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The review analyzes the role of microRNAs in the pathogenesis of bronchopulmonary diseases. The universality of the mechanisms underlying epigenetics causes a continuously growing interest in research in this field in various fields of medicine. Research in the field of epigenetics not only allows us to expand knowledge in the field of etiology and pathogenesis, but also helps to explain the heterogeneity of the disease. Currently, biomarkers used in determining the phenotype of bronchial asthma or COPD are not able to display the variety of pathological processes involved in the pathogenesis of the disease at the molecular level. It is noteworthy that microRNAs retain their stability in various body environments, are resistant to high temperatures, pH fluctuations, and freeze-thaw cycles, which greatly simplifies the process of detecting these molecules in biological fluids. The amount of detected microRNA is highly specific for a particular pathological process occurring intracellularly. Currently, biomarkers used in determining the phenotype of bronchial asthma or chronic obstructive pulmonary disease are not able to reflect the variety of pathological processes involved in the pathogenesis of the disease at the molecular level. For both diseases, the key links are known to be inflammation, airway remodeling, and an abnormal response of epithelial cells to external stimuli. Thus, there is a great potential for using microRNAs in clinical practice: as noninvasive biomarkers reflecting key points of pathogenesis, as a prognostic biomarker predicting response to therapy, and possibly in the future as new therapeutic targets.

Patients with severe bronchial asthma, which remains uncontrolled despite the optimal basic therapy, carry a significant healthcare burden and require substantial financial investments. Severe asthma is a heterogeneous airway disease with complex pathophysiological mechanisms that can be broadly divided into inflammatory pathways with eosinophilic and non-eosinophilic inflammation.Aim. This study aimed to analyze the literature data on the use of targeted genetic engineering therapy in patients with severe bronchial asthma, as well as to analyze the organization of immunobiological therapy in the Krasnoyarsk Territory. The addition of targeted drugs for severe eosinophilic bronchial asthma based on phenotyping has proven to be effective and is recommended by all current guidelines. Today, several biologics targeting specific endotypes and phenotypes has been approved for the treatment of severe eosinophilic asthma worldwide. These are antibodies binding immunoglobulin E (omalizumab), antagonists of interleukin-5 (mepolizumab, reslizumab) and its receptor (benralizumab), as well as antibodies selectively binding to the IL-4 and IL-13 receptors (dupilumab). Eosinophilic inflammation therapy is a relatively new direction of asthma treatment, and understanding its long-term efficacy and safety is important.Conclusion. It is essential to differentiate patients with severe eosinophilic asthma from the general cohort of asthma patients, timely refer them to specialists who can prescribe this therapy and have experience with it, select the drug correctly, and monitor the patients during the treatment. This article describes organization of biological therapy for patients with severe eosinophilic bronchial asthma in the Krasnoyarsk Territory.

Bronchial asthma is a current problem of health care in connection with high prevalence and heterogeneity of a disease. Development and deployment in clinical practice of genetically engineered biological medicines for treatment of patients with severe eosinophilic bronchial asthma allowed to change cardinally the course of a disease and to considerably improve quality of life of such patients. The presented clinical case focuses on the experience of using benralizumab, an interleukin-5 receptor antagonist in a patient with T2-endotype of severe bronchial asthma in combination with polypous rhinosinusitis. The diagnosis of bronchial asthma was established to the patient in 36 years. The patient had the burdened allergological personal and family anamnesis, intolerance of nonsteroid anti-inflammatory medicines, polyps in a nose were revealed later. It is known that the clinical phenotype of a combination of bronchial asthma to a polypous rhinosinusitis is difficult for treatment in connection with the inflammation which was more expressed, difficult giving in to control in airways. Over time the course of a disease was made heavier, control of symptoms was lost and, despite the therapy volume corresponding to the 5th step on GINA, including reception of system glucocorticosteroids, an exception of all factors interfering achievement of control regular symptoms and frequent aggravations remained. In accordance with the Federal Guidelines, the patient was prescribed targeted therapy with benralizumab, which suppresses eosinophilic inflammation in the respiratory tract. During the treatment, a rapid significant improvement in the patient’s condition was noted in the form of a decrease in asthma symptoms, normalization of spirography indicators, and cessation of exacerbations. The persistent clinical effect allowed to abandon the use of systemic glucocorticosteroids without losing control of the disease. There were no adverse reactions to the drug administration. Thus, therapy with benralizumab in patients with the T2-endotype of severe bronchial asthma in combination with polypous rhinosinusitis is safe and highly effective and allows it to be recommended for widespread use in clinical practice.

The review provides current data on new options for the treatment of severe bronchial asthma. The prevalence of severe asthma ranges from 3% to 10%, but it is for the treatment of this group of patients that more than 80% of the funds allocated for the treatment of the disease as a whole are spent. Patients with severe bronchial asthma make up a special category, since traditional therapy, effective in most patients with bronchial asthma, does not allow controlling the disease. Heterogeneity and multivariate disease dictate the need to develop a personalized approach, which is impossible without significant financial and personnel investments. Understanding the pathogenetic pathways underlying the development of inflammation in asthma was the impetus for the development of targeted therapies. Five genetically engineered immunobiological drugs have been developed and approved for patients with severe allergic and/or eosinophilic bronchial asthma. The choice of the right medication should depend on the correct diagnosis of severe asthma, understanding the patient’s endotype, and accounting for patient-specific factors. It is worth noting that all approved biologics and most biologics currently in development focus on T2-immune response. To be sure, there is a huge pool of patients who register a different type of inflammation. And therefore, despite the rapid development of knowledge in the field of targeted therapy of bronchial asthma, further decoding and deepening of knowledge about the pathophysiological mechanisms, in particular non-T2 inflammation, as well as an analysis of the experience of using existing drugs to clearly understand the indications, as well as to assess the effectiveness and safety of existing treatments.

The aim. To determine the level of cathepsin S and to identify its possible relationships with clinical, functional and laboratory indicators in patients with severe bronchial asthma.Methods. 114 patients with severe bronchial asthma were examined. 96 women (84.2%) and 18 (15.8%) men were divided into 2 groups: allergic and non-allergic severe bronchial asthma. The external respiration function was assessed with whole-body plethysmography (“Erich Jaeger”, Germany). The plasma concentration of cytokines IL-4, IL-5, IL-13, periostin, cathepsin S, TGF-β was estimated with ELISA (“eBioscience”, USA).Results. Fixed obstruction is reported in 48% and 50% of cases of allergic and non-allergic severe asthma, respectively. Peripheral blood eosinophilia occurs in 41.5% of cases with allergic and in 25% of cases with non-allergic asthma. IL-5, IL-13, and cathepsin S levels were increased in both groups. An increase in IL-4 and TGF-β levels was revealed in non-allergic asthma. Periostin levels were increased in patients with allergic asthma as compared with the control and the second group. Positive correlation between cathepsin S and concentration of IL-4, IL-5 was established in both groups. We identified weak positive correlation between cathepsin S levels and clinical symptoms of the disease, such as frequency of SABA use and asphyxiation attacks, only in the allergic asthma group. A positive correlation between cathepsin S and TGF-β was established in both groups.Conclusion. A positive correlation between serum cathepsin S and TGF-β was established in both allergic and non-allergic severe bronchial asthma. The found moderate relationship may indirectly indicate the involvement of cathepsin S in airway remodeling processes regardless of the disease type.

The medical and social significance of cardiovascular diseases remains high. One of the factors that determine cardiovascular risks is metabolic syndrome. As a result of excessive accumulation of lipid and carbohydrate metabolism products in metabolic syndrome, oxidative (oxidative) stress develops. The article considers both domestic and foreign scientific studies, which highlight various aspects of the influence of reactive oxygen and nitrogen species, as well as other free radicals on the formation of oxidative stress in pathological conditions that are part of the metabolic syndrome complex. This describes the mechanisms of the formation of chronic inflammation through excessive secretion of pro-inflammatory cytokines and adipokines, activation of the transcription factor NF-kB, as well as damage to the antioxidant system in obesity. Separately, a number of mechanisms of the stimulating effect of adipokines: leptin, adiponectin, chimerine, omentin 1, resistin, on the formation of oxidative stress have been noted. The ways of activating the polyol pathway, as well as diacyl-glycerol — protein kinase C — the signaling pathway of oxidative stress, the formation of mitochondrial dysfunction is described. As a result of which there is an excessive production of free radicals in insulin resistance, diabetes mellitus and macroand microvascular complications of diabetes. In addition, the influence of oxidative stress directly on the formation of cardiovascular diseases of atherosclerotic genesis, as well as arterial hypertension, has been shown.

Chronic spontaneous urticaria is an urgent health problem. Recurrent urticarial rashes, angioedema and severe itching reduce the quality of life of patients. The ineffectiveness of standard therapy requires the search for new modern methods of treating this disease. Taking into account the current data on the pathogenesis, the third line of therapy for chronic spontaneous urticaria is the addition of anti-IgE therapy (omalizumab) to antihistamines of the 2nd generation. The presented clinical case is devoted to the experience of long-term use of omalizumab in a patient with chronic spontaneous urticaria. Having a disease duration of about a year, the patient was thoroughly examined, all concomitant diseases were identified and compensated, parasitic invasion was treated, but this did not lead to a regression of symptoms. Antihistamines of the 2nd generation in standard and increased doses (up to 4 times) did not control the disease, systemic glucocorticosteroids stopped the symptoms for a short time, and therefore, in the future, the patient began to use them independently and uncontrollably. Almost daily use of corticosteroids for 6 months caused the development of complications in the form of weight gain and Cushing’s syndrome. Omalizumab completely stopped all the symptoms during the first day, no side effects were detected. The clinical effect lasted from 3 to 4 weeks. Thus, omalizumab therapy allowed the patient to almost completely get rid of the symptoms of CSC, which significantly improved the quality of life and made it possible to cancel systemic glucocorticosteroids. The peculiarity of the presented case is the duration of the use of omalizumab (more than 2 years) with the inability to cancel due to the return of urticarial rashes and itching.

Chronic obstructive pulmonary disease (COPD) is one of the most important problems of modern medicine associated with a high mortality rate, high costs of treatment and relief of exacerbations of COPD. The main objectives of COPD treatment are symptom control, reduce the frequency of exacerbations and hospitalizations, and reduced risk of exacerbation in the future. The recommendations of the GOLD initiative propose a treatment approach based on the assessment of exacerbation rates external respiratory function indicators (spirometric classification of GOLD), the severity of symptoms assessed on the CAT test and mMRC. When choosing therapy, the physician must first of all take into account the effectiveness, safety of the drug, adherence to treatment in order to achieve the therapeutic goals of treating patients with COPD. The change in therapeutic approaches in COPD treatment is associated with the accumulation of knowledge in physiology, clinical pharmacology, and the isolation of new clinical phenotypes of COPD. Currently, the main classes of drugs for the treatment of COPD are long-acting beta-agonists (LABA), longacting anticholinergics (LAMA), and inhaled glucocorticosteroids (ICS). The evolution of therapeutic approaches in COPD treatment has led to the creation of new fixed inhalation combinations of the main groups of drugs for COPD treatment. The therapeutic strategies recommended by GOLD and the Russian Federal Guidelines determine the long-term goals of COPD treatment – the impact on the risk of exacerbations in the future. The presented clinical observation of a patient with severe COPD demonstrates the effectiveness of a triple fixed combination vilanterol/umeclidinium/fluticasone furoate 55/22/92 μg as a basic therapy. The chosen treatment strategy not only reduces the severity of the symptoms of the disease, but also reduces the risk of exacerbations in the future.

Chronic obstructive pulmonary disease (COPD) today remains one of the most important problems of modern medicine. The social significance of this disease is determined by the annual health care costs for treating patients with exacerbated COPD, as well as the still high mortality and disability rates worldwide. The main goals of COPD treatment are to slow the rate of disease progression, control the symptoms, reduce the frequency of exacerbations and hospitalizations, and reduce the risk of future exacerbations. Currently, the main groups of drugs for basic therapy of COPD are inhaled prolonged bronchodilators from the groups of β2-adrenergic agonists and M-anticholinergics, as well as their combinations. Patients with COPD and bronchial asthma, as well as patients with COPD with elevated levels of eosinophils and frequent exacerbations, inhaled glucocorticosteroids (ICS) are used. It has been proven that the addition of corticosteroids to LABA in patients with moderate to severe COPD and frequent exacerbations has a more effective influence on pulmonary function and the number of exacerbations. Clinical studies have shown the relationship between the level of blood eosinophilia and the clinical effects of preventing future exacerbations when using iCS in combination with LABA. In our clinical observation, in patient with moderate COPD and blood eosinophilia > 300 cells/μL, when prescribing monotherapy with long-acting agonists, frequent exacerbations of the disease were noted. The addition of corticosteroids to monotherapy with a long-acting agonist made it possible to influence the frequency of exacerbations and reduce the level of eosinophils in the blood.

Bronchial obstructive syndrome is a violation of bronchial patency of functional or organic origin, which is manifested by shortness of breath, suffocation attacks, cough, tachycardia. The most common cause of bronchial obstructive syndrome is chronic obstructive pulmonary disease and bronchial asthma. In some cases, the cause of bronchial obstruction is tumors or tumor metastases to the lungs. The article describes a clinical case of bronchial obstructive syndrome, showing that all patients with bronchial asthma, in the absence of an effect from the prescribed adequate basic therapy, with no control over the disease, should be well examined for an alternative diagnosis. In our case, a thorough examination of the patient allowed the allergist to diagnose central lung cancer with metastases to the lymph nodes of the mediastinum. A feature of the case is the primary resistance to tyrosine kinase inhibitors, revealed during a genetic study, which determined the scheme of further polychemotherapy. This clinical case proves the need for differential diagnosis, with a comprehensive approach and the use of various examination methods.

Given a persistent global trend towards an increase in the number of patients with bronchial asthma (BA) over the past decades, researchers are facing challenges related to a comprehensive study of the pathogenesis of BA. Numerous studies have shown that BA is associated with long-term persistence of leukocytes (lymphocytes, macrophages, and eosinophils) in the bronchial tissues. However, the causes of this phenomenon remain understudied. The article provides an overview of modern research on the mechanisms of disorders of lymphocyte apoptosis in patients with BA. Our study considers the main mechanisms of molecular regulation of lymphocyte apoptosis, including transcription factors, the Fas/FasL system, and bcl-2/bcl-XL factors. We present the data on the role of reduced lymphocyte apoptosis in the formation of a severe BA phenotype. Taking into account high prevalence of obesity among patients with BA, we analyzed a few existing articles on the apoptosis of immunocompetent cells in obesity. In addition, the article highlights the key mechanisms of development of lymphocyte plasma membrane blebbing (PMB) with formation of microvesicles, as well as their influence on the course of pathological processes in BA. The authors believe that further in-depth study of apoptosis, lymphocyte necrosis, and plasma membrane blebbing can help improve the principles of diagnosis and treatment of BA.

Primary immunodeficiency is a rare congenital pathology associated with failure of immune system, manifested by disturbances of its functions. These defects lead to increased susceptibility of patients to various infectious agents, as well as the development of autoimmune, malignant and other diseases. Primary immunodeficiency is classified as a rare disease, which was previously associated with a poor prognosis with a high risk of mortality in childhood. To date, the emergence of highly effective treatment methods has changed the course and prognosis of these diseases. Clinicians of various specialties increasingly meet with this pathology in everyday practice, including adult age cohorts. In this regard, early diagnosis of primary immunodeficiency in adults becomes relevant, being associated with choosing optimal therapy, prevention of severe internal organ damage, determination of management strategy for the patient, as well as the need to identify inherited disorders and provide information to the patient’s family. Delayed verification of the diagnosis may cause disability of the patient and development of irreversible, often fatal complications. This article presents our own clinical case with a newly diagnosed clinical condition: Common variable immunodeficiency disorder (CVID), the most common form of primary immunodeficiency in adults. The symptoms of common variable immunodeficiency disorder appear in these patients in adulthood, but a high-quality collected history of the disease will allow you to trace symptoms in the patients even since early childhood. There is a common gap for several years between the onset of the disease and clinical diagnosis, since erroneous diagnosis is often made due to non-specific clinical symptoms that resemble other, more frequent diseases. The prognosis of patients with CVID depends on several factors: frequency of infections, structural disorders in the lungs, the occurrence of autoimmune diseases and the success of infection prevention. Thus, a variety of clinical forms of primary immunodeficiency, lack of awareness of doctors about this pathology, complexity of immunological examination in the general medical network lead to the fact that CVID is not diagnosed for long terms, and patients do not receive the necessary pathogenetic therapy. There is a need for drawing attention of doctors of various disciplines to the fact that the recurrent inflammatory processes of various localization, which are difficult to respond to adequate traditional therapy, may be caused by changes in the immune system, including congenital, genetically determined immunodeficiency.

Currently, the analysis of respiratory function of lungs at suspicion of obstructive pulmonary diseases is recommended to start with spirometry as the most sensitive method of obstruction detection. However, data on informative value and specificity of a method are contradictory. To obtain reliable results good cooperation of the patient and health professionals is necessary. Impulse oscillometry is a noninvasive method of general respiratory resistance assessment, which does not require forced exhalations. The sensitivity and specificity of this method remain undecided as well as the obtained parameter interpretation. Theobjectiveof this work was to study opportunities of impulse oscillometry in diagnostics of early respiratory dysfunctions of ist most informative indicators correlating with parameters of spirometry and body plethysmography.Materials and methods.Patients with the established diagnosis of mild asthma (n=68) were examined. In 71% of patients, obstructive respiratory dysfunction was revealed. In the control group (n=41) there were no abnormalities.Results.In most of patients with revealed via spirometry and body plethysmography obstructive disturbances the increase in indicators of absolute frequency dependence of the resistive component of the respiratory impedance at the oscillation frequency of 5 and 20 Hz (Rrs5-Rrs20) and the reactance area (AX). Increase in Rrs5-Rrs20 was revealed in 48 (71%) patients and the increase in AX was observed in 44 (65%) of the surveyed, patients with 42 (61%) patients without the increase of reactance (Xrs5) and resistance (Rrs5).Conclusion. The absolute frequency dependence of Rrs5-Rrs20 and AX are the most informative parameters of impulse oscillometry. In some patients the IOM findings were more significant in comparison with spirometry ones.

Complex studies were carried out in the southern part of Onega Bay (White Sea) in the summer seasons of 2003–2006 and 2011–2013. These studies revealed the dynamics of oil pollution of the water area after an accidental fuel oil spill in September 2003 and its long-term adverse effects on organisms of different trophic levels of the coastal ecosystem (benthos, fish, and sea mammal populations) in the most polluted southeastern part of the bay. The deterioration of the status of the top trophic-level white whale population (a decrease in numbers) and the accumulation of oil hydrocarbons in tissues of benthic organisms are described.

Clinical presentation of myxomas is diverse, so it is not easy to diagnose this pathology even with available modern instrumental methods. With its “natural” course this pathology is associated with poor outcome, most patients die in several years from the first clinical signs onset.

A case of late manifestation ofmucoviscidosis is reported. In the past, this pathology was dealt with by pediatricians, but to-day the management of this problem involves a number of different specialists. The progress in clinical practice makes it possible to significantly prolong the life span of patients with this condition. The present case shows that its clinical manifestations may appear at any age.

Background. To study the cytokines profile in the peripheral blood of patients with severe asthma and obesity. Methods.139 patients with severe bronchial asthma have been examined, including 66 patients with severe bronchial asthma and body mass index (BMI) 30 (2nd group). The control group was formed from 40 healthy volunteers. The respiratory function, the cytokine integral index and the levels of TNFα, IL4, IL6, IL2, IL10, IFN-γ, IL8, IL17 in the peripheral blood of patients in and out of an exacerbation were studied. Results. More significant systemic inflammation signs expressed in increased levels of TNFα, IL6, IL4, IL2 and IFN-γ were found in exacerbation period of the disease. In obese patients the increased level of proinflammatory cytokine IL17 in exacerbation period was estimated. Conclusion. We have demonstrated the presence of systemic inflammation in patients with severe BA, regardless of the presence of obesity, increased level of proinflammatory cytokine IL17 in patients with severe bronchial asthma and obesity in the period of exacerbation. It can be a reason of the low effect of steroid therapy in patients with BMI >30.

Background. To estimate interrelation of clinical and functional parameters and vessel tome regulating function of endothelium in patients with bronchial asthma. Methods. 126 patients with bronchial asthma have been examined, including 29 patients with mild bronchial asthma (the first group), 32 persons with moderate bronchial asthma (the second group), 40 respondents with severe asthma (the third group) and 25 patients with steroiddependent asthma (fourth group). The control group included 27 healthy volunteers. We have assessed the parameters of external respiration, vasodilatation function, and the levels of TNFa, IL4, sCD31 in the plasma. Results. The results of the research of vessel tome regulating function in patients with bronchial asthma are presented. The existence of endothelial function of an endothelium are characterized by disturbance of vasomotor activity of endothelium, rising of sCD31 and levels of cytokines (Il-4, TNFa) in plasma was revealed. These changes deteriorate within the ages and the course of bronchial asthma. Conclusion. We have demonstrated that endothelial dysfunction is developed even at the early stages of bronchial asthma.

The purpose of the study was to examine the relationship between functional parameters, arterial rigidity, lipid profile, markers of systemic inflammation and endothelial dysfunction in patients with COPD and COPD + coronary heart disease. We examined 110 subjects divided into 3 groups. G group 1 included 40 patients with severe and very severe COPD, group 2 consisted of 40 patients with severe and very severe COPD + coronary artery disease, the control group was comprised of 30 healthy volunteers. We studied parameters of respiratory function, the level of blood oxygenation, the main characteristics of arterial rigidity plasma lipid, TNF-α, CRP, fibrinogen, sPECAM-1 levels and the expression of CD38/ADP-ribosylcyclase in peripheral blood lymphocytes. The study revealed increased rigidity of the central arteries in the patients of groups 1and 2 regardless of the duration of observation and the presence of coronary artery disease, as evidenced by the increase of the pulse wave velocity in the aorta. Patients of both groups had elevated levels of TNF-α, CRP and fibrinogen indicating systemic inflammatory response. Taken together, the enhanced expression of CD38 in peripheral blood lymphocytes, elevated concentration of soluble CD31 (sPECAM-1) in both groups related to bronchial obstruction and neutrophil elastase activity as well as increased rigidity of the vascular bed gives evidence that the CD38 and sCD31 relationship plays a role in the formation of endothelial dysfunction, and dysregulation of vascular tone in COPD patients. Disorders of lipid metabolism combined with increased rigidity of the vascular wall, elevated levels of markers of systemic inflammation and endothelia dysfunction, suggest that patients with COPD are at risk of cardiovascular events.

This study aimed at the evaluation of the state of the respiratory system and its possible influence on the structural and functional characteristics of the right heart in patients with atopic bronchial asthma (BA) with a view to optimizing diagnostics and prevention of cardiovascular complications. The study included 189 subjects of whom 148 with BA were divided into 3 groups depending on the severity of the disease. Forty practically healthy volunteers comprised the control group. The external respiration function and right ventricle functional parameters were the main variables measured in all the participants of the study. It was shown that disorders of external respiration and pulmonary hyperinflation progressed with severity of BA and thereby promoted right ventricular myocardium remodeling and dysfunction that in turn led to chronic cardiac insufficiency. It is concluded that functional changes in the right heart in of patients with BA of different severity are associated with remodeling of the respiratory tract.

The aim of the study which included 2311 patients (aged 18—80 yrs), examined by 100 physicians (57% allergists, 37% pulmonologists and 7% general practitioner) in 18 Russian cities, was to assess the prevalence of allergic rhinitis in patients with asthma, as well as to evaluate the specifics of the course of these diseases, when concomitant or not. The study design included one outpatient visit, followed by the completion of studyspecific case report forms and Asthma Control Questionnaire (ACQ) validated for use in Russia. The vast majority (88%)of asthma patients had concomitant allergic rhinitis (Group 1). Patients with asthma only (Group 2) were older (50,6±0,78 vs 41,9±0,35 yr, p

Background. The objective of this study was to estimate a vascular wall status of large arteries and function of endothelium in patients with different clinical forms of bronchial asthma throughout the disease progression. 220 patients with bronchial asthma have been examined, including 106 persons with moderate asthma ( 1 st group), 61 persons with severe asthma (2 nd group), and 53 persons with steroid-dependent asthma. Control group was formed from 40 healthy donors. Methods. We have assessed parameters of external respiration, arterial rigidity, and the levels of TNFα, IL-6, sCD31 (sPECAM-1), CRP in the peripheral blood at the time of exacerbation and 48 weeks later. Results. We found elevation of IL-6 and TNFα levels in all the tested groups in the period of exacerbation comparing to the control group (p

This paper reports on a theoretical study of conduction electron scattering by a system of dipoles formed by closely spaced positively and negatively charged centers in a quantum well.

The paper analyses immediate and remote (from 3 to 10 years) results of sinusotrabeculectomy in initial open-angle glaucoma in 184 patients (300 eyes). Normalization of intraocular pressure was achieved in 77.7% of cases (20.12 +/- 2.1 mm Hg, at the average). Tonographic and rheographic values in the operated patients achieved the normal levels (P0 = 15.3 +/- 0.68 mm Hg, C = 0.28 +/- 0.03 mm3/min., P0/c = 68.08 +/- 3.12, RC = 2.7 +/- 06.09). The dynamics of visual functions showed stabilization of the process in 85.1% of cases. However, in 15% of cases the glaucomatous process progressed, mainly in persons who failed to receive medicamentous treatment regularly in the postoperative period.

The paper analyses results of long-term general and local medicamentous treatment of 86 patients with open-angle initial glaucoma. The hypotensive preparations were miotics, sympathomimetics, beta-blockers, carbonic anhydrase inhibitors. Regulation of intraocular pressure by means of miotics was achieved in 30% of cases and by means of sympathomimetics--in 53%. The best hypotensive effect with a long-term regulation of intraocular pressure was achieved by means of beta-blockers. In order to correct vascular disturbances, angioprotectors, cavinton, rheopolyglucin, 2 courses a year were used. A systematic, pathogenetically grounded medicamentous treatment of initial glaucoma allows to achieve stabilization of glaucomatous process in 88% of cases.