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Коморбидный пациент в практике невролога: возможности лечения
Чуканова А.С., Чуканова Е.И. Коморбидный пациент в практике невролога: возможности лечения. Consilium Medicum. 2019; 21 (2): 53–58. DOI: 10.26442/20751753.2019.2.190266
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Chukanova A.S., Chukanova E.I. Comorbid patient in neurologist practice: possibilities of treatment. Consilium Medicum. 2019; 21 (2): 53–58. DOI: 10.26442/20751753.2019.2.190266
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Аннотация
У пациентов с хронической цереброваскулярной недостаточностью (ХЦВН), формирующейся на фоне различных факторов риска, нередко диагностируется от 4 до 8 заболеваний, относящихся к разным медицинским специальностям. Важность рассмотрения проблемы коморбидности у пациентов с ХЦВН обусловлена ухудшением прогноза течения заболевания, резким удорожанием лечения за счет проведения полифармакотерапии. Наиболее распространенными факторами риска развития как сердечно-сосудистых заболеваний в целом, так и ХЦВН являются артериальная гипертензия и сахарный диабет – две взаимосвязанные патологии, которые обладают взаимоусиливающим повреждающим действием на различные органы и системы организма, приводящие к ранней инвалидизации и смертности данных пациентов. ХЦВН, протекающая на фоне артериальной гипертензии и сахарного диабета, в подавляющем большинстве случаев сопровождается развитием диабетической полинейропатии. При выборе лечения пациентам с коморбидной патологией необходимо учитывать наличие имеющихся плейотропных эффектов у назначаемых препаратов, что может способствовать эффективному лечению и снизить процент полипрогмазии. Такие препараты, как дипиридамол и тиоктовая кислота, благодаря своим многочисленным эффектам могут быть эффективны в лечении коморбидных пациентов с хроническим нарушением мозгового кровообращения и диабетической полинейропатией.
Ключевые слова: хроническая цереброваскулярная недостаточность, диабетическая полинейропатия, факторы риска, коморбидность, полифармакотерапия, микроангиопатии, эндотелиальная дисфункция, оксидативный стресс, антитромботическая терапия, дипиридамол, тиоктовая кислота.
Ключевые слова: хроническая цереброваскулярная недостаточность, диабетическая полинейропатия, факторы риска, коморбидность, полифармакотерапия, микроангиопатии, эндотелиальная дисфункция, оксидативный стресс, антитромботическая терапия, дипиридамол, тиоктовая кислота.
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From 4 to 8 comorbid diseases of various categories are commonly diagnosed in patients with chronic cerebrovascular insufficiency (CVI) that develops at the background of various risk factors. The importance of comorbidity problem in patients with chronic CVI is explained with worse disease prognosis and increase of treatment cost due to the use of many different medications. The most common risk factors of both cardiovascular disorders and chronic CVI development are arterial hypertension and diabetes mellitus. These are two correlated pathologies with synergic damaging effect on various organs and systems that result in early disability and mortality of these patients. Chronic CVI comorbid with arterial hypertension and diabetes mellitus is in most cases accompanied by diabetic polyneuropathy development. When selecting treatment for patients with comorbid pathology it is necessary to consider the existing pleiotropic effects of prescribed medications that may contribute to successful treatment and reduce the percent of polypharmacy. Such medications as dipiridamol and alpha-lipoic acid may be effective in treatment of comorbid patients with chronic cerebrovascular disease and diabetic polyneuropathy due to their multiple effects.
Key words: chronic cerebrovascular insufficiency, diabetic polyneuropathy, risk factors, comorbidity, polipharmacotherapy, microangiopathies, endothelial dysfunction, oxidative stress, antithrombotic therapy, dipiridamol, alpha-lipoic acid.
Key words: chronic cerebrovascular insufficiency, diabetic polyneuropathy, risk factors, comorbidity, polipharmacotherapy, microangiopathies, endothelial dysfunction, oxidative stress, antithrombotic therapy, dipiridamol, alpha-lipoic acid.
Полный текст
Список литературы
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[Komorbidnaia patologiia v klinicheskoi praktike. Klinicheskie rekomendatsii. Rabochaia gruppa pod rukovodstvom R.G.Oganova. Kardiovaskuliarnaia terapiia i profilaktika. 2017; 16 (6). http://dx.doi.org/10.15829/1728-8800 (in Russian).]
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[Vorob'eva O.V. Pleiotropnye effekty dipiridamola: klinicheskie perspektivy. Effektivnaia farmakoterapiia. Nevrologiia. 2016; 3 (25): 15–8 (in Russian).]
27. Arivazhagan P, Juliet P, Panneerselvam C. Effect of DL alpha-lipoic acid on the status of lipid peroxidation and antioxidants in aged rats. Pharmacol Res 2000; 41 (3): 299–303.
28. Gurer H, Ozgunes H, Oztezcan S et al. Antioxidant role of alpha-lipoic acid in lead toxicity. Free Radic Biol Med 1999; 27 (1–2): 75–81.
29. Tesfaye S, Stevens LK, Stephenson JM et al. Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study. Diabetologia 1996; 39: 1377–84.
30. Biewenga GP, Haenen GR, Bast A. The pharmacology of the antioxidant lipoic acid. Gen Pharmacol 1997; 29: 315–31.
31. Javed S, Petropoulos IN, Alam U, Malik RA. Treatment of painful diabetic neuropathy. Ther Adv Chronic Dis 2015; 6 (1): 15–28. DOI: 10.1177/2040622314552071
32. Nagamatsu M, Nickander КК, Schmelzer JD et al. Lipoic acid improves nerve blood ow, reduces oxidative stress and improves distal nerve conduction in experimental diabetic neuropathy. Diabetes Care 1995; 18: 1160–7.
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34. Ziegler D, Hanefeld M, Ruhnau KJ et al.; ALADIN Study Group. Treatment of symptomatic diabetic peripheral neuropathy with the antioxidant alpha-lipoic acid. A 3-week multicentre randomised controlle trial (ALADIN study). Diabetologia 1995; 38: 1425–33.
35. Reljanovic M, Reichel G, Rett K et al. Treatment of diabetic polyneuropathy with the antioxidant thioctic acid (alpha-lipoic acid): a two year multicenter randomized doubleblind placebo-controlled trial (ALADIN II). Alpha Lipoic Acid in Diabetic Neuropathy. Free Radic Res 1999; 31 (3): 171–9.
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38. Ziegler D, Nowak H, Kempler P et al. Treatment of symptomatic dia¬betic polyneuropathy with the antioxidant alpha-lipoic acid: a meta-analysis. Diabetic Medicine 2004; 21: 114–21.
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[Barantsevich E.R., Posokhina O.V. Podkhody k terapii nevrologicheskikh proiavlenii sakharnogo diabeta. Zhurn. nevrologii i psikhiatrii. 2010; 110 (4): 63–6 (in Russian).]
40. Чуканова Е.И. Эффективность тиоктацида при лечении больных с дисциркуляторной энцефалопатией. Журн. неврологии и психиатр. им. С.С.Корсакова. 2001; 101 (11): 31–5.
[Chukanova E.I. Effektivnost' tioktatsida pri lechenii bol'nykh s distsirkuliatornoi entsefalopatiei. Zhurn. nevrologii i psikhiatr. im. S.S.Korsakova. 2001; 101 (11): 31–5 (in Russian).]
41. Чуканова Е.И. Фармакоэкономический анализ влияния тиоктацида и солкосерила на риск развития инсульта и прогрессирование ДЭ. В кн.: Международный форум неврологов. Ереван, 2004; с. 195–99.
[Chukanova E.I. Farmakoekonomicheskii analiz vliianiia tioktatsida i solkoserila na risk razvitiia insul'ta i progressirovanie DE. V kn.: Mezhdunarodnyi forum nevrologov. Yerevan, 2004; p. 195–99 (in Russian).]
[Vsemirnaia organizatsiia zdravookhraneniia. 63-ia sessiia Vsemirnoi assamblei zdravookhraneniia, Zheneva, 17–21 maia 2010 g. Rezoliutsii i resheniia. Prilozheniia (WHA63/2010/REC/1). Pril. 4. Geneva, 2010 (in Russian).]
2. Левин О.С. Дисциркуляторная энцефалопатия. Методическое пособие. М., 2010.
[Levin O.S. Distsirkuliatornaia entsefalopatiia. Metodicheskoe posobie. Moscow, 2010 (in Russian).]
3. Dzau V, Braunwald E. Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. Am Heart J 1991; 121: 1244–63.
4. Белялов Ф.И. Лечение внутренних болезней в условиях коморбидности. Иркутск: РИО ИГМАПО, 2013.
[Belialov F.I. Lechenie vnutrennikh boleznei v usloviiakh komorbidnosti. Irkutsk: RIO IGMAPO, 2013 (in Russian).]
5. Журавлев Ю.И., Тхорикова В.Н. Современные проблемы измерения полиморбидности. Научные ведомости БелГУ. Серия Медицина. Фармация. 2013; 11 (154), вып. 22: 214–19.
[Zhuravlev Iu.I., Tkhorikova V.N. Sovremennye problemy izmereniia polimorbidnosti. Nauchnye vedomosti BelGU. Seriia Meditsina. Farmatsiia. 2013; 11 (154), vyp. 22: 214–19 (in Russian).]
6. Payne R et al. Prevalence of polypharmacy in a Scottish primary care population. Eur J Clin Pharm 2014; 70 (5): 575–81.
7. Bushardt RL et al. Polypharmacy: misleading, but manageable. Clin Int Aging 2008; 3 (2): 383–9.
8. Gnjidic D. Polypharmacy cutoff and outcomes: five or more medicines were used to identify community-dwelling older men at risk of different adverse outcomes. J Clin Epidemiol 2012; 65 (9): 989–95.
9. Zinman B, Wanner C, Lachin JM et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. N Engl J Med 2015; 373 (22): 2117–28.
10. Коморбидная патология в клинической практике. Клинические рекомендации. Рабочая группа под руководством Р.Г.Оганова. Кардиоваскулярная терапия и профилактика. 2017; 16 (6): 5–56. http://dx.doi.org/10.15829/1728-8800.
[Komorbidnaia patologiia v klinicheskoi praktike. Klinicheskie rekomendatsii. Rabochaia gruppa pod rukovodstvom R.G.Oganova. Kardiovaskuliarnaia terapiia i profilaktika. 2017; 16 (6). http://dx.doi.org/10.15829/1728-8800 (in Russian).]
11. Левин О.С. Полиневропатия. М.: Мед. информ. агентство, 2011.
[Levin O.S. Polinevropatiia. Moscow: Med. inform. agentstvo, 2011 (in Russian).]
12. Kramer H, Rolke R, Hecht M. Follow-up of advanced diabetic neuropathy. J Neurol 2005; 252 (3): 315–20.
13. Vinik AI, Mehrabyan A. Diabetic neuropathies. Med Clin North Am 2004; 88: 947–99.
14. Чуканова Е.И. Отдельные механизмы патогенеза формирования недостаточности мозгового кровообращения. Фарматека (кардиология/неврология). 2014; 13: 14–20.
[Chukanova E.I. Otdel'nye mekhanizmy patogeneza formirovaniia nedostatochnosti mozgovogo krovoobrashcheniia. Farmateka (kardiologiia/nevrologiia). 2014; 13: 14–20. (in Russian).]
15. Гусев Е.И., Скворцова В.И. Ишемия головного мозга. М.: Медицина, 2001.
[Gusev E.I., Skvortsova V.I. Ishemiia golovnogo mozga. Moscow: Meditsina, 2001 (in Russian).]
16. Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. Cerebrovasc Dis 2008; 25 (5): 457–507.
17. Hasday JD, Sitrin RG. Dipyridamole stimulates urokinase production and suppresses procoagulant activity of rabbit alveolar macrophages: a possible mechanism of antithrombotic action. Blood 1987; 69 (2): 660–7.
18. Ariesen MJ, Algra A, Kappelle LJ. Antiplatelet drugs in the secondary prevention after stroke: differential efficacy in large versus small vessel disease? A subgroup analysis from ESPS-2. Stroke 2006; 37 (1): 134–8.
19. ESPS Group. European Stroke Prevention Study. Stroke 1990; 21: 1122–30.
20. Aktas B, Utz A, Hoenig-Liedl P. Dipyridamole enhances NO/cGMP-mediated vasodilator-stimulated phosphoprotein phosphorylation and signaling in human platelets: in vitro and in vivo/ex vivo studies. Stroke 2003; 34 (3): 764–9.
21. Chakrabarti S, Freedman JE. Dipyridamole, cerebrovascular disease, and the vasculature. Vascul Pharmacol 2008; 48 (4–6): 143–9.
22. Kusmic C, Petersen C, Picano E et al. Antioxidant effect of oral dipyridamole during cerebral hypoperfusion with human carotid endarterectomy. J Cardiovasc Pharmacol 2000; 36 (2): 141–5.
23. Nelson CW, Wei EP, Povlishock JT et al. Oxygen radicals in cerebral ischemia. Am J Physiol 1992; 263 (5), pt. 2: H1356–62.
24. Weisbrot-Lefkowitz M, Reuhl K, Perry B et al. Overexpression of human glutathione peroxidase protects transgenic mice against focal cerebral ischemia/reperfusion damage. Brain Res Mol Brain Res 1998; 53 (1–2): 333–8.
25. Balakumar P, Nyo YH, Renushia R et al. Classical and pleiotropic actions of dipyridamole: Not enough light to illuminate the dark tunnel? Pharmacol Res 2014; 87: 144–50.
26. Воробьева О.В. Плейотропные эффекты дипиридамола: клинические перспективы. Эффективная фармакотерапия. Неврология. 2016; 3 (25): 15–8.
[Vorob'eva O.V. Pleiotropnye effekty dipiridamola: klinicheskie perspektivy. Effektivnaia farmakoterapiia. Nevrologiia. 2016; 3 (25): 15–8 (in Russian).]
27. Arivazhagan P, Juliet P, Panneerselvam C. Effect of DL alpha-lipoic acid on the status of lipid peroxidation and antioxidants in aged rats. Pharmacol Res 2000; 41 (3): 299–303.
28. Gurer H, Ozgunes H, Oztezcan S et al. Antioxidant role of alpha-lipoic acid in lead toxicity. Free Radic Biol Med 1999; 27 (1–2): 75–81.
29. Tesfaye S, Stevens LK, Stephenson JM et al. Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study. Diabetologia 1996; 39: 1377–84.
30. Biewenga GP, Haenen GR, Bast A. The pharmacology of the antioxidant lipoic acid. Gen Pharmacol 1997; 29: 315–31.
31. Javed S, Petropoulos IN, Alam U, Malik RA. Treatment of painful diabetic neuropathy. Ther Adv Chronic Dis 2015; 6 (1): 15–28. DOI: 10.1177/2040622314552071
32. Nagamatsu M, Nickander КК, Schmelzer JD et al. Lipoic acid improves nerve blood ow, reduces oxidative stress and improves distal nerve conduction in experimental diabetic neuropathy. Diabetes Care 1995; 18: 1160–7.
33. Ruhnau KJ, Meissner HP, Finn JR et al. Effects of 3-week oral treatment with the antioxidant thioctic acid (alpha-lipoic acid) in symptomatic diabetic polyneuropathy. Diabet Med 1999; 16: 1040–3.
34. Ziegler D, Hanefeld M, Ruhnau KJ et al.; ALADIN Study Group. Treatment of symptomatic diabetic peripheral neuropathy with the antioxidant alpha-lipoic acid. A 3-week multicentre randomised controlle trial (ALADIN study). Diabetologia 1995; 38: 1425–33.
35. Reljanovic M, Reichel G, Rett K et al. Treatment of diabetic polyneuropathy with the antioxidant thioctic acid (alpha-lipoic acid): a two year multicenter randomized doubleblind placebo-controlled trial (ALADIN II). Alpha Lipoic Acid in Diabetic Neuropathy. Free Radic Res 1999; 31 (3): 171–9.
36. Andreassen CS, Jakobsen J, Andersen H. Muscle Weakness – A Progressive Late Complication in Diabetic Distal Symmetric Polyneuropathy. Diabetes 2006, 55: 806–12.
37. Ametov A, Barinov A, O’brien P et al.; SYDNEY Trial Study Group. The sensory symptoms of diabetic polyneuropathy are improved with alpha-lipoic acid: The SYDNEY Trial. Diabetes Care 2003; 26: 770–6.
38. Ziegler D, Nowak H, Kempler P et al. Treatment of symptomatic dia¬betic polyneuropathy with the antioxidant alpha-lipoic acid: a meta-analysis. Diabetic Medicine 2004; 21: 114–21.
39. Баранцевич Е.Р., Посохина О.В. Подходы к терапии неврологических проявлений сахарного диабета. Журн. неврологии и психиатрии. 2010; 110 (4): 63–6.
[Barantsevich E.R., Posokhina O.V. Podkhody k terapii nevrologicheskikh proiavlenii sakharnogo diabeta. Zhurn. nevrologii i psikhiatrii. 2010; 110 (4): 63–6 (in Russian).]
40. Чуканова Е.И. Эффективность тиоктацида при лечении больных с дисциркуляторной энцефалопатией. Журн. неврологии и психиатр. им. С.С.Корсакова. 2001; 101 (11): 31–5.
[Chukanova E.I. Effektivnost' tioktatsida pri lechenii bol'nykh s distsirkuliatornoi entsefalopatiei. Zhurn. nevrologii i psikhiatr. im. S.S.Korsakova. 2001; 101 (11): 31–5 (in Russian).]
41. Чуканова Е.И. Фармакоэкономический анализ влияния тиоктацида и солкосерила на риск развития инсульта и прогрессирование ДЭ. В кн.: Международный форум неврологов. Ереван, 2004; с. 195–99.
[Chukanova E.I. Farmakoekonomicheskii analiz vliianiia tioktatsida i solkoserila na risk razvitiia insul'ta i progressirovanie DE. V kn.: Mezhdunarodnyi forum nevrologov. Yerevan, 2004; p. 195–99 (in Russian).]
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Авторы
А.С.Чуканова, Е.И.Чуканова*
ФГБОУ «Российский национальный исследовательский медицинский университет им. Н.И.Пирогова», Москва, Россия
ФГБОУ «Российский национальный исследовательский медицинский университет им. Н.И.Пирогова», Москва, Россия
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Anna S. Chukanova, Elena I. Chukanova*
Pirogov Russian National Research Medical University, Moscow, Russia
Pirogov Russian National Research Medical University, Moscow, Russia
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