 asthmatic patients (the latter had given informed consent). The expression of Bcl-2, Bax, and CPP32 (caspase-3 activity) was determined in the bronchial epithelial cells by the immunohistochemical technique using the DAKO kits. Allergic asthma is characterized by higher Bcl-2 and lower Bax expression than non-allergic asthma and in patients receiving systemic glucocorticosteroids. The similar nature of changes was found in the analysis of the Bcl2/Bax ratio. Regardless of the type of asthma, the expression of caspase-3 was rather high. The specific features of impaired bronchial epithelial cell apoptosis in different types of asthma can determine the pathogenetic value of apoptotic disorders in the persistence of allergic inflammation.

To reveal disturbances of peripheral blood lymphocytes apoptosis in different variants of bronchial asthma (BA).Apoptosis was studied in 20 healthy subjects, 70 BA patients: 32 patients with allergic BA (ABA) and 26 patients with non-allergic (NABA), 12 patients with BA treated with oral glucocorticosteroids. The following parameters of apoptosis were assessed: cell readiness for apoptosis (expression of CD95/Fas/APO-1 receptors), an early reversible stage of apoptosis (expression of phosphatidylserine on outer leaflet of lymphocyte membrane) and a late stage of apoptosis (the key effector caspase 3 activity).ABA is characterized by increased peripheral blood lymphocytes resistance to apoptosis: a decrease in expression of CD95/Fas/APO-1 receptors and phosphatidylserine on lymphocyte surface and caspase 3 activity. NABA is characterized by peripheral blood lymphocyte apoptosis activation at all stages: high expression of CD95/Fas/APO-1 receptors, expression of phosphatidylserine and caspase 3 activity. BA patients on systemic glucocorticosteroids are characterized by maximal expression of CD95/Fas/APO-1 receptors and phosphatidylserine on lymphocyte surface and the highest caspase 3 activity.The findings allow more accurate definition of the features of peripheral blood lymphocytes apoptosis in different variants of bronchial asthma and characteristics of relations between disturbed apoptosis and inflammation. Disturbances of apoptosis may be of pathogenetic importance in persistence ofallergic inflammation.

The aim of the study is to establish the features of expression of GATA-3 in peripheral lymphocytes from bronchial asthma patients (BA). Material and methods. 10 healthy controls, 15 patients with allergic (atopic) and 15 persons with non-allergic BA were examined. A transcription factor GATA-3 expressed in peripheral lymphocytes was analyzed by Western blot after the lymphocytes were lysed. Preparation of cell lysates, and Western blotting were performed by means of a standard procedure (Amersham). An antibody against GATA-3 (Abcam, UK) was used. Levels of the protein were analyzed versus β-actin levels using anti-actin antibody (Sigma Aldrich, USA). Results. Expression of GATA-3 was significantly increased in lymphocytes of patients with allergic BA as compared to healthy persons and non-allergic BA patients. The level of GATA-3 negatively correlated with the degree of airflow obstruction and positively correlated with dosage of parenteral steroids administered. Conclusion. GATA-3 may play a key role in the pathophysiology of BA. One may suggest that increased expression of GATA-3 transcription factor in atopic BA underlie high levels of Th2-cytokines production in allergic disease

Magnesium and calcium levels in the serum, red cells, lymphocytes, circadian urine and exhaled air condensate were measured in 40 patients with hormone-dependent bronchial asthma (BA) and 15 BA patients receiving glucocorticoids in inhalations (beclamete, becotide) and injections (hydrocortisone, prednisolone, dexasone). Nuclear absorption spectrophotometry (AAC-508, Hitachi, Japan) and selective ionometry (Mycrolyte, Kone, Finland) were employed. Short-term (10-14 days) intravenous infusions and inhalations of steroids in medium therapeutic doses do not change much homeostasis of two-valent cations. Complications resultant from disturbance of mineral metabolism developed more frequently in BA patients on long-term (4 years more longer) oral glucocorticoids. Increased renal and bronchial excretion of magnesium and calcium in patients with hormone-dependent BA having complications of glucocorticoid therapy suggests that derangement of mineral metabolism is involved in the onset of steroid osteopathy and myopathy.

The development of nonspecific bronchial hypersensitivity and hyperreactivity in bronchial asthma and effectiveness of its correction with acupuncture were investigated in 152 patients with asthma and preasthma. 94 of them were subjected to acupuncture. The authors employed a complex of diagnostic methods with determination of 241 parameters processed later with the use of systemic modelling. Bronchial hypersensitivity as indicated by the response to acetylcholine was related to impaired coordination of bronchomotor tone regulating systems: parasympathetic part of the autonomic nervous system, eosinophilic and monocytic bronchial inflammation, glucocorticoid homeostatic alterations. The corrective role of acupuncture consists in reduction of nonspecific bronchial hyperreactivity, normalization of blood acetylcholine, resensitization of cell beta-adrenergic receptors, elevation of mean concentrations of 11-OCS and T-lymphocytes.

Nuclear-absorption spectrophotometry (AAC-508, Hitachi, Japan) and selective ionometry (microlyte, Kone, Finland) were employed to measure magnesium and calcium concentrations in the serum, red cells, lymphocytes, 24-h urine and exhaled air moisture in 40 patients with hormone-dependent asthma (BA) and 15 BA patients given beclomet, becotid in inhalations and injections of hydrocortisone, prednisolone and dexason. Intravenous infusions and steroid inhalations in moderate doses for 10-14 days induce only insignificant changes in bivalent cation homeostasis. Complications associated with deranged mineral metabolism occurred more frequently in BA patients on long-term (at least 4 years) courses of oral glucocorticoids. Increased renal and bronchial excretion of magnesium and calcium in patients with hormone-dependent BA with complications of glucocorticoid therapy shows its significant contribution to development of steroid osteopathy and myopathy.

Altered bronchial sensitivity and reactivity are the basis of different variations of bronchospasm. In addition to exogenous agents, endogenous regulation factors such as adrenal and ovarian hormones are believed to make an important contribution to their development. Asthmatics showed the lowest sensitivity and the highest hyperreactivity to acetylcholine as compared to patients with preasthmatic conditions or chronic bronchitis and healthy consanguins of asthmatic patients. Disturbances of glucocorticoid homeostasis, related to various (adrenal, extra-adrenal (transcortin) and cellular) mechanisms of corticosteroid insufficiency, occurred in the majority of asthmatics and asthmatic bronchitis patients. Identification of various mechanisms of glucocorticoid insufficiency opens up actual approaches to increasing the efficiency of an individual therapy.

Hydrocortisone absorption by lymphocytes and red blood cells was reduced in patients with bronchial asthma (BA). Adrenaline produced the stimulatory effect on hydrocortisone absorption by lymphocytes and red blood cells in practically normal subjects and in BA patients in whom that effect was decreased. In patients with the steroid-dependent clinico-pathogenetic pattern of BA, hydrocortisone absorption by lymphocytes was reduced to a considerable degree. It is stressed that cellular mechanisms of glucocorticoid insufficiency are implicated in the BA pathogenesis.

A total of 31 patients with bronchial asthma were examined with the use of the brief dexamethasone test. Some patients with bronchial asthma seemed to have impaired glucocorticoid function of the adrenals. Based on the own investigations and the reported data it is concluded that patients with bronchial asthma may have different types of glucocorticoid deficiency, particularly at the expense of the impairment of the central mechanism of the regulation of glucocorticoid hormones. It has been demonstrated that the brief dexamethasone test can be used for studying the disorders of glucocorticoid function of the adrenals.