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Эффективность плазмафереза у пациентов с аритмиями и синдромом дилатационной кардиомиопатии иммуновоспалительного генеза
Эффективность плазмафереза у пациентов с аритмиями и синдромом дилатационной кардиомиопатии иммуновоспалительного генеза
Куликова В.А., Недоступ А.В., Благова О.В. и др. Эффективность плазмафереза у пациентов с аритмиями и синдромом дилатационной кардиомиопатии иммуновоспалительного генеза. Consilium Medicum. 2018; 20 (12): 39–46. DOI: 10.26442/20751753.2018.12.180159
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Аннотация
Цель – изучить эффективность плазмафереза (ПФ) в качестве основного вида патогенетического лечения или в сочетании с иммуносупрессивной терапией у больных с дилатационной кардиомиопатией (ДКМП) и аритмиями иммуновоспалительного генеза.
Материалы и методы. В исследование были включены 20 больных с аритмическим вариантом миокардита – с наджелудочковой/желудочковой экстрасистолией более 3000 в сутки (n=3/8) и мерцательной аритмией (n=9); 14 пациентов с синдромом ДКМП (конечный диастолический размер левого желудочка – 6,3±0,6 см, фракция выброса – ФВ 33,5±8,1%). Критерием включения было повышение титров хотя бы 2 видов антикардиальных антител в 2 и более раза. Миокардит диагностирован с применением биопсии миокарда, магнитно-резонансной томографии, мультиспиральной компьютерной томографии, сцинтиграфии, для исключения ишемической природы ДКМП дополнительно выполнялась коронарография. Проведен курс дискретного ПФ. Динамика оценивалась через 6 и 12 мес.
Результаты. В обеих группах отмечено достоверное снижение титров антикардиальных антител непосредственно после ПФ и при контрольных исследованиях (p<0,05). У больных с аритмиями хороший эффект (уменьшение количества экстрасистол и частоты мерцательной аритмии на 75% и более) отмечен у 65% больных основной группы. Предиктором эффективности ПФ был титр специфического антинуклеарного фактора от 1:40 и более (чувствительность – 92,3%, специфичность – 71,4%, площадь под кривой AUC – 0,813, р<0,05). Метилпреднизолон назначен 45% больным после ПФ в дозе 8 [4; 16] мг в день. У больных с синдромом ДКМП получено достоверное (p<0,05) возрастание ФВ (до 41,4±8,2% и 46,3±12,7%) и дистанции теста с 6-минутной ходьбой. Хороший эффект (возрастание ФВ на 10% и более) отмечен у 50% пациентов. Предиктором эффективности ПФ стало систолическое давление в легочной артерии 28,5 мм рт. ст. и более (чувствительность – 100%, специфичность – 71,4%, площадь под кривой AUC – 0,893, p<0,05). После ПФ метилпреднизолон назначен 43% больных в средней дозе 8 [8; 17,25] мг/сут.
Заключение. Хороший клинический ответ на ПФ отмечен у 65% больных с аритмиями и у 50% пациентов с синдромом ДКМП иммуновоспалительного генеза. У больных с различными вариантами миокардита проведение ПФ повышает эффективность антиаритмической и иммуносупрессивной терапии и позволяет воздержаться от агрессивных режимов иммуносупрессии.Материалы и методы. В исследование были включены 20 больных с аритмическим вариантом миокардита – с наджелудочковой/желудочковой экстрасистолией более 3000 в сутки (n=3/8) и мерцательной аритмией (n=9); 14 пациентов с синдромом ДКМП (конечный диастолический размер левого желудочка – 6,3±0,6 см, фракция выброса – ФВ 33,5±8,1%). Критерием включения было повышение титров хотя бы 2 видов антикардиальных антител в 2 и более раза. Миокардит диагностирован с применением биопсии миокарда, магнитно-резонансной томографии, мультиспиральной компьютерной томографии, сцинтиграфии, для исключения ишемической природы ДКМП дополнительно выполнялась коронарография. Проведен курс дискретного ПФ. Динамика оценивалась через 6 и 12 мес.
Результаты. В обеих группах отмечено достоверное снижение титров антикардиальных антител непосредственно после ПФ и при контрольных исследованиях (p<0,05). У больных с аритмиями хороший эффект (уменьшение количества экстрасистол и частоты мерцательной аритмии на 75% и более) отмечен у 65% больных основной группы. Предиктором эффективности ПФ был титр специфического антинуклеарного фактора от 1:40 и более (чувствительность – 92,3%, специфичность – 71,4%, площадь под кривой AUC – 0,813, р<0,05). Метилпреднизолон назначен 45% больным после ПФ в дозе 8 [4; 16] мг в день. У больных с синдромом ДКМП получено достоверное (p<0,05) возрастание ФВ (до 41,4±8,2% и 46,3±12,7%) и дистанции теста с 6-минутной ходьбой. Хороший эффект (возрастание ФВ на 10% и более) отмечен у 50% пациентов. Предиктором эффективности ПФ стало систолическое давление в легочной артерии 28,5 мм рт. ст. и более (чувствительность – 100%, специфичность – 71,4%, площадь под кривой AUC – 0,893, p<0,05). После ПФ метилпреднизолон назначен 43% больных в средней дозе 8 [8; 17,25] мг/сут.
Ключевые слова: миокардит, дилатационная кардиомиопатия, аритмии, плазмаферез, иммуносупрессивная терапия.
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Objective – to study effectiveness of plasmapheresis (PH) use as the main pathogenic treatment option or combined with immunosuppressive therapy in patients with dilated cardiomyopathy (DCM) and arrhythmias of immunoinflammatory nature.
Materials and methods. The study included 20 patients with arrhythmic myocarditis – supraventricular/ventricular extrasystoles numbered more than 3000 per day (n=3/8) and atrial fibrillation (n=9); 14 patients with DCM (left ventricle end-diastolic diameter – 6.3±0.6 cm, ejection fraction – EF 33.5±8.1%). Inclusion criterion was 2-fold or more titer increase of at least 2 types of anti-cardiac antibodies. Myocarditis was diagnosed using myocardium biopsy, magnetic resonance imaging, multispiral computed tomography, and scintigraphy. Coronarography was performed for ischemic nature of DCM exclusion. A course of discrete PH was performed. Patients’ dynamics was estimated after 6 and 12 months.
Results. A significant decrease of anti-cardiac antibodies titers was observed in both groups of patients right after plasmapheresis and in follow-up (p<0.05). In patients with arrhythmias good effect (decrease of extrasystoles number and atrial fibrillation frequency by 75% and more) was observed in 65% of the study group patients. Specific antinuclear antibody titer from 1:40 and more was a predictor for PH effectiveness (sensitivity – 92.3%, specificity – 71.4%, area under curve AUC – 0.813, р<0.05). Methylprednisolone was administered in 45% of patients at a dose of 8 [4; 16] mg per day. In patients with DCM a significant (p<0.05) increase of EF (up to 41.4±8.2% and 46.3±12.7%) and 6-minute walk test distance was observed. Good effect (EF increase on 10% and more) was observed in 50% of patients. Pulmonary artery systolic pressure more than 28.5 mm Hg was a predictor for PH effectiveness (sensitivity – 100%, specificity – 71.4%, area under curve AUC – 0.893, p<0.05). Methylprednisolone was administered in 43% of patients at a mean dose of 8 [8; 17.25] mg per day.
Conclusion. Good clinical effect of PH was observed in 65% of patients with arrhythmias and in 50% of patients with DCM syndrome of immunoinflammatory nature. In patients with different myocarditis variants PH increases effectiveness of antiarrhythmic and immunosuppressive therapy and allows to refrain from aggressive immunosuppression regimen.
Key words: myocarditis, dilated cardiomyopathy, arrhythmias, plasmapheresis, immunosuppressive therapy.
Materials and methods. The study included 20 patients with arrhythmic myocarditis – supraventricular/ventricular extrasystoles numbered more than 3000 per day (n=3/8) and atrial fibrillation (n=9); 14 patients with DCM (left ventricle end-diastolic diameter – 6.3±0.6 cm, ejection fraction – EF 33.5±8.1%). Inclusion criterion was 2-fold or more titer increase of at least 2 types of anti-cardiac antibodies. Myocarditis was diagnosed using myocardium biopsy, magnetic resonance imaging, multispiral computed tomography, and scintigraphy. Coronarography was performed for ischemic nature of DCM exclusion. A course of discrete PH was performed. Patients’ dynamics was estimated after 6 and 12 months.
Results. A significant decrease of anti-cardiac antibodies titers was observed in both groups of patients right after plasmapheresis and in follow-up (p<0.05). In patients with arrhythmias good effect (decrease of extrasystoles number and atrial fibrillation frequency by 75% and more) was observed in 65% of the study group patients. Specific antinuclear antibody titer from 1:40 and more was a predictor for PH effectiveness (sensitivity – 92.3%, specificity – 71.4%, area under curve AUC – 0.813, р<0.05). Methylprednisolone was administered in 45% of patients at a dose of 8 [4; 16] mg per day. In patients with DCM a significant (p<0.05) increase of EF (up to 41.4±8.2% and 46.3±12.7%) and 6-minute walk test distance was observed. Good effect (EF increase on 10% and more) was observed in 50% of patients. Pulmonary artery systolic pressure more than 28.5 mm Hg was a predictor for PH effectiveness (sensitivity – 100%, specificity – 71.4%, area under curve AUC – 0.893, p<0.05). Methylprednisolone was administered in 43% of patients at a mean dose of 8 [8; 17.25] mg per day.
Conclusion. Good clinical effect of PH was observed in 65% of patients with arrhythmias and in 50% of patients with DCM syndrome of immunoinflammatory nature. In patients with different myocarditis variants PH increases effectiveness of antiarrhythmic and immunosuppressive therapy and allows to refrain from aggressive immunosuppression regimen.
Key words: myocarditis, dilated cardiomyopathy, arrhythmias, plasmapheresis, immunosuppressive therapy.
Полный текст
Список литературы
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15. Недоступ А.В., Царегородцев Д.А., Рагимов А.А. и др. Использование плазмафереза при лечении нарушений ритма сердца, резистентных к лекарственной терапии. Терапевтический архив. 2002; 74 (12): 41–6. PMID: 12577839 / Nedostup A.V., Tsaregorodtsev D.A., Ragimov A.A. i dr. Plasma exchange in patients with arrhythmias resistant to antiarrhythmic drugs. Therapeutic Archive. 2002; 74 (12): 41–6. PMID: 12577839 [in Russian]
16. Благова О.В., Осипова Ю.В., Недоступ А.В. и др. Клинические, лабораторные и инструментальные критерии миокардита, установленные в сопоставлении с биопсийным исследованием миокарда (алгоритм неинвазивной диагностики). Терапевтический архив. 2017; 89 (9): 30–40. / Blagova O.V., Osipova Iu.V., Nedostup A.V. i dr. Clinical, laboratory and instrumental criteria for myocarditis, established in comparison with myocardial biopsy: A non-invasive diagnostic algorithm. Therapeutic Archive. 2017; 89 (9): 30–40. [in Russian]
2. Escher F, Tschöepe C, Lassner D et al. Myocarditis and inflammatory cardiomyopathy: from diagnosis to treatment. Turk Kardiyol Dern Ars 2015; 43 (8): 739–48 DOI: 10.5543/tkda.2015.47750
3. Rusconi P, Wilkinson J, Sleeper LA et al. Differences in Presentation and Outcomes between Children with Familial Dilated Cardiomyopathy and Children with Idiopathic Dilated Cardiomyopathy: A Report from the Pediatric Cardiomyopathy Registry Study Group. Circ Heart Fail 2017; 10 (2): e002637. DOI: 10.1161/CIRCHEARTFAILURE.115.002637
4. Shaboodien G, Maske C, Wainwright H et al. Prevalence of myocarditis and cardiotropic virus infection in Africans with HIV-associated cardiomyopathy, idiopathic dilated cardiomyopathy and heart transplant recipients: a pilot study: cardiovascular topic. Cardiovasc J Afr 2013; 24 (6): 218–3. DOI: 10.5830/CVJA-2013-039
5. Caforio AL, Pankuweit S, Arbustini E et al. Current state of knowledge onaetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2013; 34: 2636–48. DOI: 10.1093/eurheartj/eht210
6. Jahns R, Boivin V, Schwarzbach V et al. Pathological autoantibodies in cardiomyopathy. Autoimmunity 2008; 41 (6): 454–61. DOI: 10.1080/08916930802031603
7. Schwartz J, Winters JL, Padmanabhan A et al. Guidelines on the use of therapeutic apheresis in clinical practice – evidence based approach from the writing committee of the American Society for Apheresis: The Sixth Special Issue. J Clin Apher 2013; 28 (3): 145–284. DOI: 10.1002/jca.21276
8. Ohlow MA, Brunelli M, Schreiber M et al. Therapeutic effect of immunoadsorption and subsequent immunoglobulin substitution in patients with dilated cardiomyopathy: Results from the observational prospective Bad Berka Registry. J Cardiol 2017; 69 (2): 409–16. DOI: 10.1016/j.jjcc.2016.07.014
9. Pei J, Li N, Chen J et al. The predictive values of beta1-adrenergic and M2 muscarinic receptor autoantibodies for sudden cardiac death in patients with chronic heart failure. Eur J Heart Fail 2012; 14 (8): 887–94. DOI: 10.1093/eurjhf/hfs082
10. Koizumi K, Hoshiai M, Toda T et al. Outcomes of plasma exchange for severe dilated cardiomyopathy in children. Heart Vessels 2017; 32 (1): 61–7. DOI: 10.1007/s00380-016-0830-1
11. Ameling S, Herda LR, Hammer E et al. Myocardial gene expression profiles and cardiodepressant autoantibodies predict response of patients with dilated cardiomyopathy to immunoadsorption therapy. Eur Heart J 2013; 34: 666–75. DOI: 10.1093/eurheartj/ehs330
12. Chimenti C, Russo MA, Carpi A , et al. Histological substrate of human atrial fibrillation. Biomed Pharmacother 2010; 64 (3): 177–83. DOI: 10.1016/j.biopha.2009.09.017
13. Cooper LT, Baughman KL, Feldman AM et al. The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Endorsed by the Heart Failure Society of America and the Heart Failure Association of the European Society of Cardiology. J Am Coll Cardiol 2007; 50 (19): 1914–31. DOI: 10.1016/j.jacc.2007.09.008
14. Lewek J, Kaczmarek K, Cygankiewicz I et al. Inflammation and arrhythmias: potential mechanisms and clinical implications. Expert Rev Cardiovasc Ther 2014; 12 (9): 1077–85. DOI: 10.1586/14779072.2014.942286
15. Nedostup A.V., Tsaregorodtsev D.A., Ragimov A.A. i dr. Plasma exchange in patients with arrhythmias resistant to antiarrhythmic drugs. Therapeutic Archive. 2002; 74 (12): 41–6. PMID: 12577839 [in Russian]
16. Blagova O.V., Osipova Iu.V., Nedostup A.V. i dr. Clinical, laboratory and instrumental criteria for myocarditis, established in comparison with myocardial biopsy: A non-invasive diagnostic algorithm. Therapeutic Archive. 2017; 89 (9): 30–40. [in Russian]
2. Escher F, Tschöepe C, Lassner D et al. Myocarditis and inflammatory cardiomyopathy: from diagnosis to treatment. Turk Kardiyol Dern Ars 2015; 43 (8): 739–48 DOI: 10.5543/tkda.2015.47750
3. Rusconi P, Wilkinson J, Sleeper LA et al. Differences in Presentation and Outcomes between Children with Familial Dilated Cardiomyopathy and Children with Idiopathic Dilated Cardiomyopathy: A Report from the Pediatric Cardiomyopathy Registry Study Group. Circ Heart Fail 2017; 10 (2): e002637. DOI: 10.1161/CIRCHEARTFAILURE.115.0026374. Shaboodien G, Maske C, Wainwright H et al. Prevalence of myocarditis and cardiotropic virus infection in Africans with HIV-associated cardiomyopathy, idiopathic dilated cardiomyopathy and heart transplant recipients: a pilot study: cardiovascular topic. Cardiovasc J Afr 2013; 24 (6): 218–3. DOI: 10.5830/CVJA-2013-039
5. Caforio AL, Pankuweit S, Arbustini E et al. Current state of knowledge onaetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2013; 34: 2636–48. DOI: 10.1093/eurheartj/eht210
6. Jahns R, Boivin V, Schwarzbach V et al. Pathological autoantibodies in cardiomyopathy. Autoimmunity 2008; 41 (6): 454–61. DOI: 10.1080/08916930802031603
7. Schwartz J, Winters JL, Padmanabhan A et al. Guidelines on the use of therapeutic apheresis in clinical practice – evidence based approach from the writing committee of the American Society for Apheresis: The Sixth Special Issue. J Clin Apher 2013; 28 (3): 145–284. DOI: 10.1002/jca.21276
8. Ohlow MA, Brunelli M, Schreiber M et al. Therapeutic effect of immunoadsorption and subsequent immunoglobulin substitution in patients with dilated cardiomyopathy: Results from the observational prospective Bad Berka Registry. J Cardiol 2017; 69 (2): 409–16. DOI: 10.1016/j.jjcc.2016.07.014
9. Pei J, Li N, Chen J et al. The predictive values of beta1-adrenergic and M2 muscarinic receptor autoantibodies for sudden cardiac death in patients with chronic heart failure. Eur J Heart Fail 2012; 14 (8): 887–94. DOI: 10.1093/eurjhf/hfs082
10. Koizumi K, Hoshiai M, Toda T et al. Outcomes of plasma exchange for severe dilated cardiomyopathy in children. Heart Vessels 2017; 32 (1): 61–7. DOI: 10.1007/s00380-016-0830-1
11. Ameling S, Herda LR, Hammer E et al. Myocardial gene expression profiles and cardiodepressant autoantibodies predict response of patients with dilated cardiomyopathy to immunoadsorption therapy. Eur Heart J 2013; 34: 666–75. DOI: 10.1093/eurheartj/ehs330
12. Chimenti C, Russo MA, Carpi A , et al. Histological substrate of human atrial fibrillation. Biomed Pharmacother 2010; 64 (3): 177–83. DOI: 10.1016/j.biopha.2009.09.017
13. Cooper LT, Baughman KL, Feldman AM et al. The role of endomyocardial biopsy in the management of cardiovascular disease: a scientific statement from the American Heart Association, the American College of Cardiology, and the European Society of Cardiology. Endorsed by the Heart Failure Society of America and the Heart Failure Association of the European Society of Cardiology. J Am Coll Cardiol 2007; 50 (19): 1914–31. DOI: 10.1016/j.jacc.2007.09.008
14. Lewek J, Kaczmarek K, Cygankiewicz I et al. Inflammation and arrhythmias: potential mechanisms and clinical implications. Expert Rev Cardiovasc Ther 2014; 12 (9): 1077–85. DOI: 10.1586/14779072.2014.942286
15. Недоступ А.В., Царегородцев Д.А., Рагимов А.А. и др. Использование плазмафереза при лечении нарушений ритма сердца, резистентных к лекарственной терапии. Терапевтический архив. 2002; 74 (12): 41–6. PMID: 12577839 / Nedostup A.V., Tsaregorodtsev D.A., Ragimov A.A. i dr. Plasma exchange in patients with arrhythmias resistant to antiarrhythmic drugs. Therapeutic Archive. 2002; 74 (12): 41–6. PMID: 12577839 [in Russian]
16. Благова О.В., Осипова Ю.В., Недоступ А.В. и др. Клинические, лабораторные и инструментальные критерии миокардита, установленные в сопоставлении с биопсийным исследованием миокарда (алгоритм неинвазивной диагностики). Терапевтический архив. 2017; 89 (9): 30–40. / Blagova O.V., Osipova Iu.V., Nedostup A.V. i dr. Clinical, laboratory and instrumental criteria for myocarditis, established in comparison with myocardial biopsy: A non-invasive diagnostic algorithm. Therapeutic Archive. 2017; 89 (9): 30–40. [in Russian]
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2. Escher F, Tschöepe C, Lassner D et al. Myocarditis and inflammatory cardiomyopathy: from diagnosis to treatment. Turk Kardiyol Dern Ars 2015; 43 (8): 739–48 DOI: 10.5543/tkda.2015.47750
3. Rusconi P, Wilkinson J, Sleeper LA et al. Differences in Presentation and Outcomes between Children with Familial Dilated Cardiomyopathy and Children with Idiopathic Dilated Cardiomyopathy: A Report from the Pediatric Cardiomyopathy Registry Study Group. Circ Heart Fail 2017; 10 (2): e002637. DOI: 10.1161/CIRCHEARTFAILURE.115.002637
4. Shaboodien G, Maske C, Wainwright H et al. Prevalence of myocarditis and cardiotropic virus infection in Africans with HIV-associated cardiomyopathy, idiopathic dilated cardiomyopathy and heart transplant recipients: a pilot study: cardiovascular topic. Cardiovasc J Afr 2013; 24 (6): 218–3. DOI: 10.5830/CVJA-2013-039
5. Caforio AL, Pankuweit S, Arbustini E et al. Current state of knowledge onaetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2013; 34: 2636–48. DOI: 10.1093/eurheartj/eht210
6. Jahns R, Boivin V, Schwarzbach V et al. Pathological autoantibodies in cardiomyopathy. Autoimmunity 2008; 41 (6): 454–61. DOI: 10.1080/08916930802031603
7. Schwartz J, Winters JL, Padmanabhan A et al. Guidelines on the use of therapeutic apheresis in clinical practice – evidence based approach from the writing committee of the American Society for Apheresis: The Sixth Special Issue. J Clin Apher 2013; 28 (3): 145–284. DOI: 10.1002/jca.21276
8. Ohlow MA, Brunelli M, Schreiber M et al. Therapeutic effect of immunoadsorption and subsequent immunoglobulin substitution in patients with dilated cardiomyopathy: Results from the observational prospective Bad Berka Registry. J Cardiol 2017; 69 (2): 409–16. DOI: 10.1016/j.jjcc.2016.07.014
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Авторы
В.А.Куликова*1, А.В.Недоступ1, О.В.Благова1, В.А.Зайденов2, А.Г.Куприянова3, И.А.Нечаев1, А.А.Рагимов1
1 ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М.Сеченова» Минздрава России. 119991, Россия, Москва, ул. Трубецкая, д. 8, стр. 2;
2 ФГБУ «Национальный медицинский исследовательский центр трансплантологии и искусственных органов им. акад. В.И.Шумакова» Минздрава России. 123182, Россия, Москва, ул. Щукинская, д. 1;1 ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М.Сеченова» Минздрава России. 119991, Россия, Москва, ул. Трубецкая, д. 8, стр. 2;
3 ФГБОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И.Пирогова» Минздрава России. 117997, Россия, Москва, ул. Островитянова, д. 1
*kulikova-victoria@mail.ru
________________________________________________
V.A.Kulikova*1, A.V.Nedostup1, O.V.Blagova1, V.A.Zaidenov2, A.G.Kupriyanova3, I.A.Nechaev1, A.A.Ragimov1
1 I.M.Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation. 119991, Russian Federation, Moscow, ul. Trubetskaia, d. 8, str. 2;
2 V.I.Shumakov National Medical Research Center Transplantology and artificial organs of the Ministry of Health of the Russian Federation. 123182, Russian Federation, Moscow, ul. Shchukinskaya, d. 1;1 I.M.Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation. 119991, Russian Federation, Moscow, ul. Trubetskaia, d. 8, str. 2;
3 N.I.Pirogov Russian National Research Medical University of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Ostrovitianova, d. 1
*kulikova-victoria@mail.ru
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