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Postmyocardial syndrome (Dressler syndrome) is a form of secondary pericarditis with or without pericardial effusion resulting from myocardial damage. Dressler syndrome is not a common disease, but it should be suspected in patients with pathognomonic symptoms after a myocardial infarction (MI). The article presents a clinical case of a 65-year-old man, a smoker who is overweight, with a history of hypertension, MI with ST segment elevation, stenting of the envelope branch of the left coronary artery, thrombospiration. According to coronary angiography, the patient revealed a multivessel lesion of the coronary arteries. Two weeks after stenting, the patient’s condition worsened: shortness of breath, pain in the left half of the chest, fever appeared. During the examination at the outpatient stage, bilateral hydrothorax and hydropericardium were revealed. He was hospitalized, was treated with ibuprofen 600 mg 3 times a day for 7 days, with a positive effect. Ten days after discharge, the patient noted an increase in shortness of breath, an increase in body temperature, a recurrence of dull chest pain. He was hospitalized at the Vorokhobov City Clinical Hospital No. 67, where bilateral hydrothorax, hydropericardium, pneumonitis were detected during the examination. the diagnosis "Postmyocardial syndrome, recurrent course" was established. Hospital treatment was carried out with colchicine, methylprednisolone, acetylsalicylic acid, ticagrelor, losartan, bisoprolol, amlodipine, spironolactone. Against the background of the therapy, the condition improved, the patient began to notice an increase in exercise tolerance, a gradual regression of dull chest pain on the left, body temperature decrease to subfebrile figures. Positive dynamics of laboratory parameters was noted.

Phosphopenic osteomalacia (PPOM) is a rare variant of paraneoplastic syndrome caused by tumor synthesis of fibroblast growth factor 23 (FGF23). FGF23 secretion leads to a decrease in phosphate reabsorption and calcitriol levels, which leads to the development of severe hypophosphataemia and hypocalcaemia. FGF23 synthesis is predominantly associated with benign mesenchymal tumors, but has also been described in malignant neoplasms. The main clinical manifestations of PPOM are generalized myalgias and myopathy, ostealgia, pathological fractures, etc. The diagnosis of the disease requires a step-by-step investigation using somatostatin receptor-based imaging techniques, as these have the highest sensitivity for the detection of neoplasms causing osteomalacia. Surgical intervention is clearly the treatment of choice. Promising non-surgical methods include treatment with burosumab and somatostatin analogues.

The medical and social significance of systemic sclerosis (SSc) is high. The progressive disease has a significant impact on the functional status, work participation and leads to early disability in patients of working age. The article presents data on the prevalence of work disability in patients with SSc in comparison with other rheumatic diseases, the frequency of separation from work and work transitions due to the problems connected with SSc, the socio-economic burden of SSc in different countries. The article specifies the components of the disease which affect the ability to work, the main approaches to quantify the indicators of working ability, describes the instruments most commonly used for this purpose. The data of various authors on working ability measurement and predictors of work disability in patients with SSc are presented.

On August 31,2023 in V.A. Nasonova Research Institute of Rheumatology a meeting of the Expert Council was held at which the principal investigators and co-investigators of the ARTNEO-2021 protocol "Multicenter randomized double-blind, placebo-controlled study of ARTNEO in patients with stage II-III primary knee osteoarthritis" was held. A consensus position was developed on the possibility and feasibility of using a combination of undenatured (native) type II collagen, methylsulfonylmethane, boswellic acids, vitamins C and D (ARTNEO complex) in clinical practice. Based on the results of the study, the use of the ARTNEO complex can be recommended as part of a complex therapy for patients with osteoarthritis as a course treatment with total duration up to 6 months. The results of the study can only be interpreted in relation to ARTNEO and cannot be transferred to preparations with a different composition.

Catastrophic antiphospholipid syndrome (CAPS) is a life-threatening condition associated with the development of thrombotic occlusion of microvasculature vessels, with a mortality rate of about 50%.The pathogenesis of CAPS is based on cellular activation, complement system induction, cytokine stimulation, inhibition of anticoagulant factors and fibrinolysis, which leads to progressive thrombotic microangiopathy, disseminated intravascular coagulation (DIC), and systemic inflammatory response syndrome. Classification criteria for CAPS include microthrombotic involvement of ≥3 organs (most commonly lungs, kidneys, and central nervous system) for ≤1 week with high titers of antiphospholipid antibodies.Differential diagnosis is carried out with DIC, heparin-induced thrombocytopenia, hemolytic uremic syndrome, HELLP syndrome, sepsis. Treatment of CAPS in the acute phase involves anticoagulant and immunosuppressive therapy (glucocorticoids, plasmapheresis, IV immunoglobulin, rituximab, eculizumab). Timely diagnosis and adequately selected treatment of CAPS can reduce mortality from 50 to 30%.Further study of CAPS is needed to improve the prognosis and increase the life expectancy of patients.

The impact of the transferred coronavirus infection on the musculoskeletal system still remains an urgent problem. Аrthralgia, myalgia, arthritis, autoimmune disorders and also osteonecrosis are may be development of the postCOVID period. This article discusses the case of the debut of multifocal osteonecrosis after a coronavirus infection.

Systemic scleroderma (SSD) is a rare immune-inflammatory systemic disease of connective tissue with a typical lesion of skin, blood vessels, musculoskeletal system and internal organs (lungs, heart, digestive tract, kidneys). The SSD pathogenesis is based on activation of a cascade of complex immune interactions that lead to vasculopathy. The presence of many pathophysiological links in the progression of the disease causes a variety of clinical manifestations in various patients with SSD. A full assessment of all stages of SSD development is still being carried out and every newly open element of the interaction of immunological subjects completes the overall picture of the disease. A number of studies show a correlation between level of several biomarkers and both disease prognosis and estimated therapy effectiveness. Recent data confirm importance of the biomarkers for formation of patterns of a particular disease phenotype in a specific patient. Depending on relation of the biomarkers to various biological processes, several of their categories are distinguished: biomarkers expressed in lung tissue, cellular units of immunity, nucleic acids, acute phase indicators, connective tissue growth factors, matrix proteinases and their inhibitors, chemokines and cytokines, as well as biomarkers of endothelial activation. Discovery of a novel set of the indicators can be decisive in determining the management tactics and forecasting the response to therapy of some groups of patients with SSD. By combining the most recent data on significant markers obtained in the framework of extensive studies, we have described the most significant biomarkers of SSD and their link to interstitial lung disease (ILD) that is formed in SSD.

The study objective is to demonstrate a rare cause of recurrent acute cerebrovascular diseases in a young patient – Sneddon syndrome. The patient revealed gene polymorphism: homozygous 4G/5G in the plasminogen activator inhibitor-1 (PAI-1) gene, C807T in the glycoprotein I gene (GPIa), T1565C in the glycoprotein III gene (GPIIIa), G1639A in the vitamin K epoxide reductase gene (VKORC1), increased homocysteine, which were risk factors for thrombosis.

The new coronavirus infection (COVID-19) is associated with a wide spectrum of various clinical manifestations including involvement of the musculoskeletal system which can persist for a long time after the infection. Supposedly, pathogenesis of musculoskeletal manifestations of COVID-19 is primarily caused by systemic inflammation accompanied by cytokine hyperexpression (interferon γ, interleukins 1β, 6, 8, 17, tumor necrosis factor α), as well as hypoxia leading to overproduction of inflammatory cytokines, activation of bone reabsorption by osteoclasts and subsequent decrease of mineral bone density and osteonecrosis in some cases. Additionally, some drugs prescribed to patients with COVID-19 (some antiviral drugs and glucocorticoids) should also be taken into account as they can lead to development of musculoskeletal pathology. In the acute period of COVID-19, myalgias are common, but in rare cases myositis with proximal muscular weakness and increased levels of creatine phosphokinase, lactate dehydrogenase can occur. Arthralgias in the acute period of COVID-19 are rarer than myalgias. In the studies of clinical manifestation of COVID-19, frequency of arthralgias and myalgias in the acute period is between 15.5 and 50 %. After COVID-19, frequency of arthralgias and myalgias gradually decreases, however there are cases of long-term joint and muscle pains, as well as post-viral arthritis, development of arthritis in the context of various autoimmune disorders. Myalgias and arthralgias during COVID-19 usually regress spontaneously and in most patients do not require prescription of antipain medications, but in some cases pain management is necessary. Use of non-steroid anti-inflammatory drugs and vitamin D during COVID-19 is a safe and effective method of pain management, including myalgia and arthralgia. Rehabilitation programs play an important role in improvement of functional state and patient recovery after moderate and severe COVID-19.

After suffering pulmonary embolism (PE), doctors are confronted with various consequences of the disease, from asymptomatic residual pulmonary thrombosis to the formation of chronic thromboembolic pulmonary hypertension (CTEPH). There is also a subgroup of patients who have undergone pulmonary embolism, who experience shortness of breath during physical exertion, absent before pulmonary embolism, or shortened dyspnea preceding PE, combined with residual thrombosis of pulmonary artery (PA) and normal average pressure in PA at rest during catheterization of the right heart (CRH). This condition is defined as chronic thromboembolic pulmonary disease or post thromboembolic syndrome. Pathogenetic aspects of this condition are not fully investigated. It is important to predict the development of postembolic syndrome and to develop algorithms for the diagnosis, treatment and rehabilitation of patients with symptoms and residual pulmonary thrombosis. In case of the development of pulmonary vasculopathy in some patients who have undergone pulmonary embolism, a severe life-threatening condition forms - CTEPH, characterized by an increase in pressure in the pulmonary artery, right heart failure due to the presence of organized blood clots that have entered the pulmonary vascular bed during PE. The volume of thrombotic masses does not always correlate with clinical symptoms, which indicates the importance of microvascular remodeling. If CTEPH is suspected, a diagnostic algorithm is required, including ventilation-perfusion scintigraphy, CT angiopulmonography and catheterization of the right heart. Treating a patient with CTEPH is a difficult task fora doctor. The timely referral of the patient to the center where they are involved in treatment, including surgery and CTEPH is extremely important. Timely performed thrombendarterectomy in some cases allows to completely cure the patient. In the case of inoperable CTEPH or residual pulmonary hypertension after thrombendarterectomy, balloon angioplasty of the PA is used as well as drug treatment with specific drugs that reduce the pressure in the PA (riociguat), endothelin receptor antagonists (bosentan, macitentan), prostanoids (inhalant illoprost) phosphodiesterase-5 inhibitor and combined therapy. In this article we considered some consequences directly related to PE: asymptomatic residual pulmonary thrombosis, chronic thromboembolic pulmonary disease, chronic thromboembolic pulmonary hypertension.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly used pain relievers. However, their use often threatens with serious undesirable effects, associated mainly with damage to cardiovascular system (CVS), gastrointestinal tract, kidneys and liver. Contraindications to NSAIDs prescription are clearly regulated, algorithms for their personalized appointment are determined taking into account risk factors for cardiovascular and gastrointestinal adverse events. The severity of NSAIDs side effects is mainly due to the selectivity to cyclooxygenase-2 (COX-2), as well as the physicochemical properties of various drugs. Cardiovascular adverse events differ among various NSAIDs both within commonly used drugs and among COX-2 inhibitors. It is well known that NSAIDs selective for COX-2 are safer in terms of the effect on the gastrointestinal tract than non-selective drugs. A meta-analysis showed that relatively selective COX-2 inhibitors (meloxicam, etodolac) were associated with a comparable risk of developing symptomatic ulcers and ulcers identified by endoscopy, and safety and tolerability profiles of the drugs were similar.All NSAIDs are associated with cardiovascular toxicity, however, different drugs have significant risk differences. The mechanism of NSAIDs cardiovascular adverse effects is associated with an increase of blood pressure, sodium retention, vasoconstriction, platelet activation, and prothrombotic state. It has been shown that the risk of cardiovascular adverse events when taking COX-2 inhibitors (celecoxib, etoricoxib) significantly increases. According to a study of more than 8 million people, it was found that the risk of myocardial infarction was increased in patients taking ketorolac. Further, highest to lowest risk authors list indomethacin, etoricoxib, rofecoxib (not currently used), diclofenac, a fixed combination of diclofenac with misoprostol, piroxicam, ibuprofen, naproxen, celecoxib, meloxicam, nimesulide and ketoprofen. When taking NSAIDs, the risk of heart failure decompensation increases, and it turned out to be the greatest for ketorolac, etoricoxib, and indomethacin. Meloxicam, aceclofenac, ketoprofen almost did not increase heart failure risk. It should be noted that when using the drugs (except for indomethacin and meloxicam), there is a tendency to increase the total cardiovascular and renal risks with increasing doses. Thus, it is obvious that a very careful approach is required when choosing NSAIDs. If there is an increased risk of gastrointestinal complications associated with NSAIDs, selective NSAIDs are preferred, with both coxibs and traditional selective NSAIDs showing the best safety profile in the studies. To minimize cardiovascular side effects specialists should consider the risk level of cardiovascular complications, as well as results of large clinical studies where particular NSAIDs are compared.

Patients with systemic scleroderma, or systemic sclerosis (SS), have an increased risk of developing malignant neoplasms. Cancer can be diagnosed immediately prior to SS symptoms, at the stage of diagnosis and years after SS diagnosis. The first two cases may indicate scleroderma-like paraneoplastic syndrome. In this case, the main mechanism of paraneoplastic syndrome development is associated with immune system activation by antigens, expressed by tumor cells, which leads to the development of antibodies that cross-react with body tissues, causing damage and secondary regeneration. Thus, cancer induces autoimmunity – mutation-specific T-cell immune response, and pathogenetic mechanisms can be the same for fibrogenesis and oncogenesis.SS clinical and laboratory characteristics that indicate paraneoplastic etiology include minimum time difference between diagnosing scleroderma and cancer, as well as oncopathology in a patient’s or family cancer history, late disease onset (after 50 years), SS symptoms in a man, sudden onset and rapid progression of clinical symptoms, expressed or atypical SS symptoms (malaise, fever, significant weight loss), asymmetric or absent Raynaud syndrome, antibodies against RNA polymerase III, absence of anticentromeric antibodies and anti-Scl70, deviations in laboratory tests indicating possible oncopathology (anemia, hypercalcemia, hypergammaglobulinemia), no response to SS treatment, disappearance of SS symptoms after anticancer treatment and their appearance when cancer reactivation. On the other hand, patients with scleroderma have an increased risk of all types of cancer, with men at higher risk than women. Continuous autoimmune stimulation, B-cell activation, chronic inflammatory process and fibrosis in SS patients can lead to malignant transformation in certain organ systems, especially in lungs.The most important risk factor for lung cancer in SS patients is interstitial lung disease, requiring special attention from a physician. In addition to lung cancer, SS patients more likely than the general population suffer from malignant hematologic diseases, esophageal cancer, hepatocellular carcinoma and bladder cancer. Scleroderma-like skin changes are also possible when cytotoxic drugs are used to treat cancer (docetaxel, paclitaxel, bleomycin, etc.), as well as during radiation therapy.

The aim of this study was to obtain hybridomas producing monoclonal antibodies (Mabs) to the G-protein of the respiratory syncytial virus (RSV), and to evaluate their immunological characteristics and virus-neutralizing activity.Material and methods. Mouse Mabs were obtained using hybridoma technology. The properties of Mabs were studied by enzyme-linked immunosorbent assay (ELISA), immunofluorescence staining (IF) of infected cells, as well as by biological neutralization test in vitro (NT). To identify epitopes recognized by the Mabs on G protein ELISA additivity test was used.Results. Hybridization of splenocytes with Sp2/0 myeloma cells and primary screening showed that 75 hybridomas produce antibodies interacting with purified virus, 17 of them also react with the recombinant G-protein in ELISA. In NT 4, hybridomas suppressed in vitro RSV infection by more than 50%. Cloning of these hybridomas revealed 4 monoclones producing the most active Mabs. Mab 1C11 was IgG2a, 3 others (5D4, 5G11 and 6H4) were IgM. Three IgM Mabs actively reacted with both RSV A2 and Long, and with G-protein; Mab 1C11 was less reactive with all antigens tested. All Mabs suppressed RSV infection, while Mab 5D4 supressed it almost completely (98%). IF analysis showed that all Mabs detected RSV G-protein in the cell cytoplasm, the largest number of infected cells was detected using Mab 5D4 (80%). It was shown that the isolated Mabs were directed to two non-overlapping epitopes on the RSV G-protein.Conclusion. The isolated Mabs can be used to detect RSV in clinical samples by ELISA and IF. The isolated Mabs can be used for humanized recombinant antibodies construction and for the treatment of RSV infection in future.

Introduction. Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract infections in infants and the elderly. The absence of a wide range of therapeutic drugs and vaccines indicates to the high relevance of the development of new effective drugs for the prevention and treatment of RSV infections. Purpose: to obtain highly active and specific monoclonal antibodies (MAbs) capable of detecting RSV in infected cells and neutralizing the infectious activity of the virus in vitro. Material and methods. RSV reference strains of group A 2 subgroups (A2 and Long) were propagated in HEp-2 and MA-104 cell lines, respectively. Mice were immunized with purified RSV A2 virus. MAbs were obtained using hybridoma technology. Results. A panel of 6 MAbs reacting with RSV strains А2 and Long has been obtained. Four MAbs were IgG (IgG2a or IgG2b subtype), two MAbs were IgM. All MAbs reacted with RSV F-protein in immunochemical tests. The MAbs actively reacted with RSV in ELISA, in immufluorescence and peroxidase staining of infected cells, and in immunodot test. Five out of 6 MAbs neutralized of RSV in cell culture. Different properties of MAbs suggest that they target different antigenic sites of F-protein. Discussion. Comparative analysis suggests that the obtained MAbs can be used for the development of diagnostic preparations, for RSV detection in clinical materials and confirmation of infection etiology by rapid culture method. Conclusion. High activity and specificity of MAbs indicate that they can serve as a basis for development vaccines and preventive medicines.

The objective of this study was to evaluate immunoregulatory and protective potential of mesenchymal stem cells (MSC) in a mouse model of lethal HSV1 infection. MSC were isolated from bone marrow of DBA mice and cultured in flasks with DMEM containing 10% FBS, insulin, transferrin, selenite, fibroblast growth factor, glutaminе and gentamicin. Antiviral activity was tested on HSV1-infected Vero cells. In vivo experiments were performed on DBA mice divided into 5 groups (10 animals each): group 1, intact (nave) mice; group 2, intravenous (iv) MSC injection; group 3, intraperitoneal infection with 20 LD50 HSV1 followed by MSC injection; group 4, HSV1 infection followed by acyclovir (ACV) injection; group 5, HSV1 infection and iv injection of saline. Isolated cells were consistent with MSC morphologically, by adhesive ability and surface receptors. Conditioned media from MSC collected after 4-5 passages inhibited HSV1 infection in vitro by 64-70% and contained IL-6 and TNF-, whose concentrations were 5- and 20-fold higher, respectively, than in the control. MSC and ACV injections protected 70% and 60% of DBA mice, respectively, compared with the control (group 5, 10% survival). High activity of virus neutralizing anti-HSV1 antibodies and activation of T cell proliferation were observed in survived mice from group 3. Serum levels of IL-6 and TNF- in these mice were lower and that of INF- much higher than in agonizing animals of this group (Р0.05). These findings indicate that MSC therapy is a prospective approach to the development of new effective management of generalized HSV1 infection.

The article considers the key points of the new 2018 guidelines of the European Society of Cardiology and European Society of Hypertension on management and treatment of patients with arterial hypertension (AH). The guidelines widen the possibilities for ambulatory monitoring of blood pressure (BP) and at-home measurement of BP in diagnosis of AH, especially for detection of hidden (“masked”) hypertension and white-coat hypertension. New target ranges for BP depending on age and concomitant pathology are established. For most patients, BP

The study objective is to demonstrate the difficulty of differential diagnosis in pulmonary-renal syndrome using a clinical case as an example.Materials and methods. Male patient A., 68 years old, retired, was hospitalized at the N.I. Pirogov City Clinical Hospital № 1 in December of 2017 with complaints of inefficient cough, fever of 39 °С, weakness, apnea, weight loss up 10 kg in 3 months. Examination revealed skin and mucosa paleness, calf edema, heart beat of 102 bpm, normal rhythm, arterial pressure 130/80 mm Hg, respiratory rate 22 breaths per min. Auscultation revealed harsh respiration in the lungs, weakened in the lower parts, fine moist rales. Anemia (hemoglobin – 53 g/l, erythrocytes – 1.85 × 1012/l, serum iron – 3.1 µmol/l), elevated urea up to 41.4 mmol/l, creatinine up to 843.1 µmol/l (glomerular filtration rate – 6 ml/min/1.73 m2), leukocytes up to 12.5 × 109/l, С-reactive protein up to 124.96 mg/l were diagnosed. Clinical urine analysis showed proteinuria 0.47 g/l. Computed tomography of the chest revealed pronounced infiltrative changes in tissues of both lungs, more on the right, alveolitis, bronchiolitis in the middle lobe on the right, 5th segment on the left. Lymphadenopathy mediastinal was diagnosed. After examination (multiple bacteriological blood, sputum tests, interferon-gamma release assay, echocardiography, bronchoalveolar lavage, sterna puncture, esophagogastroduodenoscopy, colonoscopy, etc.), oncological pathology, tuberculosis of the lungs, sepsis, infections endocarditis and other infectious pathologies were excluded. Antibacterial courses prescribed earlier were ineffective. Immunological blood test revealed high titers (1:1280) of antineutrophil cytoplasmic antibodies (ANCA) with perinuclear fluorescence type (myeloperoxidase specificity), negative antibodies to glomerular basal membrane which allowed to diagnose ANCA-associated vasculitis.Results. Considering the data of clinical, lab, and instrumental examination, the patient was diagnosed with microscopic polyangiitis, ANCA-associated, affecting the lungs (disseminated interstitial lung disease with bronchiolitis) and kidneys (rapidly progressive glomerulonephritis), intrathoracic lymphadenopathy, activity grade III (BVAS index – 23 points). Grade II respiratory failure. Chronic kidney disease 5D (glomerular filtration rate – 6 ml/min/1.73 m2). Grade II arterial hypertension, risk 4. Grade II pulmonary hypertension. Chronic heart failure 2А, functional class IV. Mixed anemia (iron-deficient, chronic disease), severe. Disseminated polyposis of the colon (hyperplastic type). At the hospital, antibacterial drugs (cefoperazone sulbactam), antifungal (fluticasone) were administered, anemia was corrected (iron-containing drugs and erythropoietin, hemotransfusion), hemodialysis. Cyclophosphane 400 mg was administered intravenously, a week later – 800 mg. Methylprednisolone (60 mg/day), co-trimoxazole (480 mg 3 times a week) were prescribed. A pronounced improvement was observed due to the therapy: body temperature normalization, decreased apnea, cough, weakness, increased appetite. The patient was discharged with recommendation for continuation of cytostatic therapy per the regimen and prescription for programmed hemodialysis at the place of residence.Conclusion. This clinical case demonstrates a necessity of considering ANCA-associated vasculitis during differential diagnosis of pulmonary-renal syndrome. Timely diagnosis and active cytostatic therapy play a principal role in treatment and promote deceleration of disease progression and improve prognosis.

Objective: to analyze and present a clinical case of late diagnosis of Takayasu’s arteritis in a young female patient with long-term arterial hypertension.Materials and methods. The female patient G., born in 1989, had noted elevated arterial pressure (AP) of 150/90 mm Hg since she was 14. At 21 the following diagnosis was stated: Fibro-muscular dysplasia, stenosis of the left renal artery. Stenosis of the celiac trunk. Aneurisms of the branches of the superior mesenteric artery; prosthesis of the left renal artery was performed. Since the beginning of 2016, the patient has noted elevated AP of 200/110 mm Hg despite continuing hypotensive therapy. Diagnosis of Nonspecific aortoarteritis was proposed in May of 2017. Methylprednisolone therapy was administered: 250 mg No. 2 intravenously, Prednisolone: 25 mg a day orally. Due to signs of decreased blood flow to the left kidney, in August of 2017 extracorporeal repeat prosthesis of the left renal artery, bypass of the right middle renal artery with reversed autovein were performed.Results. During examination in October of 2017, the patient complained of weakness, frequent elevated AP of 200/110 mm Hg. In blood test: hemoglobin 106 g/l, erythrocyte sedimentation rate 38 mm/h, C-reactive protein 25 mg/l. A heterozygous mutation in the methylenetetrahydropholate reductase, a heterozygous mutation in the factor V gene (G1691A) were identified. Homocysteine level was normal, infection and oncological pathology were excluded. The following diagnosis was made: Takayasu»s arteritis type IV affecting the aorta and its branches, moderate activity. Occlusion of the celiac trunk. Aneurisms of the branches of the superior mesenteric artery. Critical stenosis of the left renal artery. Thrombosis of the aorto-renal prosthesis. Hypoplasia of the left kidney. Prednisolone 50 mg a day, metoprolol 50 mg a day, valsartan 160 mg a day, acetylsalicylic acid 100 mg a day were prescribed.Conclusion. The presented clinical observation shows the importance of comprehensive examination of young patients complaining of elevated AP for many years. Due to untimely diagnosis and absence of pathogenetic therapy, the patient suffered negative consequences of surgical treatment.

The study objective is to demonstrate characteristics of prescription of nonsteroidal anti-inflammatory drugs (NSAIDs) for ankylosing spondylitis (AS) through a clinical case.Materials and methods. Male patient N., 34 years old, sought medical help complaining of pain in the cervical, thoracic, and lumbar spine, predominantly at night, at rest; limited range of motion in cervical and lumbar spine, pain in the area of external thigh surface, morning tightness longer than 2 hours. Stomachache after eating was also a complaint. The first episode of inflammatory pain was 10 years ago. Diagnosis of AS was determined 2 years ago, NSAIDs were prescribed which the patient didn’t take regularly. Based on clinical and laboratory examination, the following diagnosis was made. Main disorder: ankylosing spondylitis, late stage, stage III bilateral sacroiliitis, frontal spondylitis, high activity (BASDAI 5, 7, ASDAS-CRP 2, 7), HLA-В27-associated, with extra-articular manifestations (stage II bilateral coxitis, tendinitis of the shoulder rotator cuff muscle – superspinatus, supraspinatus, teres minor muscle, trochanteritis on both sides). Secondary diagnosis: NSAID-gastropathy, gastroesophageal reflux disease with esophagitis, gastroduodenitis associated with H. pylori. Meloxicam 15 mg/day in constant continuous regimen, methotrexate 12.5 mg SC once a week, folic acid 1 mg 5 days a week, sirdalud 4 mg 2 times a day, H. Pylori eradication therapy, glucocorticoid administration in the area of inflamed entheses were prescribed.Results. During the patient’s visit a month later, significant positive dynamics were observed: decreased pain in the lumbar, cervical, and thoracic spine, decreased pain in the shoulder joints, pain relief in the area of the greater trochanters, full active and passive range of motion in the shoulder joints. Duration of morning tightness was 1.5 hours. No complaints of pain in the epigastric region. In blood test: clinical and biochemical characteristics without abnormalities, С-reactive protein decreased from 62.5 to 20 mg/l. BASDAI 4, 3, ASDAS-CRP 2.0. Treatment with NSAIDs, methotrexate, proton pump inhibitor, folic acid was continued.Conclusion. NSAIDs are leading drugs for treatment of AS. Their prescription allows to relieve spinal pain and tightness, decreases enthesitis manifestations, exudative changes in the joints, allows to prevent or slow down structural changes in the spine. A very important treatment aspect is providing patients with information on the necessity of long-term continuous administration of NSAIDs and basic drugs, as well as on possible adverse events, regular laboratory control, necessity of gastroprotective drugs. Effectiveness of meloxicam in AS therapy was proved in a number of multicenter studies with a large number of patients. Meloxicam’s effectiveness is comparable to traditional NSAIDs – the “golden standard” (diclofenac, piroxicam, naproxem), but it’s more safe.

The article presents an overview of modern data and an analysis of the recommendations of the European Society of Cardiology and the European Association for Cardio-Thoracic Surgery published in 2017 regarding the use of antithrombotic therapy in patients with valvular heart disease. The results of studies devoted to the use of new oral anticoagulants in patients with valvular heart disease are demonstrated.

Antiviral activity of new AТ-specific fluorescent symmetric dimeric bisbenzimidazoles of DBА(n) series was assessed in the cell models of infections caused by type 1 herpes simplex virus (HSV1) and human cytomegalovirus (CMV). In DBA(n) molecules bisbenzimidazole fragments are bound to an oligomethylene liner with varied number of methylene groups in the linker (n = 1, 3, 5, 7, 9, 11). In contrast to DB(n) dimeric bisbenzimidazoles, in DBA(n) series terminal fragments of macromolecules contain N-dimethylaminopropylcarboxamide groups instead of N-methylpiperazine groups. DBА(n) compounds better dissolve in water, pass across plasma and nuclear membrane, and stain DNA in living cells. DBA(1) and DBA(7) produced therapeutic effects in HSV1 infection; DBA(7) completely suppressed the infection. DBA(11) displayed in vitro therapeutic activity in HSV1 and CMV infections. In addition, DBA(7) and DBA(1) showed microbicidal activity. Thus, DBA(11), which is active against two viruses causing severe diseases with serious health consequences for immunodeficient individuals, should be further investigated. High antiviral activity of DBA(7) in all test models indicates that this compound is a promising active agent for innovative antiviral drugs.

Objective: to describe a clinical case of chronic post-thromboembolic pulmonary hypertension (CTEPH) development and progression in a patient with recurrent pulmonary thromboembolism (PTE) and hereditary thrombophilia.Materials and methods. Patient K., female, 50 years old, was hospitalized in the 1st therapeutic department of N.I. Pirogov First City Clinical Hospital with complaints of shortness of breath, occurring at rest and exacerbating after minimal physical activity, dry cough, chest heaviness, swelling of the lower extremities (mainly right one). The patient had a history of deep venous thrombosis (DVT) of the lower extremities, PTE, splenectomy, and long glucocorticosteroid drugs intake for thrombocytopenic purpura. The patient underwent different examinations in the hospital, including evaluation of laboratory tests in dynamics, echocardiography, contrast-enhanced multislice computed tomography of the pulmonary artery and its branches, perfusion lung scintigraphy, right heart catheterization.Results. After examination the patient was diagnosed with multiple segmental and subsegmental perfusion defects of both lungs; we also observed signs of pulmonary hypertension (PH) at echocardiography, proved by right heart catheterization. Also the patient was diagnosed with inherited thrombophilia. The patient was included in the register of PH-patients, thromboendarterectomy together with administration of special medications, approved for use in patients with pulmonary arterial hypertension (PAH-specific therapy) were recommended.Conclusion. This article describes the main features of CTEPH, its diagnostics and treatment in patients with CTEPH after PTE.

Objective – review current data on the use of beta-blockers (BB) in chronic heart failure (CHF).Materials and methods. This article discusses beneficial effects of BB administration in CHF patients. It has been demonstrated that decrease in heart rate underlies clinical efficacy of BB therapy in patients with chronic heart failure. We reviewed the question of the necessity to achieve target doses of BB in the treatment of CHF patients. It has been shown that administration of BB in patients with chronic heart failure and reduced left ventricular ejection fraction increase pumping function of heart, and thus reduce the number of hospitalizations for decompensated heart failure, reducing the risk of total and sudden mortality. We demonstrated substantial advantages of β1-selective BB over nonselective ones with respect to their impact on hemodynamics, metabolic processes, rheological parameters of blood and bronchi. We also considered therapeutic tactics in case of BB administration in CHF patients.Results. Based on the data of the current studies we proved high efficiency and safety of β1-selective BBs in CHF patients.Conclusion. Correct choice of BB in patients with CHF and decrease in heart rate during the treatment can significantly increase an effectiveness of the treatment.

Data about chronic thromboembolic pulmonary hypertension (CTPH) prevalence is presented. The main CTPH clinical manifestations are described. The possible reasons and pathogenetic mechanisms of CTPH development are discussed. Features of unfavorable disease prognosis are also presented. Indications, results, limitations for CTPH surgical treatment are shown. Data of the currently completed clinical studies on bosentan, prostacyclin analogues and phosphodiesterase-5 inhibitors usage in CTPH are presented.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare life-threatening disease with a prevalence of 2 cases per 100000 population. CTEPH is a chronic, progressive disease characterized by high disability and mortality rates in young and middle-aged people, often with underlying genetic and autoimmune thrombophilic disorders. The need for pathogenetic therapy with orphan drugs that can slow the progression of the disease is supported.

Aim. To study the right heart remodeling and level of N-terminal brain natriuretic peptide (Nt-proBNP) in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Material and methods. Patients (n=79) after pulmonary embolism were included into the study. The main group consisted of patients (n=43) with an increase in systolic pulmonary artery pressure (SPAP) >30 mm Hg: 30 (37.9%) patients had pulmonary hypertension (PH) degree I, and 13 (16.5%) — PH degree II–III. Group of comparison con- sisted of 36 patients expired pulmonary embolism and having SPAP 2) were detected in 19.4%, 16.7% and 61.5% of patients of comparison group, PH I and PH II–III patients, respectively. According to myocardial tissue Doppler echocardiography Em/Am

The review presents data on the incidence of chronic thromboembolic pulmonary hypertension after pulmonary thromboembolism and describescongenital and acquired coagulation abnormalities in patients with venous thromboembolism. It considers the potential factors of development of chronic thromboembolic pulmonary hypertension and some medical conditions and diseases, which favors the development of pulmonary hypertension after prior pulmonary thromboembolism.

The article tells about incidence of pulmonary hypertension after pulmonary artery thromboembolia; congenital and acquired coagulation abnormalities in patients with venous thromboembolism; potential factors of chronic thromboembolic pulmonary hypertension; certain medical conditions and diseases contributing to the development of pulmonary hypertension after pulmonary artery thromboembolia.