Дислипидемия и атеросклероз у больных сахарным диабетом 2-го типа. Особенности терапии статинами, сравнительный анализ: взгляд эндокринолога
Дислипидемия и атеросклероз у больных сахарным диабетом 2-го типа. Особенности терапии статинами, сравнительный анализ: взгляд эндокринолога
Демидова Т.Ю., Сусарева О.В. Дислипидемия и атеросклероз у больных сахарным диабетом 2-го типа. Особенности терапии статинами, сравнительный анализ: взгляд эндокринолога. Consilium Medicum. 2018; 20 (5): 24–28. DOI: 10.26442/2075-1753_2018.5.24-28
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Demidova T.Yu., Susareva O.V. Dyslipidemia and atherosclerosis in type 2 diabetes mellitus patients. Statin therapy characteristics and comparative analysis: endocrinologist’s point of view. Consilium Medicum. 2018; 20 (5): 24–28. DOI: 10.26442/2075-1753_2018.5.24-28
Дислипидемия и атеросклероз у больных сахарным диабетом 2-го типа. Особенности терапии статинами, сравнительный анализ: взгляд эндокринолога
Демидова Т.Ю., Сусарева О.В. Дислипидемия и атеросклероз у больных сахарным диабетом 2-го типа. Особенности терапии статинами, сравнительный анализ: взгляд эндокринолога. Consilium Medicum. 2018; 20 (5): 24–28. DOI: 10.26442/2075-1753_2018.5.24-28
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Demidova T.Yu., Susareva O.V. Dyslipidemia and atherosclerosis in type 2 diabetes mellitus patients. Statin therapy characteristics and comparative analysis: endocrinologist’s point of view. Consilium Medicum. 2018; 20 (5): 24–28. DOI: 10.26442/2075-1753_2018.5.24-28
Больные, страдающие сахарным диабетом 2-го типа (СД 2), относятся к группе высокого риска по развитию сердечно-сосудистых заболеваний (ССЗ), а комбинация СД 2 и ССЗ обусловливает крайне высокий риск смерти. Назначение статинов при СД 2 для профилактики развития ССЗ является одним из ключевых принципов современной антидиабетической терапии. В международных рекомендациях и в алгоритмах лечения СД Российской диабетической ассоциации именно статины рассматриваются как средства 1-й линии гиполипидемической терапии у больных СД 2. Достижение целевых значений липидного профиля является одной из ведущих задач при проведении терапии статинами. В ходе многоцентровых рандомизированных слепых плацебо-контролируемых клинических исследований больные, получавшие розувастатин, показали наилучшие результаты по снижению холестерина липопротеинов низкой плотности, триглицеридов, С-реактивного белка. Розувастатин обладает дозозависимым эффектом и может быть рекомендован в качестве препарата выбора.
Ключевые слова: сахарный диабет 2-го типа, дислипидемия, сердечно-сосудистые заболевания, статины, розувастатин.
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Patients with type 2 diabetes mellitus (DM type 2) are in a high-risk group of cardiovascular disease (CVD) development, and coexisting DM type 2 and CVD contribute to high mortality risk. Statin use in DM type 2 patients for CVD prevention is one of the key concepts of modern antidiabetic therapy. It is statins which are considered as first line hypolipidemic therapy in DM type 2 patients according to international guidelines and DM treatment algorithm of Russian Diabetes Association. Target lipid profile values achievement is one of the major tasks in statin therapy. It was shown in multicenter randomized blind placebo-controlled clinical trials that patients who received rosuvastatin had the best results in cholesterol, triglycerides, LDL, and C-reactive protein level reduction. Rosuvastatin has a dose-dependent effect and can be recommended as treatment of choice.
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16. Tanji N, Markowitz GS, Fu C et al. Expression of advanced glycation end products and their cellular receptorRAGEin diabetic nephropathy and nondiabetic renal disease. J Am Soc Nephrol 2000; 11: 1656–66.
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22. Gotto AM, Whitney E, Stein EA et al. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Circulation 2000; 101: 477–84.
23. Walldius G, Jungner I, Holme I et al. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet 2001; 358: 2026–33.
24. Nicholls S et al. Atheroscler Suppl 2009; 10: 965.
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28. Ross R. Atherosclerosis – an inflammatory disease. N Eng J Med 1999; 340: 115–26.
29. Jager A, van Hinsbergh VW, Kostense PJ et al. von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. Arterioscler Thromb Vasc Biol 1999; 19: 3071–8.
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31. Maedler K, Sergeev P, Ris F et al. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. J Clin Invest 2002; 110: 851–60.
32. Chamaria S, Johnson KW, Vengrenyuk Y et al. Intracoronary Imaging, Cholesterol Effluxand Transcriptomics after Intensive Statin Treatment in Diabetes. Sci Rep 2017; 7 (1): 7001.
33. Davies MJ, Richardson PD, Woolf N et al. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J 1993; 69: 377–81.
34. Moreno PR, Falk E, Palacios IF et al. Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. Circ J 1994; 90: 775–8.
35. Burke AP, Kolodgie FD, Zieske A et al. Morphologic findings of coronary atherosclerotic plaques in diabetics: a postmortem study. Arterioscler Thromb Vasc Biol 2004; 24: 1266–71.
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1. Global report on diabetes. WHO, 2016. http://www.who.int/diabetes/global-report
2. Federal'naia sluzhba gosudarstvennoi statistiki. http://www.gks.ru [in Russian]
3. Haffner SM, Lehto S, Ronnemaa T et al. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med 1998; 339: 229–34.
4. Nelson AJ, Rochelau SK, Nicholls SJ. Managing Dyslipidemia in Type 2 Diabetes. Endo-crinol Metab Clin N Am 2018; 47: 153–73.
5. Anderson TJ. Assessment and Treatment of Endothelial Dysfunction in Humans. J Am Coll Cardiol 1999; 34: 631–8.
6. Katakami N. Mechanism of Development of Atherosclerosis and Cardiovascular Disease in Diabetes Mellitus. J Atheroscler Thromb 2018; 25: 27–39.
7. Ross R. Atherosclerosis – An inflammatory Disease. N Engl J Med 1999; 340: 115–26.
8. Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circ J 2002; 105: 1135.
9. Libby P, Ridker PM, Hansson GK. Progress and challenges in translating the biology of atherosclerosis. Nature 2011; 473: 317–25.
10. DeFronzo RA. Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture. 2009. Diabetologia 2010; 53: 1270–87.
11. Matsuzawa Y, Shimomura I, Nakamura T et al. Pathophysiology and Pathogenesis of Visceral Fat Obesity. Obes Res 1995; Suppl. 2: 187–94.
12. Hsueh WA, Law R. The central role of fat and effect of peroxisome proliferator-activated receptor-gamma on progression of insulin resistance and cardiovascular disease. Am J Cardiol 2003; 92: 3–9.
13. Hajer GR, van Haeften TW, Visseren FLJ. Adipose tissue dysfunction in obesity, diabetes, and vascular diseases. Eur Heart J 2008; 29: 2959–71.
14. Ritthaler U, Deng Y, Zhang Y et al. Expression of receptors for advanced glycation end products in peripheral occlusive vascular disease. Am J Pathol 1995; 146: 688–94.
15. Cipollone F, Fazia M, Iezzi A et al. Suppression of the functionally coupled cyclooxygenase-2/prostaglandin E synthase as a basis of simvastatin-dependent plaque stabilization in humans. Circ J 2003; 107: 1479–85.
16. Tanji N, Markowitz GS, Fu C et al. Expression of advanced glycation end products and their cellular receptorRAGEin diabetic nephropathy and nondiabetic renal disease. J Am Soc Nephrol 2000; 11: 1656–66.
17. Brett J, Schmidt AM, Yan SD et al. Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. Am J Pathol 1993; 143: 1699–712.
18. Algoritmy spetsializirovannoi meditsinskoi pomoshchi bol'nym sakharnym diabetom. 2017. [in Russian]
19. Jung KY, Kyoung MK, Han SK et al. Effect of Rosuvastatin on Cholesterol Efflux Capacity and Endothelial Function in Type 2 Diabetes Mellitus and Dyslipidemia. Circ J 2017. DOI: 10.1253/circj.CJ-17-0411
20. Jellinger PS, Handelsman Y, Rosenblit PD et al. American Association of clinical endocrinologists and American college of endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract 2017; 23 (Suppl. 2): 1–87.
21. Wolffenbuttel BHR, Franken AAM, Vincent HH. Cholesterol-lowering effects of rosuvastatin compared with atorvastatin in patients with type 2 diabetes – CORALL study. J Inter Med 2005; 257: 531–9.
22. Gotto AM, Whitney E, Stein EA et al. Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). Circulation 2000; 101: 477–84.
23. Walldius G, Jungner I, Holme I et al. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet 2001; 358: 2026–33.
24. Nicholls S et al. Atheroscler Suppl 2009; 10: 965.
25. Stalenhoef AF et al. A comparative study with rosuvastatin in subjects with metabolic syndrome: results of the COMETS study. Eur Heart J 2005; 26: 2664–72.
26. Nesto R. C-Reactive protein, its role in inflammation, type 2 diabetes and cardiovascular disease, and the effects of insulin-sensitizing treatment with thiazolidinediones. Diabet Med 2004; 21: 810–7.
27. Betteridge DJ, Gibson JM, Sager PT. Comparison of effectiveness of rosuvastatin versus atorvastatin on the achievement of combined C-reactive protein (<2 mg/L) and low-density lipoprotein cholesterol (<70 mg/dl) targets in patients with type 2 diabetes mellitus (from the ANDROMEDA study). Am J Cardiol 2007; 100: 1245–8.
28. Ross R. Atherosclerosis – an inflammatory disease. N Eng J Med 1999; 340: 115–26.
29. Jager A, van Hinsbergh VW, Kostense PJ et al. von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. Arterioscler Thromb Vasc Biol 1999; 19: 3071–8.
30. Jialal I, Miguelino E, Griffen SC, Devaraj S. Concomitant reduction of low-density lipoprotein-cholesterol and biomarkers of inflammation with low-dose simvastatin therapy in patients with type 1 diabetes. J Clin Endocrinol Metab 2007; 92: 3136–40.
31. Maedler K, Sergeev P, Ris F et al. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. J Clin Invest 2002; 110: 851–60.
32. Chamaria S, Johnson KW, Vengrenyuk Y et al. Intracoronary Imaging, Cholesterol Effluxand Transcriptomics after Intensive Statin Treatment in Diabetes. Sci Rep 2017; 7 (1): 7001.
33. Davies MJ, Richardson PD, Woolf N et al. Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. Br Heart J 1993; 69: 377–81.
34. Moreno PR, Falk E, Palacios IF et al. Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. Circ J 1994; 90: 775–8.
35. Burke AP, Kolodgie FD, Zieske A et al. Morphologic findings of coronary atherosclerotic plaques in diabetics: a postmortem study. Arterioscler Thromb Vasc Biol 2004; 24: 1266–71.
36. Dollery CM, McEwan JR, Henney AM. Matrix metalloproteinases and cardiovascular disease. Circ Res 1995; 77: 863–8.
37. Bellosta S, Via D, Canavesi M et al. HMG-CoA reductase inhibitors reduce MMP-9 secretion by macrophages. Arterioscler Thromb Vasc Biol 1998; 18: 1671–8.
38. Parathath S, Grauer L, Huang LS et al. Diabetes adversely affects macrophages during atherosclerotic plaque regression in mice. Diabetes 2011; 60: 1759–69.
39. Kobalava Zh.D., Villeval'de S.V. Terapiia statinami i risk razvitiia sakharnogo diabeta. Effektivnaia farmakoterapiia. Endokrinologiia. 2015; Spetsvyp. (11): 33–9. [in Russian]
40. Proekt klinicheskikh rekomendatsii. Profilaktika razvitiia sakharnogo diabeta tipa 2: rol' i mesto metformina. Endokrinologiia. Novosti. Mneniia. Obuchenie. 2017; 1: 1–9. [in Russian]
Авторы
Т.Ю.Демидова*, О.В.Сусарева
ФГБОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И.Пирогова» Минздрава России. 117997, Россия, Москва, ул. Островитянова, д. 1
*t.y.demidova@gmail.com
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T.Yu.Demidova*, O.V.Susareva
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
*t.y.demidova@gmail.com