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.
Представлены данные о частоте развития хронической тромбоэмболической легочной гипертензии (ХТЛГ). Описаны основные клинические проявления ХТЛГ. Освещены возможные причины и патогенетические механизмы формирования ХТЛГ, описаны маркеры неблагоприятного течения заболевания. Рассмотрены показания, результаты, ограничения к проведению хирургического лечения ХТЛГ. Приведены данные последних клинических исследований, посвященных применению бозентана, аналогов простациклина, ингибиторов фосфодиэстеразы-5 при этом тяжелом заболевании. Ключевые слова: легочная гипертензия, хроническая тромбоэмболическая легочная гипертензия, тромбоэмболия легочной артерии, тромбэндартерэктомия, бозентан, аналоги простациклина, ингибиторы фосфодиэстеразы-5. РФК 2011;7(2):199-203 Pathogenetic mechanisms and treatment principles of chronic thromboembolic pulmonary hypertension
Хроническая тромбоэмболическая легочная гипертензия (ХТЛГ) является редким жизнеугрожающим заболеванием с распространенностью 2 случая на 100000 населения. ХТЛГ-это хроническое прогрессирующее заболевание, характеризующееся высокой степенью инвалидизации и высокой смертностью у лиц молодого и среднего возраста, часто имеющее в основе генетические и аутоиммунные тромбофилические нарушения. Приводится обоснование необходимости применения патогенетической терапии орфанными препаратами, позволяющими замедлить прогрессирование заболевания.
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 consisted of 36 patients expired pulmonary embolism and having SPAP <30 mm Hg. The control group consisted of 20 people. 6-minute walk test (6-MWT) and Doppler echocardiography were performed in all patients. Besides myocardial tissue Doppler echocardiography and assessment of Nt-proBNP level were performed in 38 and 71 patients, respectively. Results. Dyspnea occurred in 90.7% of patients with various degrees of PH and 80.5% of patients with normal SPAP. Patients without PH and with PH I complained of palpitations, weakness, fatigue, and dizziness with similar frequency. Patients with PH I were comparable with ones of comparison group in 6-MWT distance that dramatically decreased in patients with PH II-III. Enlargement of the right atrium (RA) and/or right ventricular (RV) was observed in 76.7% of patients with PH I and 100% of patients with PH II-III. RV diastolic function abnormalities (E/A<1 and E/A>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<1 was observed in 8 (72.7%) patients of the comparison group and in 13 (76.4%) patients with PH. 33.9] fmol/ml in PH I patients and 142.1 [62.1, 171.8] fmol/ml in PH II-III patients. Nt-proBNP level was 6.5 [3.1, 18.3] fmol/mL in patients of the comparison group, and it was higher than this in patients of the control group (3.5 [1.8, 7.5 fmol/ml]. Conclusion. Various indicators of heart remodeling and RV diastolic dysfunction were found in the majority of patients after pulmonary embolism, including those with normal SPAP. Elevation of Nt-proBNP level adequately reflects the severity of RV dysfunction in CTEPH patients only in PH II-III. This marker has low diagnostic value in patients without CTEPH and PH I patients.
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.
BackgroundSystemic sclerosis (SSc) is a multisystem, connective tissue disease characterized by fibrosis of the skin and internal organ involvement, which can influence quality of life and functional capacity. SSc patients show some problems associated with reduced quality of life.ObjectivesSystemic sclerosis (SSc) is a multisystem, connective tissue disease characterized by fibrosis of the skin and internal organ involvement, which can influence quality of life and functional capacity. SSc patients show some problems associated with reduced quality of life.MethodsIn total, 51 patients with SSc were included: 50 women and 1 man (mean age: 63,2 ± 10,1 year, limited SSc 28/diffuse SSc 23, median duration since first non-Raynaud symptom: 10,1 years) who fulfilled the ACR/EULAR classification criteria (2013), filled in questionnaires assessing disability (HAQ, Health Assessment Questionnaire) and quality of life (SF-36, Medical outcomes study Short Form 36 - Physical Component Summary and Mental Component Summary).ResultsAverage HAQ in patients with limited and diffuse SSc was 0,66±0,58 and 0,9±0,59. Data analysis showed that 59% of the patients were in the mild to moderate HAQ disability category (0 ⩽ HAQ < 1), 39% in the moderate to severe disability category (1 ⩽ HAQ < 2), and 2% in the severe to very severe disability category (2 ⩽ HAQ ⩾ 3). The SF36 mean scores of the total group were 34,8±8,7 on the Mental Component Summary and 37,0±13,1 on the Physical Component Summary.ConclusionSsc and its complications decrease quality of life and functional capacity. Although validated in SSc, the HAQ disability index underestimates respiratory failure due to interstitial lung disease, gastrointestinal symptoms, cardiovascular complications and severity of Raynaud phenomenon. Alternative measures of functional impairment should be examined. Health-related quality of life, which was assessed by the SF-36 is reduced in both physical and mental domains. It should be taken into account by clinicians for further improvement of treatment and development rehabilitation program.References[1]Almeida C, Almeida I, Vasconcelos C. Quality of life in systemic sclerosis. Autoimmun Rev. 2015;14(12):1087-1096Disclosure of InterestsNone declared
Волевач Лариса Васильевна, кафедра поликлинической терапии с курсом ИДПО, зав. кафедрой, профессор, д. м. н. Сарсенбаева Айман Силкановна, декан ИДПО, кафедра терапии ИДПО, профессор, д. м. н. Габбасова Лилия Вадимовна, кафедра поликлинической терапии с курсом ИДПО, доцент, к. м. н. Демидова Надежда Александровна, кафедра поликлинической терапии с курсом ИДПО, ассистент Гарипова Роза Айратовна, кафедра поликлинической терапии с курсом ИДПО, ассистент Гурьев Ростислав Дмитриевич, кафедра поликлинической терапии с курсом ИДПО, ассистент Камалова Алиса Атласовна, кафедра поликлинической терапии с курсом ИДПО, доцент, к. м. н.
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.
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