Москва 125252, ул. Алабяна 13, корпус 1
+7 (495) 098-03-59
Заказать звонок
  • О портале
  • Контакты
  • ...
    Omnidoctor
    Библиотека
    • Издания для врачей
      • Consilium Medicum
      • Педиатрия.Consilium Medicum
      • Современная Онкология
      • Гинекология
      • Терапевтический архив
      • Газета «Участковый терапевт»
      • Газета «Женская консультация»
      • Газета «Участковый педиатр»
      • Справочник поликлинического врача
      • Cardioсоматика
      • Системные гипертензии
    • Издания для провизоров и фармацевтов
      • Газета «Первостольник»
      • Справочник провизора
    • Online-издания
      • Женская консультация
      • Участковый педиатр
      • Участковый терапевт
    Медиатека
    Мероприятия
    Спецпроекты
    • ИммуноГалактика (NEW!)
    • Гормональный оркестр
    • CardioSPACE
    • NeuroFusion (NEW!)
    • Современная Онкология
    • Урологика
    Пресс-центр
    Практикум
      Библиотека
      Медиатека
      Мероприятия
      Спецпроекты
      ИммуноГалактика (NEW!)
      Гормональный оркестр
      CardioSPACE
      NeuroFusion (NEW!)
      Современная Онкология
      Урологика
      Пресс-центр
      Практикум
      Omnidoctor
      Библиотека
      • Издания для врачей
        • Consilium Medicum
        • Педиатрия.Consilium Medicum
        • Современная Онкология
        • Гинекология
        • Терапевтический архив
        • Газета «Участковый терапевт»
        • Газета «Женская консультация»
        • Газета «Участковый педиатр»
        • Справочник поликлинического врача
        • Cardioсоматика
        • Системные гипертензии
      • Издания для провизоров и фармацевтов
        • Газета «Первостольник»
        • Справочник провизора
      • Online-издания
        • Женская консультация
        • Участковый педиатр
        • Участковый терапевт
      Медиатека
      Мероприятия
      Спецпроекты
      • ИммуноГалактика (NEW!)
      • Гормональный оркестр
      • CardioSPACE
      • NeuroFusion (NEW!)
      • Современная Онкология
      • Урологика
      Пресс-центр
      Практикум
        Omnidoctor
        • Библиотека
          • Назад
          • Библиотека
          • Издания для врачей
            • Назад
            • Издания для врачей
            • Consilium Medicum
            • Педиатрия.Consilium Medicum
            • Современная Онкология
            • Гинекология
            • Терапевтический архив
            • Газета «Участковый терапевт»
            • Газета «Женская консультация»
            • Газета «Участковый педиатр»
            • Справочник поликлинического врача
            • Cardioсоматика
            • Системные гипертензии
          • Издания для провизоров и фармацевтов
            • Назад
            • Издания для провизоров и фармацевтов
            • Газета «Первостольник»
            • Справочник провизора
          • Online-издания
            • Назад
            • Online-издания
            • Женская консультация
            • Участковый педиатр
            • Участковый терапевт
        • Медиатека
        • Мероприятия
        • Спецпроекты
          • Назад
          • Спецпроекты
          • ИммуноГалактика (NEW!)
          • Гормональный оркестр
          • CardioSPACE
          • NeuroFusion (NEW!)
          • Современная Онкология
          • Урологика
        • Пресс-центр
        • Практикум
        • Мой кабинет
        • +7 (495) 098-03-59
        Москва 125252, ул. Алабяна 13, корпус 1
        info@omnidoctor.ru
        • Вконтакте
        • Telegram
        • YouTube
        • Главная
        • Библиотека
        • Издания для врачей
        • Терапевтический архив
        • Журнал Терапевтический архив 2020 Терапевтический архив
        • Журнал Терапевтический архив №5 Вопросы ревматологии 2020
        • Преимущества терапии ингибиторами натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом 2-го типа в сочетании с гиперурикемией и подагрой - Журнал Терапевтический архив №5 Вопросы ревматологии 2020

        Преимущества терапии ингибиторами натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом 2-го типа в сочетании с гиперурикемией и подагрой - Журнал Терапевтический архив №5 Вопросы ревматологии 2020

        Паневин Т.С., Елисеев М.С., Шестакова М.В., Насонов Е.Л. Преимущества терапии ингибиторами натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом 2-го типа в сочетании с гиперурикемией и подагрой. Терапевтический архив. 2020; 92 (5): 110–118. DOI: 10.26442/00403660.2020.05.000633

        ________________________________________________

        Panevin T.S., Eliseev M.S., Shestakova M.V., Nasonov E.L. Advantages of therapy with sodium glucose cotransporter type 2 inhibitors in patients with type 2 diabetes mellitus in combination with hyperuricemia and gout. Therapeutic Archive. 2020; 92 (5): 110–118. DOI: 10.26442/00403660.2020.05.000633

        Преимущества терапии ингибиторами натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом 2-го типа в сочетании с гиперурикемией и подагрой

        Паневин Т.С., Елисеев М.С., Шестакова М.В., Насонов Е.Л. Преимущества терапии ингибиторами натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом 2-го типа в сочетании с гиперурикемией и подагрой. Терапевтический архив. 2020; 92 (5): 110–118. DOI: 10.26442/00403660.2020.05.000633

        ________________________________________________

        Panevin T.S., Eliseev M.S., Shestakova M.V., Nasonov E.L. Advantages of therapy with sodium glucose cotransporter type 2 inhibitors in patients with type 2 diabetes mellitus in combination with hyperuricemia and gout. Therapeutic Archive. 2020; 92 (5): 110–118. DOI: 10.26442/00403660.2020.05.000633

        • Читать PDF
          Преимущества терапии ингибиторами натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом  2-го типа в сочетании с гиперурикемией и подагрой

        Материалы доступны только для специалистов сферы здравоохранения.
        Чтобы посмотреть материал полностью Авторизуйтесь или зарегистрируйтесь.

        • Аннотация
        • Список литературы
        • Авторы
        Аннотация
        В настоящее время в Российской Федерации зарегистрировано только два препарата для снижения мочевой кислоты (МК) – аллопуринол и фебуксостат, однако их использование позволяет достичь целевого уровня МК не во всех случаях. Согласно результатам многочисленных рандомизированных исследований гиперурикемия и подагра ассоциированы со многими компонентами метаболического синдрома, включая сахарный диабет. Указанные факторы диктуют необходимость поиска новых препаратов, оказывающих комплексное влияние сразу на несколько компонентов метаболического синдрома. Потенциально привлекательной в этом плане является новая группа препаратов для лечения сахарного диабета 2-го типа – ингибиторы натрий-глюкозного котранспортера 2-го типа, которые помимо основного сахароснижающего действия показали положительные эффекты в отношении сердечно-сосудистой системы, почек, а также снижения уровня МК.

        Ключевые слова: подагра, гиперурикемия, мочевая кислота, натрий-глюкозный котранспортер 2-го типа, дапаглифлозин, эмпаглифлозин, канаглифлозин, ипраглифлозин.

        ________________________________________________

        Currently, only two drugs for reducing uric acid (UA), allopurinol and febuxostat, are registered in the Russian Federation, but their use does not allow to achieve the target level of UA in all cases. According to the results of numerous randomized trials, hyperuricemia and gout are associated with the corresponding components of the metabolic syndrome, including diabetes mellitus. The influence of factors is due to the need to search for new drugs that have a complex effect on several components of metabolic syndrome at once. Potentially attractive in this regard is a new group of drugs for the treatment of type 2 diabetes mellitus – inhibitors of the sodium-glucose cotransporter of type 2, which, in addition to the main hypoglycemic actions, showed positive effects on the cardiovascular system, kidneys, as well as lowering UA.

        Кeywords: gout, hyperuricemia, uric acid, sodium glucose cotransporter type 2, dapagliflozin, empaglizflozin, canagliflozin, ipragliflozin.


        Список литературы
        1. Насонова В.А., Барскова В.Г. Ранние диагностика и лечение подагры – научно обоснованное требование улучшения трудового и жизненного прогноза больных. Научно-практическая ревматология. 2004;42(1):5-7 [Nasonova VA, Barskova VG. Early diagnostic and treatment of gout – is scientifically based reguirements for improvement of labour and living prognosis of patients. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2004;42(1):5-7 (In Russ.)]. doi: 10.14412/1995-4484-2004-1374
        2. Насонов Е.Л., Елисеев М.С. Роль интерлейкина 1 в развитии заболеваний человека. Научно-практическая ревматология. 2016;54(1):60-77 [Nasonov EL, Eliseev MS. Role of interleukin 1 in the development ofhuman diseases. Nauchno-prakticheskaya revmatologiya = Rheumatology Science and Practice. 2016;54(1):60-77 (In Russ.)]. doi: 10.14412/1995-4484-2016-60-77
        3. Shiozawa A, Szabo SM, Bolzani A, et al. Serum Uric Acid and the Risk of Incident and Recurrent Gout: A Systematic Review. J Rheumatol. 2017;44(3):388-96. doi: 10.3899/jrheum.160452
        4. Loeb JN. The influence of temperature on the solubility of monosodium urate. Arthritis Rheumatism. 1972;15(2):189-92. doi: 10.1002/art.1780150209
        5. Cicero AFG, Fogacci F, Giovannini M, et al. Serum uric acid predicts incident metabolic syndrome in the elderly in an analysis of the Brisighella Heart Study. Sci Reports. 2018;8(1). doi: 10.1038/s41598-018-29955-w
        6. Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014;26(2):186-91. doi: 10.1097/bor.0000000000000028
        7. Laws A, Reaven GM. Evidence for an independent relationship between insulin resistance and fasting plasma HDL-cholesterol, triglyceride and insulin concentrations. J Int Med. 1992;231(1):25-30. doi: 10.1111/j.1365-2796.1992.tb00494.x
        8. Abbasian M, Ebrahimi H, Delvarianzadeh M, et al. Association between serum uric acid (SUA) levels and metabolic syndrome (MetS) components in personnel of Shahroud University of Medical Sciences. Diabetes & Metabolic Syndrome. Clin Res Rev. 2016;10(3):132-6. doi: 10.1016/j.dsx.2016.01.003
        9. Verdecchia P, Schillaci G, Reboldi G, et al. Relation Between Serum Uric Acid and Risk of Cardiovascular Disease in Essential Hypertension. Hypertension. 2000;36(6):1072-8. doi: 10.1161/01.hyp.36.6.1072
        10. Zuo T, Liu X, Jiang L, et al. Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies. BMC Cardiovasc Dis. 2016;16(1):207. doi: 10.1186/s12872-016-0379-z71
        11. White J, Sofat R, Hemani G, et al. Plasma urate concentration and risk of coronary heart disease: a Mendelian randomisation analysis. Lancet Diabet Endocrinol. 2016;4(4):327-36. doi: 10.1016/S2213-8587(15)00386-1
        12. Hyndman D, Liu S, Miner JN. Urate Handling in the Human Body. Curr Rheumatol Rep. 2016;18:34. doi: 10.1007/s11926-016-0587-7
        13. Richette P, Doherty M, Pascual E, et al. 2018 updated European League Against Rheumatism evidence-based recommendations for the diagnosis of gout. Ann Rheum Dis. 2020;79(Issue 1). doi: 10.1136/annrheumdis-2019-215315
        14. Khanna D, Fitzgerald JD, Khanna PP, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic non pharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res. 2012;64(10):1431-46. doi: 10.1002/acr.21772
        15. Елисеев М.С. Подагра. В кн.: Ревматология. Российские клинические рекомендации. Под ред. Е.Л. Насонова. М.: ГЭОТАР-Медиа, 2017; с. 253-64 [Eliseev MS. Podagra. V kn.: Revmatologiia. Rossiiskie klinicheskie rekomendatsii. Pod red. EL Nasonova. Moscow: GEOTAR-Media, 2017; p. 253-64 (In Russ.)].
        16. Барскова В.Г., Елисеев М.С., Кудаева Ф.М. и др. Влияние метформина на течение подагры и инсулинорезистентность. Клиническая медицина. 2009;87(7):41-6 [Barskova VG, Eliseev MS, Kudaeva FM, et al. Effect of metformine on the clinical course of gout and insulin resistance. Clinical medicine. 2009;87(7):41-6 (In Russ.)].
        17. Niu S-W, Chang K-T, Lin HY-H, et al. Decreased incidence of gout in diabetic patients using pioglitazone. Rheumatology. 2017;57(1):92-9. doi: 10.1093/rheumatology/kex363
        18. Vallon V. The Mechanisms and Therapeutic Potential of SGLT2 Inhibitors in Diabetes Mellitus. Ann Rev Med. 2015;66(1):255-70. doi: 10.1146/annurev-med-051013-110046
        19. Buchanan KD. Diabetes mellitus and gout. Semin Arthritis Rheumatism. 1972;2(2):157-63. doi: 10.1016/0049-0172(72)90007-8
        20. Tung Y-C, Lee S-S, Tsai W-C, et al. Association Between Gout and Incident Type 2 Diabetes Mellitus: A Retrospective Cohort Study. Am J Med. 2016;129(11):1219.e17-1219.e25. doi: 10.1016/j.amjmed.2016.06.041
        21. Collier A, Stirling A, Cameron L, et al. Gout and diabetes: a common combination. Postgrad Med J. 2016;92(1089):372-8. doi: 10.1136/
        postgradmedj-2015-133691
        22. Bhole V, Choi JWJ, Woo Kim S, et al. Serum Uric Acid Levels and the Risk of Type 2 Diabetes: A Prospective Study. Am J Med. 2010;123(10):957-61. doi: 10.1016/j.amjmed.2010.03.027
        23. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15. doi: 10.1002/art.22466
        24. Елисеев М.С., Барскова В.Г. Нарушения углеводного обмена при подагре: частота выявления и клинические особенности. Терапевтический архив. 2010;82(5):50-4 [Eliseev MS, Barskova VG. Carbo-hydrate metabolic disturbances in gout: Detection rate and clinical features. Therapeutic Archive. 2010;82(5):50-4 (In Russ.)].
        25. Liu J, Tao L, Zhao Z, et al. Two-Year Changes in Hyperuricemia and Risk of Diabetes: A Five-Year Prospective Cohort Study. J Diabet Res. 2018;2018:1-7. doi: 10.1155/2018/6905720
        26. Choi BG, Kim DJ, Baek MJ, et al. Hyperuricaemia and development of type 2 diabetes mellitus in Asian population. Clin Exper Pharmacol Physiol. 2018;45(6):499-506. doi: 10.1111/1440-1681.12911
        27. Shani M, Vinker S, Dinour D, et al. High Normal Uric Acid Levels Are Associated with an Increased Risk of Diabetes in Lean, Normoglycemic Healthy Women. J Clin Endocrinol Metab. 2016;101(10):3772-8. doi: 10.1210/jc.2016-2107
        28. Li L, Yang C, Zhao Y, et al. Is hyperuricemia an independent risk factor for new-onset chronic kidney disease: a systematic review and meta-analysis based on observational cohort studies. BMC Nephrology. 2014;15(1). doi: 10.1186/1471-2369-15-122
        29. De Cosmo S, Viazzi F, Pacilli A, et al. Serum Uric Acid and Risk of CKD in Type 2 Diabetes. Clin J Am Soc Nephrol. 2015;10(11):1921-9. doi: 10.2215/cjn.03140315
        30. Ito H, Abe M, Mifune M, et al. Hyperuricemia Is Independently Associated with Coronary Heart Disease and Renal Dysfunction in Patients with Type 2 Diabetes Mellitus. Sesti G, editor. PLoS ONE. 2011;6(11):e27817. doi: 10.1371/journal.pone.0027817
        31. Choi Y-J, Yoon Y, Lee K-Y, et al. Uric acid induces endothelial dysfunction by vascular insulin resistance associated with the impairment of nitric oxide synthesis. FASEB J. 2014;28(7):3197-204. doi: 10.1096/fj.13-247148
        32. Fabbrini E, Serafini M, Colic Baric I, et al. Effect of Plasma Uric Acid on Antioxidant Capacity, Oxidative Stress, and Insulin Sensitivity in Obese Subjects. Diabetes. 2013;63(3):976-81. doi: 10.2337/db13-1396
        33. Glantzounis G, Tsimoyiannis E, Kappas A, Galaris D. Uric Acid and Oxidative Stress. Curr Pharm Design. 2005;11(32):4145-51. doi: 10.2174/138161205774913255
        34. Kuwabara M, Niwa K, Hisatome I, et al. Asymptomatic Hyperuricemia Without Comorbidities Predicts Cardiometabolic Diseases. Hypertension. 2017;69(6):1036-44. doi: 10.1161/hypertensionaha.116.08998
        35. Fonseca VA. Defining and Characterizing the Progression of Type 2 Diabetes. Diabetes Care. 2009;32(Suppl. 2):S151-S156. doi: 10.2337/dc09-s301
        36. Li C, Hsieh MC, Chang SJ. Metabolic syndrome, diabetes, and hyperuricemia. Curr Opin Rheumatol. 2013;25(2):210-6. doi: 10.1097/BOR.0b013e32835d951e
        37. Dessein PH. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000;59(7):539-43. doi: 10.1136/ard.59.7.539
        38. Bruderer SG, Bodmer M, Jick SS, Meier CR. Poorly controlled type 2 diabetes mellitus is associated with a decreased risk of incident gout: a population-based case-control study. Ann Rheum Dis. 2014;74(9):1651-8. doi: 10.1136/annrheumdis-2014-205337
        39. Lin S-D, Tsai D-H, Hsu S-R. Association between serum uric acid level and components of the metabolic syndrome. J Chin Med Assoc. 2006;69(11):512-6. doi: 10.1016/s1726-4901(09)70320-x
        40. Rodríguez G, Soriano LC, Choi HK. Impact of diabetes against the future risk of developing gout. Ann Rheum Dis. 2010;69(12):2090-4. doi: 10.1136/ard.2010.130013
        41. Chen W, Liu X, Ye S. Effects of metformin on blood and urine proinflammatory mediators in patients with type 2 diabetes. J Inflamm (Lond). 2016;13:34. doi: 10.1186/s12950-016-0142-3
        42. Matsuura F, Yamashita S, Nakamura T, et al. Effects of visceral fat accumulation on uric acid metabolism in male obese subjects: visceral fat obesity is linked more closely to overproduction of uric acid than sub-cutaneous fat obesity. Metabolism. 1998;47:929-33. doi: 10.1016/S0026-0495(98)90346-8
        43. Chung YH, Kim DH, Lee WW. Monosodium urate crystal-induced pro-interleukin-1β production is post-transcriptionally regulated via the p38 signaling pathway in human monocytes. Sci Reports. 2016;6(1). doi: 10.1038/srep34533
        44. Vazirpanah N, Ottria A, van der Linden M, et al. mTOR inhibition by metformin impacts monosodium urate crystal-induced inflammation and cell death in gout: a prelude to a new add-on therapy? Ann Rheum Dis. 2019;78(5):663-71. doi: 10.1136/annrheumdis-2018-214656
        45. Мадянов И.В., Балаболкин М.И., Марков Д.С., Маркова Т.Н. Основные причины гиперурикемии при сахарном диабете. Терапевтический архив. 2000;72(2):55-8 [Madianov IV, Balabolkin MI, Markov DS, Markova TN. Main causes of hyperuricemia in diabetes mellitus. Therapeutic Archive. 2000;72(2):55-8 (In Russ.)].
        46. Feig DI. Uric Acid and Hypertension. Semin Nephrol. 2011;31(5):441-6. doi: 10.1016/j.semnephrol.2011.08.008
        47. Washburn WN, Poucher SM. Differentiating sodium-glucose co-transporter-2 inhibitors in development for the treatment of type 2 diabetes mellitus. Expert Opin Invest Drugs. 2013;22(4):463-86. doi: 10.1517/13543784.2013.774372
        48. Scheen AJ, Paquot N. Metabolic effects of SGLT-2 inhibitors beyond increased glucosuria: A review of the clinical evidence. Diabet Metab. 2014;40(6):S4-S11. doi: 10.1016/s1262-3636(14)72689-8
        49. Vasilakou D, Karagiannis T, Athanasiadou E, et al. Sodium-Glucose Cotransporter 2 Inhibitors for Type 2 Diabetes. Ann Intern Med. 2013;159(4):262. doi: 10.7326/0003-4819-159-4-201308200-00007
        50. Berhan A, Barker A. Sodium glucose co-transport 2 inhibitors in the treatment of type 2 diabetes mellitus: a meta-analysis of randomized double-blind controlled trials. BMC Endocrine Dis. 2013;13(1). doi: 10.1186/1472-6823-13-58
        51. Idris I, Donnelly R. Sodium-glucose co-transporter-2 inhibitors: an emerging new class of oral antidiabetic drug. Diabet Obes Metab. 2009;11(2):79-88. doi: 10.1111/j.1463-1326.2008.00982.x
        52. Kalra S. Sodium Glucose Co-Transporter-2 (SGLT2) Inhibitors: A Review of Their Basic and Clinical Pharmacology. Diabet Ther. 2014;5(2):355-66. doi: 10.1007/s13300-014-0089-4
        53. Дедов И.И., Шестакова М.В., Майоров А.Ю. и др. Алгоритмы специализированной медицинской помощи больным сахарным диабетом. 
        9-й вып. Сахарный диабет. 2019;22(1S1):1-144 [Dedov II, Shestakova, MV, Mayorov AY, et al. Standards of specialized diabetes care. 9th edition. Diabetes Mellitus. 2019;22(1S1):1-144 (In Russ.)]. doi: 10.14341/DM221S1
        54. List JF, Woo V, Morales E, et al. Sodium-Glucose Cotransport Inhibition With Dapagliflozin in Type 2 Diabetes. Diabetes Care. 2008;32(4):650-7. doi: 10.2337/dc08-1863
        55. Roden M, Merker L, Christiansen AV, et al. Safety, tolerability and effects on cardiometabolic risk factors of empagliflozin monotherapy in drug-naïve patients with type 2 diabetes: a double-blind extension of a Phase III randomized controlled trial. Cardiovasc Diabetol. 2015;14(1). doi: 10.1186/s12933-015-0314-0
        56. Davies MJ, Trujillo A, Vijapurkar U, et al. Effect of canagliflozin on serum uric acid in patients with type 2 diabetes mellitus. Diabet Obes Metab. 2015;17(4):426-9. doi: 10.1111/dom.12439
        57. Zhao Y, Xu L, Tian D, et al. Effects of sodium-glucose co-transporter 2 (SGLT2) inhibitors on serum uric acid level: A meta-analysis of randomized controlled trials. Diabet Obes Metab. 2017;20(2):458-62. doi: 10.1111/dom.13101
        58. Xin Y, Guo Y, Li Y, et al. Effects of sodium glucose cotransporter-2 inhibitors on serum uric acid in type 2 diabetes mellitus: A systematic review with an indirect comparison meta-analysis. Saudi J Biol Sci. 2019;26(2):421-6. doi: 10.1016/j.sjbs.2018.11.013
        59. Li J, Badve SV, Zhou Z, et al. The effects of canagliflozin on gout in type 2 diabetes: a post-hoc analysis of the CANVAS Program. Lancet Rheum. 2019;1(4):e220-e228. doi: 10.1016/s2665-9913(19)30078-5
        60. Chao EC. SGLT-2 Inhibitors: A New Mechanism for Glycemic Control. Clin Diabet. 2014;32(1):4-11. doi: 10.2337/diaclin.32.1.4
        61. Poudel R. Renal glucose handling in diabetes and sodium glucose cotransporter 2 inhibition. Ind J Endocrin Metab. 2013;17(4):588. doi: 10.4103/2230-8210.113725
        62. McGill JB. The SGLT2 Inhibitor Empagliflozin for the Treatment of Type 2 Diabetes Mellitus: a Bench to Bedside Review. Diabet Ther. 2014;5(1):43-63. doi: 10.1007/s13300-014-0063-1
        63. Doblado M, Moley KH. Facilitative glucose transporter 9, a unique hexose and urate transporter. Am J Physiol-Endocrinol Metab. 2009;297(4):E831-E835. doi: 10.1152/ajpendo.00296.2009
        64. Caulfield MJ, Munroe PB, O’Neill D, et al. SLC2A9 Is a High-Capacity Urate Transporter in Humans. Hattersley A, editor. PLoS Med. 2008;5(10):e197. doi: 10.1371/journal.pmed.0050197
        65. Chino Y, Samukawa Y, Sakai S, et al. SGLT2 inhibitor lowers serum uric acid through alteration of uric acid transport activity in renal tubule by increased glycosuria. Biopharm Drug Disposit. 2014;35(7):391-404. doi: 10.1002/bdd.1909
        66. Li S, Sanna S, Maschio A, et al. The GLUT9 Gene Is Associated with Serum Uric Acid Levels in Sardinia and Chianti Cohorts. PLoS Genet. 2007;3(11):e194. doi: 10.1371/journal.pgen.0030194
        67. Satirapoj B, Adler SG. Comprehensive approach to diabetic nephropathy. Kidney Res Clin Pract. 2014;33:121-31. doi: 10.1016/j.krcp.2014.08.001
        68. Maeda S, Matsui T, Takeuchi M, Yamagishi S. Sodium-glucose cotransporter 2-mediated oxidative stress augments advanced glycation end products-induced tubular cell apoptosis. Diabet Metab Res Rev. 2013;29(5):406-12. doi: 10.1002/dmrr.2407
        69. Kawanami D, Matoba K, Takeda Y, et al. SGLT2 Inhibitors as a Therapeutic Option for Diabetic Nephropathy. Int J Mol Sci. 2017;18(5):1083. doi: 10.3390/ijms18051083
        70. Ojima A, Matsui T, Nishino Y, et al. Empagliflozin, an Inhibitor of Sodium-Glucose Cotransporter 2 Exerts Anti-Inflammatory and Antifibrotic Effects on Experimental Diabetic Nephropathy Partly by Suppressing AGEs-Receptor Axis. Hormone Metab Res. 2015;47(09):686-92. doi: 10.1055/s-0034-1395609
        71. Dekkers CJ, Petrykiv S, Laverman GD, et al. Effects of the SGLT-2 inhibitor dapagliflozin on glomerular and tubular injury markers. Diabet Obes Metab. 2018;20(8):1988-93. doi: 10.1111/dom.13301
        72. Shimazu T, Hirschey MD, Newman J, et al. Suppression of Oxidative Stress by-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor. Science. 2012;339(6116):211-4. doi: 10.1126/science.1227166
        73. Hill NR, Fatoba ST, Oke JL, et al. Global Prevalence of Chronic Kidney Disease – A Systematic Review and Meta-Analysis. Remuzzi G, editor. PLOS One. 2016;11(7):e0158765. doi: 10.1371/journal.pone.0158765
        74. Vallon V, Gerasimova M, Rose MA, et al. SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice. Am J Physiol-Renal Physiol. 2014;306(2):F194-F204. doi: 10.1152/ajprenal.00520.2013
        75. Liao X, Wang X, Li H, et al. Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor Increases Circulating Zinc-Α2-Glycoprotein Levels in Patients with Type 2 Diabetes. Sci Reports. 2016;6(1). doi: 10.1038/srep32887
        76. Mancini SJ, Boyd D, Katwan OJ, et al. Canagliflozin inhibits interleukin-1β-stimulated cytokine and chemokine secretion in vascular endothelial cells by AMP-activated protein kinase-dependent and -independent mechanisms. Sci Reports. 2018;8(1). doi: 10.1038/s41598-018-23420-4
        77. Maldonado-Cervantes MI, Galicia OG, Moreno-Jaime B, et al. Autocrine modulation of glucose transporter SGLT2 by IL-6 and TNF-α in LLC-PK1 cells. J Physiol Biochem. 2012;68(3):411-20. doi: 10.1007/s13105-012-0153-3
        78. Scheen AJ, Van Gaal LF. Combating the dual burden: therapeutic targeting of common pathways in obesity and type 2 diabetes. Lancet Diabet Endocrinol. 2014;2(11):911-22. doi: 10.1016/s2213-8587(14)70004-x
        79. Barnett AH. Impact of sodium glucose cotransporter 2 inhibitors on weight in patients with type 2 diabetes mellitus. Postgrad Med. 2013;125:92-100. doi: 10.3810/pgm.2013.09.2698
        80. Vasilakou D, Karagiannis T, Athanasiadou E, et al. Sodium-Glucose Cotransporter 2 Inhibitors for Type 2 Diabetes. Ann Int Med. 2013;159(4):262. doi: 10.7326/0003-4819-159-4-201308200-00007
        81. Liu X-Y, Zhang N, Chen R, et al. Efficacy and safety of sodium–glucose cotransporter 2 inhibitors in type 2 diabetes: a meta-analysis of randomized controlled trials for 1 to 2 years. J Diabet Complicat. 2015;29(8):1295-303. doi: 10.1016/j.jdiacomp.2015.07.011
        82. Ferrannini G, Hach T, Crowe S, et al. Energy Balance After Sodium-Glucose Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1730-5. doi: 10.2337/dc15-0355
        83. Ladwig K-H, Marten-Mittag B, Löwel H, et al. Influence of depressive mood on the association of CRP and obesity in 3205 middle aged healthy men. Brain, Behav Immun. 2003;17(4):268-75. doi: 10.1016/s0889-1591(03)00056-4
        84. Bochud M, Marquant F, Marques-Vidal P-M, et al. Association between C-Reactive Protein and Adiposity in Women. J Clin Endocrinol Metab. 2009;94(10):3969-77. doi: 10.1210/jc.2008-2428
        85. Jung U, Choi M-S. Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease. Int J Mol Sci. 2014;15(4):6184-223. doi: 10.3390/ijms15046184
        86. Yaribeygi H, Butler AE, Atkin SL, et al. Sodium-glucose cotransporter 2 inhibitors and inflammation in chronic kidney disease: Possible molecular pathways. J Cell Physiol. 2018;234(1):223-30. doi: 10.1002/jcp.26851
        87. Kuriyama S. Protection of the kidney with sodium-glucose cotransporter 2 inhibitors: potential mechanisms raised by the large-scaled randomized control trials. Clin Exper Nephrol. 2018;23(3):304-12. doi: 10.1007/s10157-018-1673-0
        88. Maliha G, Townsend RR. SGLT2 inhibitors: their potential reduction in blood pressure. J Am Soc Hypertens. 2015;9(1):48-53. doi: 10.1016/j.jash.2014.11.001
        89. Baker WL, Smyth LR, Riche DM, et al. Effects of sodium-glucose co-transporter 2 inhibitors on blood pressure: A systematic review and meta-analysis. J Am Soc Hypertens. 2014;8(4):262-75.e9. doi: 10.1016/j.jash.2014.01.007
        90. Sano M, Chen S, Imazeki H, et al. Changes in heart rate in patients with type 2 diabetes mellitus after treatment with luseogliflozin: Subanalysis of placebo-controlled, double-blind clinical trials. J Diabet Invest. 2018;9(3):638-41. doi: 10.1111/jdi.12726
        91. Wu JHY, Foote C, Blomster J, et al. Effects of sodium-glucose cotransporter-2 inhibitors on cardiovascular events, death, and major safety outcomes in adults with type 2 diabetes: a systematic review and meta-analysis. Lancet Diabet Endocrinol. 2016;4(5):411-9. doi: 10.1016/s2213-8587(16)00052-8
        92. Ptaszynska A, Johnsson KM, Parikh SJ, et al. Safety Profile of Dapagliflozin for Type 2 Diabetes: Pooled Analysis of Clinical Studies for Overall Safety and Rare Events. Drug Safety. 2014;37(10):815-29. doi: 10.1007/s40264-014-0213-4
        93. Johnsson KM, Ptaszynska A, Schmitz B, et al. Urinary tract infections in patients with diabetes treated with dapagliflozin. J Diabet Complicat. 2013;27:473-8. doi: 10.1016/j.jdiacomp.2013.05.004
        94. Peters AL, Buschur EO, Buse JB, et al. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With Sodium-Glucose 
        Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1687-93. doi: 10.2337/dc15-0843
        95. Bonner C, Kerr-Conte J, Gmyr V, et al. Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion. Nature Med. 2015;21(5):512-7. doi: 10.1038/nm.3828
        96. Kalra S, Gupta Y, Patil S. Sodium-glucose cotransporter-2 inhibition and the insulin: Glucagon ratio: Unexplored dimensions. Ind J Endocrinol Metab. 2015;19(3):426. doi: 10.4103/2230-8210.152793
        97. Rosenstock J, Ferrannini E. Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, and Preventable Safety Concern With SGLT2 Inhibitors. Diabet Care. 2015;38(9):1638-42. doi: 10.2337/dc15-1380
        98. Zhang M, Zhang L, Wu B, et al. Dapagliflozin treatment for type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials. Diabet/Metab Res Rev. 2014;30(3):204-21. doi: 10.1002/dmrr.2479
        99. Meier C, Schwartz AV, Egger A, Lecka-Czernik B. Effects of diabetes drugs on the skeleton. Bone. 2016;82:93-100. doi: 10.1016/j.bone.2015.04.026
        100. Ljunggren Ö, Bolinder J, Johansson L, et al. Dapagliflozin has no effect on markers of bone formation and resorption or bone mineral density in patients with inadequately controlled type 2 diabetes mellitus on metformin. Diabet Obes Metab. 2012;14(11):990-9. doi: 10.1111/j.1463-1326.2012.01630.x
        101. Bolinder J, Ljunggren Ö, Johansson L, et al. Dapagliflozin maintains glycaemic control while reducing weight and body fat mass over 2 years in patients with type 2 diabetes mellitus inadequately controlled on metformin. Diabet Obes Metab. 2013;16(2):159-69. doi: 10.1111/dom.12189
        102. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. New Engl J Med. 2015;373(22):2117-28. doi: 10.1056/nejmoa1504720
        103. Wanner C, Inzucchi SE, Lachin JM, et al. Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes. New Engl J Med. 2016;375(4):323-34. doi: 10.1056/nejmoa1515920
        104. Ptaszynska A, Cohen SM, Messing EM, et al. Assessing Bladder Cancer Risk in Type 2 Diabetes Clinical Trials: the Dapagliflozin Drug Development Program as a "Case Study". Diabet Ther. 2015;6(3):357-75. doi: 10.1007/s13300-015-0128-9
        105. Yang H-C, Nguyen PAA, Islam M, et al. Gout drugs use and risk of cancer: A case-control study. Joint Bone Spine. 2018;85(6):747-53. doi: 10.1016/j.jbspin.2018.01.008
        106. Lin H-W, Tseng C-H. A Review on the Relationship between SGLT2 Inhibitors and Cancer. Int J Endocrinol. 2014;2014:1-6. doi: 10.1155/2014/719578
        107. Neal B, Perkovic V, Mahaffey KW, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes. New Engl J Med. 2017;377(7):644-57. doi: 10.1056/nejmoa1611925
        108. Hallow KM, Helmlinger G, Greasley PJ, et al. Why do SGLT2 inhibitors reduce heart failure hospitalization? A differential volume regulation hypothesis. Diabet Obes Metab. 2018;20(3):479-87. doi: 10.1111/dom.13126


        ________________________________________________

        1. Nasonova VA, Barskova VG. Early diagnostic and treatment of gout – is scientifically based reguirements for improvement of labour and living prognosis of patients. Nauchno-Prakticheskaya Revmatologiya = Rheumatology Science and Practice. 2004;42(1):5-7 (In Russ.) doi: 10.14412/1995-4484-2004-1374
        2. Nasonov EL, Eliseev MS. Role of interleukin 1 in the development ofhuman diseases. Nauchno-prakticheskaya revmatologiya = Rheumatology Science and Practice. 2016;54(1):60-77 (In Russ.) doi: 10.14412/1995-4484-2016-60-77
        3. Shiozawa A, Szabo SM, Bolzani A, et al. Serum Uric Acid and the Risk of Incident and Recurrent Gout: A Systematic Review. J Rheumatol. 2017;44(3):388-96. doi: 10.3899/jrheum.160452
        4. Loeb JN. The influence of temperature on the solubility of monosodium urate. Arthritis Rheumatism. 1972;15(2):189-92. doi: 10.1002/art.1780150209
        5. Cicero AFG, Fogacci F, Giovannini M, et al. Serum uric acid predicts incident metabolic syndrome in the elderly in an analysis of the Brisighella Heart Study. Sci Reports. 2018;8(1). doi: 10.1038/s41598-018-29955-w
        6. Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol. 2014;26(2):186-91. doi: 10.1097/bor.0000000000000028
        7. Laws A, Reaven GM. Evidence for an independent relationship between insulin resistance and fasting plasma HDL-cholesterol, triglyceride and insulin concentrations. J Int Med. 1992;231(1):25-30. doi: 10.1111/j.1365-2796.1992.tb00494.x
        8. Abbasian M, Ebrahimi H, Delvarianzadeh M, et al. Association between serum uric acid (SUA) levels and metabolic syndrome (MetS) components in personnel of Shahroud University of Medical Sciences. Diabetes & Metabolic Syndrome. Clin Res Rev. 2016;10(3):132-6. doi: 10.1016/j.dsx.2016.01.003
        9. Verdecchia P, Schillaci G, Reboldi G, et al. Relation Between Serum Uric Acid and Risk of Cardiovascular Disease in Essential Hypertension. Hypertension. 2000;36(6):1072-8. doi: 10.1161/01.hyp.36.6.1072
        10. Zuo T, Liu X, Jiang L, et al. Hyperuricemia and coronary heart disease mortality: a meta-analysis of prospective cohort studies. BMC Cardiovasc Dis. 2016;16(1):207. doi: 10.1186/s12872-016-0379-z71
        11. White J, Sofat R, Hemani G, et al. Plasma urate concentration and risk of coronary heart disease: a Mendelian randomisation analysis. Lancet Diabet Endocrinol. 2016;4(4):327-36. doi: 10.1016/S2213-8587(15)00386-1
        12. Hyndman D, Liu S, Miner JN. Urate Handling in the Human Body. Curr Rheumatol Rep. 2016;18:34. doi: 10.1007/s11926-016-0587-7
        13. Richette P, Doherty M, Pascual E, et al. 2018 updated European League Against Rheumatism evidence-based recommendations for the diagnosis of gout. Ann Rheum Dis. 2020;79(Issue 1). doi: 10.1136/annrheumdis-2019-215315
        14. Khanna D, Fitzgerald JD, Khanna PP, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic non pharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res. 2012;64(10):1431-46. doi: 10.1002/acr.21772
        15. Eliseev MS. Podagra. V kn.: Revmatologiia. Rossiiskie klinicheskie rekomendatsii. Pod red. EL Nasonova. Moscow: GEOTAR-Media, 2017; p. 253-64 (In Russ.)
        16. Barskova VG, Eliseev MS, Kudaeva FM, et al. Effect of metformine on the clinical course of gout and insulin resistance. Clinical medicine. 2009;87(7):41-6 (In Russ.)
        17. Niu S-W, Chang K-T, Lin HY-H, et al. Decreased incidence of gout in diabetic patients using pioglitazone. Rheumatology. 2017;57(1):92-9. doi: 10.1093/rheumatology/kex363
        18. Vallon V. The Mechanisms and Therapeutic Potential of SGLT2 Inhibitors in Diabetes Mellitus. Ann Rev Med. 2015;66(1):255-70. doi: 10.1146/annurev-med-051013-110046
        19. Buchanan KD. Diabetes mellitus and gout. Semin Arthritis Rheumatism. 1972;2(2):157-63. doi: 10.1016/0049-0172(72)90007-8
        20. Tung Y-C, Lee S-S, Tsai W-C, et al. Association Between Gout and Incident Type 2 Diabetes Mellitus: A Retrospective Cohort Study. Am J Med. 2016;129(11):1219.e17-1219.e25. doi: 10.1016/j.amjmed.2016.06.041
        21. Collier A, Stirling A, Cameron L, et al. Gout and diabetes: a common combination. Postgrad Med J. 2016;92(1089):372-8. doi: 10.1136/
        postgradmedj-2015-133691
        22. Bhole V, Choi JWJ, Woo Kim S, et al. Serum Uric Acid Levels and the Risk of Type 2 Diabetes: A Prospective Study. Am J Med. 2010;123(10):957-61. doi: 10.1016/j.amjmed.2010.03.027
        23. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15. doi: 10.1002/art.22466
        24. Елисеев М.С., Барскова В.Г. Нарушения углеводного обмена при подагре: частота выявления и клинические особенности. Терапевтический архив. 2010;82(5):50-4 [Eliseev MS, Barskova VG. Carbo-hydrate metabolic disturbances in gout: Detection rate and clinical features. Therapeutic Archive. 2010;82(5):50-4 (In Russ.)].
        25. Liu J, Tao L, Zhao Z, et al. Two-Year Changes in Hyperuricemia and Risk of Diabetes: A Five-Year Prospective Cohort Study. J Diabet Res. 2018;2018:1-7. doi: 10.1155/2018/6905720
        26. Choi BG, Kim DJ, Baek MJ, et al. Hyperuricaemia and development of type 2 diabetes mellitus in Asian population. Clin Exper Pharmacol Physiol. 2018;45(6):499-506. doi: 10.1111/1440-1681.12911
        27. Shani M, Vinker S, Dinour D, et al. High Normal Uric Acid Levels Are Associated with an Increased Risk of Diabetes in Lean, Normoglycemic Healthy Women. J Clin Endocrinol Metab. 2016;101(10):3772-8. doi: 10.1210/jc.2016-2107
        28. Li L, Yang C, Zhao Y, et al. Is hyperuricemia an independent risk factor for new-onset chronic kidney disease: a systematic review and meta-analysis based on observational cohort studies. BMC Nephrology. 2014;15(1). doi: 10.1186/1471-2369-15-122
        29. De Cosmo S, Viazzi F, Pacilli A, et al. Serum Uric Acid and Risk of CKD in Type 2 Diabetes. Clin J Am Soc Nephrol. 2015;10(11):1921-9. doi: 10.2215/cjn.03140315
        30. Ito H, Abe M, Mifune M, et al. Hyperuricemia Is Independently Associated with Coronary Heart Disease and Renal Dysfunction in Patients with Type 2 Diabetes Mellitus. Sesti G, editor. PLoS ONE. 2011;6(11):e27817. doi: 10.1371/journal.pone.0027817
        31. Choi Y-J, Yoon Y, Lee K-Y, et al. Uric acid induces endothelial dysfunction by vascular insulin resistance associated with the impairment of nitric oxide synthesis. FASEB J. 2014;28(7):3197-204. doi: 10.1096/fj.13-247148
        32. Fabbrini E, Serafini M, Colic Baric I, et al. Effect of Plasma Uric Acid on Antioxidant Capacity, Oxidative Stress, and Insulin Sensitivity in Obese Subjects. Diabetes. 2013;63(3):976-81. doi: 10.2337/db13-1396
        33. Glantzounis G, Tsimoyiannis E, Kappas A, Galaris D. Uric Acid and Oxidative Stress. Curr Pharm Design. 2005;11(32):4145-51. doi: 10.2174/138161205774913255
        34. Kuwabara M, Niwa K, Hisatome I, et al. Asymptomatic Hyperuricemia Without Comorbidities Predicts Cardiometabolic Diseases. Hypertension. 2017;69(6):1036-44. doi: 10.1161/hypertensionaha.116.08998
        35. Fonseca VA. Defining and Characterizing the Progression of Type 2 Diabetes. Diabetes Care. 2009;32(Suppl. 2):S151-S156. doi: 10.2337/dc09-s301
        36. Li C, Hsieh MC, Chang SJ. Metabolic syndrome, diabetes, and hyperuricemia. Curr Opin Rheumatol. 2013;25(2):210-6. doi: 10.1097/BOR.0b013e32835d951e
        37. Dessein PH. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000;59(7):539-43. doi: 10.1136/ard.59.7.539
        38. Bruderer SG, Bodmer M, Jick SS, Meier CR. Poorly controlled type 2 diabetes mellitus is associated with a decreased risk of incident gout: a population-based case-control study. Ann Rheum Dis. 2014;74(9):1651-8. doi: 10.1136/annrheumdis-2014-205337
        39. Lin S-D, Tsai D-H, Hsu S-R. Association between serum uric acid level and components of the metabolic syndrome. J Chin Med Assoc. 2006;69(11):512-6. doi: 10.1016/s1726-4901(09)70320-x
        40. Rodríguez G, Soriano LC, Choi HK. Impact of diabetes against the future risk of developing gout. Ann Rheum Dis. 2010;69(12):2090-4. doi: 10.1136/ard.2010.130013
        41. Chen W, Liu X, Ye S. Effects of metformin on blood and urine proinflammatory mediators in patients with type 2 diabetes. J Inflamm (Lond). 2016;13:34. doi: 10.1186/s12950-016-0142-3
        42. Matsuura F, Yamashita S, Nakamura T, et al. Effects of visceral fat accumulation on uric acid metabolism in male obese subjects: visceral fat obesity is linked more closely to overproduction of uric acid than sub-cutaneous fat obesity. Metabolism. 1998;47:929-33. doi: 10.1016/S0026-0495(98)90346-8
        43. Chung YH, Kim DH, Lee WW. Monosodium urate crystal-induced pro-interleukin-1β production is post-transcriptionally regulated via the p38 signaling pathway in human monocytes. Sci Reports. 2016;6(1). doi: 10.1038/srep34533
        44. Vazirpanah N, Ottria A, van der Linden M, et al. mTOR inhibition by metformin impacts monosodium urate crystal-induced inflammation and cell death in gout: a prelude to a new add-on therapy? Ann Rheum Dis. 2019;78(5):663-71. doi: 10.1136/annrheumdis-2018-214656
        45. Madianov IV, Balabolkin MI, Markov DS, Markova TN. Main causes of hyperuricemia in diabetes mellitus. Therapeutic Archive. 2000;72(2):55-8 (In Russ.)
        46. Feig DI. Uric Acid and Hypertension. Semin Nephrol. 2011;31(5):441-6. doi: 10.1016/j.semnephrol.2011.08.008
        47. Washburn WN, Poucher SM. Differentiating sodium-glucose co-transporter-2 inhibitors in development for the treatment of type 2 diabetes mellitus. Expert Opin Invest Drugs. 2013;22(4):463-86. doi: 10.1517/13543784.2013.774372
        48. Scheen AJ, Paquot N. Metabolic effects of SGLT-2 inhibitors beyond increased glucosuria: A review of the clinical evidence. Diabet Metab. 2014;40(6):S4-S11. doi: 10.1016/s1262-3636(14)72689-8
        49. Vasilakou D, Karagiannis T, Athanasiadou E, et al. Sodium-Glucose Cotransporter 2 Inhibitors for Type 2 Diabetes. Ann Intern Med. 2013;159(4):262. doi: 10.7326/0003-4819-159-4-201308200-00007
        50. Berhan A, Barker A. Sodium glucose co-transport 2 inhibitors in the treatment of type 2 diabetes mellitus: a meta-analysis of randomized double-blind controlled trials. BMC Endocrine Dis. 2013;13(1). doi: 10.1186/1472-6823-13-58
        51. Idris I, Donnelly R. Sodium-glucose co-transporter-2 inhibitors: an emerging new class of oral antidiabetic drug. Diabet Obes Metab. 2009;11(2):79-88. doi: 10.1111/j.1463-1326.2008.00982.x
        52. Kalra S. Sodium Glucose Co-Transporter-2 (SGLT2) Inhibitors: A Review of Their Basic and Clinical Pharmacology. Diabet Ther. 2014;5(2):355-66. doi: 10.1007/s13300-014-0089-4
        53. Dedov II, Shestakova, MV, Mayorov AY, et al. Standards of specialized diabetes care. 9th edition. Diabetes Mellitus. 2019;22(1S1):1-144 (In Russ.) doi: 10.14341/DM221S1
        54. List JF, Woo V, Morales E, et al. Sodium-Glucose Cotransport Inhibition With Dapagliflozin in Type 2 Diabetes. Diabetes Care. 2008;32(4):650-7. doi: 10.2337/dc08-1863
        55. Roden M, Merker L, Christiansen AV, et al. Safety, tolerability and effects on cardiometabolic risk factors of empagliflozin monotherapy in drug-naïve patients with type 2 diabetes: a double-blind extension of a Phase III randomized controlled trial. Cardiovasc Diabetol. 2015;14(1). doi: 10.1186/s12933-015-0314-0
        56. Davies MJ, Trujillo A, Vijapurkar U, et al. Effect of canagliflozin on serum uric acid in patients with type 2 diabetes mellitus. Diabet Obes Metab. 2015;17(4):426-9. doi: 10.1111/dom.12439
        57. Zhao Y, Xu L, Tian D, et al. Effects of sodium-glucose co-transporter 2 (SGLT2) inhibitors on serum uric acid level: A meta-analysis of randomized controlled trials. Diabet Obes Metab. 2017;20(2):458-62. doi: 10.1111/dom.13101
        58. Xin Y, Guo Y, Li Y, et al. Effects of sodium glucose cotransporter-2 inhibitors on serum uric acid in type 2 diabetes mellitus: A systematic review with an indirect comparison meta-analysis. Saudi J Biol Sci. 2019;26(2):421-6. doi: 10.1016/j.sjbs.2018.11.013
        59. Li J, Badve SV, Zhou Z, et al. The effects of canagliflozin on gout in type 2 diabetes: a post-hoc analysis of the CANVAS Program. Lancet Rheum. 2019;1(4):e220-e228. doi: 10.1016/s2665-9913(19)30078-5
        60. Chao EC. SGLT-2 Inhibitors: A New Mechanism for Glycemic Control. Clin Diabet. 2014;32(1):4-11. doi: 10.2337/diaclin.32.1.4
        61. Poudel R. Renal glucose handling in diabetes and sodium glucose cotransporter 2 inhibition. Ind J Endocrin Metab. 2013;17(4):588. doi: 10.4103/2230-8210.113725
        62. McGill JB. The SGLT2 Inhibitor Empagliflozin for the Treatment of Type 2 Diabetes Mellitus: a Bench to Bedside Review. Diabet Ther. 2014;5(1):43-63. doi: 10.1007/s13300-014-0063-1
        63. Doblado M, Moley KH. Facilitative glucose transporter 9, a unique hexose and urate transporter. Am J Physiol-Endocrinol Metab. 2009;297(4):E831-E835. doi: 10.1152/ajpendo.00296.2009
        64. Caulfield MJ, Munroe PB, O’Neill D, et al. SLC2A9 Is a High-Capacity Urate Transporter in Humans. Hattersley A, editor. PLoS Med. 2008;5(10):e197. doi: 10.1371/journal.pmed.0050197
        65. Chino Y, Samukawa Y, Sakai S, et al. SGLT2 inhibitor lowers serum uric acid through alteration of uric acid transport activity in renal tubule by increased glycosuria. Biopharm Drug Disposit. 2014;35(7):391-404. doi: 10.1002/bdd.1909
        66. Li S, Sanna S, Maschio A, et al. The GLUT9 Gene Is Associated with Serum Uric Acid Levels in Sardinia and Chianti Cohorts. PLoS Genet. 2007;3(11):e194. doi: 10.1371/journal.pgen.0030194
        67. Satirapoj B, Adler SG. Comprehensive approach to diabetic nephropathy. Kidney Res Clin Pract. 2014;33:121-31. doi: 10.1016/j.krcp.2014.08.001
        68. Maeda S, Matsui T, Takeuchi M, Yamagishi S. Sodium-glucose cotransporter 2-mediated oxidative stress augments advanced glycation end products-induced tubular cell apoptosis. Diabet Metab Res Rev. 2013;29(5):406-12. doi: 10.1002/dmrr.2407
        69. Kawanami D, Matoba K, Takeda Y, et al. SGLT2 Inhibitors as a Therapeutic Option for Diabetic Nephropathy. Int J Mol Sci. 2017;18(5):1083. doi: 10.3390/ijms18051083
        70. Ojima A, Matsui T, Nishino Y, et al. Empagliflozin, an Inhibitor of Sodium-Glucose Cotransporter 2 Exerts Anti-Inflammatory and Antifibrotic Effects on Experimental Diabetic Nephropathy Partly by Suppressing AGEs-Receptor Axis. Hormone Metab Res. 2015;47(09):686-92. doi: 10.1055/s-0034-1395609
        71. Dekkers CJ, Petrykiv S, Laverman GD, et al. Effects of the SGLT-2 inhibitor dapagliflozin on glomerular and tubular injury markers. Diabet Obes Metab. 2018;20(8):1988-93. doi: 10.1111/dom.13301
        72. Shimazu T, Hirschey MD, Newman J, et al. Suppression of Oxidative Stress by-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor. Science. 2012;339(6116):211-4. doi: 10.1126/science.1227166
        73. Hill NR, Fatoba ST, Oke JL, et al. Global Prevalence of Chronic Kidney Disease – A Systematic Review and Meta-Analysis. Remuzzi G, editor. PLOS One. 2016;11(7):e0158765. doi: 10.1371/journal.pone.0158765
        74. Vallon V, Gerasimova M, Rose MA, et al. SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice. Am J Physiol-Renal Physiol. 2014;306(2):F194-F204. doi: 10.1152/ajprenal.00520.2013
        75. Liao X, Wang X, Li H, et al. Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor Increases Circulating Zinc-Α2-Glycoprotein Levels in Patients with Type 2 Diabetes. Sci Reports. 2016;6(1). doi: 10.1038/srep32887
        76. Mancini SJ, Boyd D, Katwan OJ, et al. Canagliflozin inhibits interleukin-1β-stimulated cytokine and chemokine secretion in vascular endothelial cells by AMP-activated protein kinase-dependent and -independent mechanisms. Sci Reports. 2018;8(1). doi: 10.1038/s41598-018-23420-4
        77. Maldonado-Cervantes MI, Galicia OG, Moreno-Jaime B, et al. Autocrine modulation of glucose transporter SGLT2 by IL-6 and TNF-α in LLC-PK1 cells. J Physiol Biochem. 2012;68(3):411-20. doi: 10.1007/s13105-012-0153-3
        78. Scheen AJ, Van Gaal LF. Combating the dual burden: therapeutic targeting of common pathways in obesity and type 2 diabetes. Lancet Diabet Endocrinol. 2014;2(11):911-22. doi: 10.1016/s2213-8587(14)70004-x
        79. Barnett AH. Impact of sodium glucose cotransporter 2 inhibitors on weight in patients with type 2 diabetes mellitus. Postgrad Med. 2013;125:92-100. doi: 10.3810/pgm.2013.09.2698
        80. Vasilakou D, Karagiannis T, Athanasiadou E, et al. Sodium-Glucose Cotransporter 2 Inhibitors for Type 2 Diabetes. Ann Int Med. 2013;159(4):262. doi: 10.7326/0003-4819-159-4-201308200-00007
        81. Liu X-Y, Zhang N, Chen R, et al. Efficacy and safety of sodium–glucose cotransporter 2 inhibitors in type 2 diabetes: a meta-analysis of randomized controlled trials for 1 to 2 years. J Diabet Complicat. 2015;29(8):1295-303. doi: 10.1016/j.jdiacomp.2015.07.011
        82. Ferrannini G, Hach T, Crowe S, et al. Energy Balance After Sodium-Glucose Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1730-5. doi: 10.2337/dc15-0355
        83. Ladwig K-H, Marten-Mittag B, Löwel H, et al. Influence of depressive mood on the association of CRP and obesity in 3205 middle aged healthy men. Brain, Behav Immun. 2003;17(4):268-75. doi: 10.1016/s0889-1591(03)00056-4
        84. Bochud M, Marquant F, Marques-Vidal P-M, et al. Association between C-Reactive Protein and Adiposity in Women. J Clin Endocrinol Metab. 2009;94(10):3969-77. doi: 10.1210/jc.2008-2428
        85. Jung U, Choi M-S. Obesity and Its Metabolic Complications: The Role of Adipokines and the Relationship between Obesity, Inflammation, Insulin Resistance, Dyslipidemia and Nonalcoholic Fatty Liver Disease. Int J Mol Sci. 2014;15(4):6184-223. doi: 10.3390/ijms15046184
        86. Yaribeygi H, Butler AE, Atkin SL, et al. Sodium-glucose cotransporter 2 inhibitors and inflammation in chronic kidney disease: Possible molecular pathways. J Cell Physiol. 2018;234(1):223-30. doi: 10.1002/jcp.26851
        87. Kuriyama S. Protection of the kidney with sodium-glucose cotransporter 2 inhibitors: potential mechanisms raised by the large-scaled randomized control trials. Clin Exper Nephrol. 2018;23(3):304-12. doi: 10.1007/s10157-018-1673-0
        88. Maliha G, Townsend RR. SGLT2 inhibitors: their potential reduction in blood pressure. J Am Soc Hypertens. 2015;9(1):48-53. doi: 10.1016/j.jash.2014.11.001
        89. Baker WL, Smyth LR, Riche DM, et al. Effects of sodium-glucose co-transporter 2 inhibitors on blood pressure: A systematic review and meta-analysis. J Am Soc Hypertens. 2014;8(4):262-75.e9. doi: 10.1016/j.jash.2014.01.007
        90. Sano M, Chen S, Imazeki H, et al. Changes in heart rate in patients with type 2 diabetes mellitus after treatment with luseogliflozin: Subanalysis of placebo-controlled, double-blind clinical trials. J Diabet Invest. 2018;9(3):638-41. doi: 10.1111/jdi.12726
        91. Wu JHY, Foote C, Blomster J, et al. Effects of sodium-glucose cotransporter-2 inhibitors on cardiovascular events, death, and major safety outcomes in adults with type 2 diabetes: a systematic review and meta-analysis. Lancet Diabet Endocrinol. 2016;4(5):411-9. doi: 10.1016/s2213-8587(16)00052-8
        92. Ptaszynska A, Johnsson KM, Parikh SJ, et al. Safety Profile of Dapagliflozin for Type 2 Diabetes: Pooled Analysis of Clinical Studies for Overall Safety and Rare Events. Drug Safety. 2014;37(10):815-29. doi: 10.1007/s40264-014-0213-4
        93. Johnsson KM, Ptaszynska A, Schmitz B, et al. Urinary tract infections in patients with diabetes treated with dapagliflozin. J Diabet Complicat. 2013;27:473-8. doi: 10.1016/j.jdiacomp.2013.05.004
        94. Peters AL, Buschur EO, Buse JB, et al. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With Sodium-Glucose 
        Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1687-93. doi: 10.2337/dc15-0843
        95. Bonner C, Kerr-Conte J, Gmyr V, et al. Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion. Nature Med. 2015;21(5):512-7. doi: 10.1038/nm.3828
        96. Kalra S, Gupta Y, Patil S. Sodium-glucose cotransporter-2 inhibition and the insulin: Glucagon ratio: Unexplored dimensions. Ind J Endocrinol Metab. 2015;19(3):426. doi: 10.4103/2230-8210.152793
        97. Rosenstock J, Ferrannini E. Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, and Preventable Safety Concern With SGLT2 Inhibitors. Diabet Care. 2015;38(9):1638-42. doi: 10.2337/dc15-1380
        98. Zhang M, Zhang L, Wu B, et al. Dapagliflozin treatment for type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials. Diabet/Metab Res Rev. 2014;30(3):204-21. doi: 10.1002/dmrr.2479
        99. Meier C, Schwartz AV, Egger A, Lecka-Czernik B. Effects of diabetes drugs on the skeleton. Bone. 2016;82:93-100. doi: 10.1016/j.bone.2015.04.026
        100. Ljunggren Ö, Bolinder J, Johansson L, et al. Dapagliflozin has no effect on markers of bone formation and resorption or bone mineral density in patients with inadequately controlled type 2 diabetes mellitus on metformin. Diabet Obes Metab. 2012;14(11):990-9. doi: 10.1111/j.1463-1326.2012.01630.x
        101. Bolinder J, Ljunggren Ö, Johansson L, et al. Dapagliflozin maintains glycaemic control while reducing weight and body fat mass over 2 years in patients with type 2 diabetes mellitus inadequately controlled on metformin. Diabet Obes Metab. 2013;16(2):159-69. doi: 10.1111/dom.12189
        102. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. New Engl J Med. 2015;373(22):2117-28. doi: 10.1056/nejmoa1504720
        103. Wanner C, Inzucchi SE, Lachin JM, et al. Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes. New Engl J Med. 2016;375(4):323-34. doi: 10.1056/nejmoa1515920
        104. Ptaszynska A, Cohen SM, Messing EM, et al. Assessing Bladder Cancer Risk in Type 2 Diabetes Clinical Trials: the Dapagliflozin Drug Development Program as a "Case Study". Diabet Ther. 2015;6(3):357-75. doi: 10.1007/s13300-015-0128-9
        105. Yang H-C, Nguyen PAA, Islam M, et al. Gout drugs use and risk of cancer: A case-control study. Joint Bone Spine. 2018;85(6):747-53. doi: 10.1016/j.jbspin.2018.01.008
        106. Lin H-W, Tseng C-H. A Review on the Relationship between SGLT2 Inhibitors and Cancer. Int J Endocrinol. 2014;2014:1-6. doi: 10.1155/2014/719578
        107. Neal B, Perkovic V, Mahaffey KW, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes. New Engl J Med. 2017;377(7):644-57. doi: 10.1056/nejmoa1611925
        108. Hallow KM, Helmlinger G, Greasley PJ, et al. Why do SGLT2 inhibitors reduce heart failure hospitalization? A differential volume regulation hypothesis. Diabet Obes Metab. 2018;20(3):479-87. doi: 10.1111/dom.13126


        Авторы
        Т.С. Паневин1,2, М.С. Елисеев1, М.В. Шестакова2, Е.Л. Насонов1

        1 ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», Москва, Россия;
        2 ФГБУ «Национальный медицинский исследовательский центр эндокринологии», Москва, Россия

        ________________________________________________

        T.S. Panevin1,2, M.S. Eliseev1, M.V. Shestakova2, E.L. Nasonov1

        1 Nasonova Research Institute of Rheumatology, Moscow, Russia;
        2 National Medical Research Center for Endocrinology, Moscow, Russia


        Поделиться
        Назад к списку
        Цель портала OmniDoctor – предоставление профессиональной информации врачам, провизорам и фармацевтам.

        Ключевые слова

        артериальная гипертензия дети артериальная гипертония лечение сахарный диабет COVID-19 ишемическая болезнь сердца диагностика беременность ожирение сердечно-сосудистые заболевания хроническая сердечная недостаточность рак молочной железы факторы риска метаболический синдром хроническая болезнь почек хроническая обструктивная болезнь легких качество жизни профилактика сахарный диабет 2-го типа фибрилляция предсердий инфаркт миокарда бесплодие антигипертензивная терапия прогноз сердечная недостаточность химиотерапия атеросклероз бронхиальная астма неалкогольная жировая болезнь печени таргетная терапия эффективность амлодипин нестероидные противовоспалительные препараты витамин D бактериальный вагиноз ревматоидный артрит гастроэзофагеальная рефлюксная болезнь реабилитация вирус папилломы человека безопасность коморбидность болезнь Крона атопический дерматит эндометриоз пробиотики эндотелиальная дисфункция язвенный колит инсулинорезистентность инсульт
        Узнавайте первым
        Подпишитесь, чтобы получать информацию о самых интересных событиях, последних новостях.
        Рассылка
        Новости
        Мероприятия
        Актуальные вебинары, конференции, семинары и т.д.
        Медиатека
        Записи вебинаров, подкасты, статьи и интервью.
        Библиотека
        Материалы для врачей-клиницистов:
        — Электронная...
        Наши контакты
        +7 (495) 098-03-59
        Заказать звонок
        Москва 125252, ул. Алабяна 13, корпус 1
        info@omnidoctor.ru
        Портал
        О портале
        История
        Лицензии
        Партнеры
        Реквизиты
        Об издательстве "Консилиум Медикум"
        Политика обработки ПД
        Пресс-центр
        Медиатека
        Библиотека
        Издания для врачей
        Издания для провизоров и фармацевтов
        Online-издания
        Мероприятия
        © 2025 Все права защищены.
        Подождите секунду, мы ищем Расширенный поиск
        Мы используем инструмент веб-аналитики Яндекс Метрика, который посредством обработки файлов «cookie» позволяет анализировать данные о посещаемости сайта, что помогает нам улучшить работу сайта, повысить его удобство и производительность. Соответственно, продолжая пользоваться сайтом, вы соглашаетесь на использование файлов «cookie» и их дальнейшую обработку сервисом Яндекс Метрика. Вы можете блокировать и (или) удалять файлы «cookie» в настройках своего веб-браузера.
        Я согласен(-на)