Генетический базис при хронических заболеваниях вен (ХЗВ) является на сегодняшний день до конца не изученным. Определенные генные мутации играют важную роль, являясь факторами риска для возникающей в дальнейшем картины ХЗВ. Феномен генетической детерминированности к ремоделированию венозной стенки стал активно изучаться с накоплением и углублением наших знаний о геноме. Помимо генетической предрасположенности огромное значение имеет и действие факторов внешней среды. Механизм их взаимодействия с геномом изучается эпигенетикой.
Изучение патофизиологии ХЗВ является основой для эффективного лечения. На сложные молекулярные процессы, которые запускаются при нарушении гемодинамики в патогенезе ХЗВ, мы можем воздействовать с применением определенного ряда веноактивных препаратов. Доказательная база по этим препаратам на сегодняшний день должна не только обязательно включать в себя возможности влияния и коррекции субъективных симптомов ХЗВ, но и объяснять этот положительный эффект с рассмотрением механизма их действия на патофизиологическом уровне.
The genetic basis concerning chronic venousdiseases (CVI) has not been investigated enough yet. Certain genetic mutations play an important role as risk factors for the appearance of CVI in the future. The phenomenon of genetic determinism of venous wall remodeling is actively studied with accumulation and deepening the genome knowledge. The effect of environmental factors is a great importance in addition to genetic predisposition. The mechanism of their interaction with the genome is studied by epigenetics.
Study of CVI pathophysiology is the basis for effective treatment. We can affect the complex molecular processes that run in violation of hemodynamics in the pathogenesis of CVI using specialtypes of veno-active drugs. Nowadays, the evidence base for these drugs should not only be possible to include managing and correction of CVI subjective symptoms, and to explain this positive effect studying the mechanism of their action at the pathophysiological level.
1. Schultz-Ehrenburg U, Weindorf N, Matthes U, Hirche H. An epidemiologic study of the pathogenesis of varices. The Bochum study I–III]. Phlebologie 1992; 45 (4): 497–500.
2. Scott TE, LaMorte WW, Gorin DR, Menzoian JO. Risk factors for chronic venous insufficiency: a dual case–control study. J Vasc Surg 1995; 22: 622–8.
3. Hirai M, Naiki K, Nakayama R. Prevalence and risk factors of varicose veins in Japanese women. Angiology 1990; 41: 228–32.
4. Cornu-Thenard A, Boivin P, Baud JM et al. Importance of familial factor in varicose diseas. Clinical study of 134 families. J Dermatol Surg Oncol 1994; 20: 318–26.
5. Criqui MH et al. Chronic venous disease in an ethnically diverse population: the San Diego Population Study. Am J Epidemiol 2003; 158: 448–56.
6. Anwar MA, Georgiadis KA, Shalhoub J et al. A review of familial, genetic, and congenital aspects of primary varicose vein disease. Circ Cardiovasc Genet 2012; 5 (4): 460–6.
7. Svejcar J. Biochemicalanalysis of the blood vessel wall. ArztlForsch 1963; 10 (17): 588–94.
8. Zsotér T, Cronin RF. Venous distensibility in patients with varicose veins. Can Med Assoc J 1966; 94 (25): 1293–7.
9. Blöchl-Daum B, Schuller-Petrovic S, Wolzt M et al. Primary defect in alpha-adrenergic responsiveness in patients with varicose veins. Clin Pharmacol Ther 1991; 49 (1): 49–52.
10. Kirsch D, Wahl W, Böttger T, Junginger T. Primary varicose veins-changes in the venous wall and elastic behavior. Chirurg 2000; 71 (3): 300–5.
11. Sansilvestri-Morel P, Rupin A, Badier-Commander C et al. Imbalance in the synthesis of collagen type I and collagen type III in smooth muscle cells derived from human varicose veins. J Vasc Res 2001; 38 (6): 560–8.
12. Kostas TI, Ioannou CV, Drygiannakis I et al. Chronic venous disease progression and modification of predisposing factors. J Vasc Surg 2010; 51: 900–7.
13. Савельев В.С., Кириенко А.И., Золотухин И.А. Селиверстов Е.И. Проспективное обсервационное исследование СПЕКТР: регистр пациентов с хроническими заболеваниями вен нижних конечностей. Флебология. 2012; 1: 4–9. / Savel'ev V.S., Kirienko A.I., Zolotukhin I.A. Seliverstov E.I. Prospektivnoe observatsionnoe issledovanie SPEKTR: registr patsientov s khronicheskimi zabolevaniiami ven nizhnikh konechnostei. Flebologiia. 2012; 1: 4–9. [in Russian]
14. Raffetto JD, Khalil RA. Mechanisms of varicose vein formation: valve dysfunction and wall dilation. Phlebology 2008; 23 (2): 85–98.
15. Pascarella L, Lulic D, Penn AH et al. Mechanisms in Experimental Venous Valve Failure and their Modification by Daflon 500 mg. Eur
J Vasc Endovasc Surg 2008; 35; 102–10.
16. Management of chronic venous disorders of the lower limbs. Guidelines acoording to scientific evidence. Int Angiology 2014; 33 (2): 1–208.
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1. Schultz-Ehrenburg U, Weindorf N, Matthes U, Hirche H. An epidemiologic study of the pathogenesis of varices. The Bochum study I–III]. Phlebologie 1992; 45 (4): 497–500.
2. Scott TE, LaMorte WW, Gorin DR, Menzoian JO. Risk factors for chronic venous insufficiency: a dual case–control study. J Vasc Surg 1995; 22: 622–8.
3. Hirai M, Naiki K, Nakayama R. Prevalence and risk factors of varicose veins in Japanese women. Angiology 1990; 41: 228–32.
4. Cornu-Thenard A, Boivin P, Baud JM et al. Importance of familial factor in varicose diseas. Clinical study of 134 families. J Dermatol Surg Oncol 1994; 20: 318–26.
5. Criqui MH et al. Chronic venous disease in an ethnically diverse population: the San Diego Population Study. Am J Epidemiol 2003; 158: 448–56.
6. Anwar MA, Georgiadis KA, Shalhoub J et al. A review of familial, genetic, and congenital aspects of primary varicose vein disease. Circ Cardiovasc Genet 2012; 5 (4): 460–6.
7. Svejcar J. Biochemicalanalysis of the blood vessel wall. ArztlForsch 1963; 10 (17): 588–94.
8. Zsotér T, Cronin RF. Venous distensibility in patients with varicose veins. Can Med Assoc J 1966; 94 (25): 1293–7.
9. Blöchl-Daum B, Schuller-Petrovic S, Wolzt M et al. Primary defect in alpha-adrenergic responsiveness in patients with varicose veins. Clin Pharmacol Ther 1991; 49 (1): 49–52.
10. Kirsch D, Wahl W, Böttger T, Junginger T. Primary varicose veins-changes in the venous wall and elastic behavior. Chirurg 2000; 71 (3): 300–5.
11. Sansilvestri-Morel P, Rupin A, Badier-Commander C et al. Imbalance in the synthesis of collagen type I and collagen type III in smooth muscle cells derived from human varicose veins. J Vasc Res 2001; 38 (6): 560–8.
12. Kostas TI, Ioannou CV, Drygiannakis I et al. Chronic venous disease progression and modification of predisposing factors. J Vasc Surg 2010; 51: 900–7.
13. Savel'ev V.S., Kirienko A.I., Zolotukhin I.A. Seliverstov E.I. Prospektivnoe observatsionnoe issledovanie SPEKTR: registr patsientov s khronicheskimi zabolevaniiami ven nizhnikh konechnostei. Flebologiia. 2012; 1: 4–9. [in Russian]
14. Raffetto JD, Khalil RA. Mechanisms of varicose vein formation: valve dysfunction and wall dilation. Phlebology 2008; 23 (2): 85–98.
15. Pascarella L, Lulic D, Penn AH et al. Mechanisms in Experimental Venous Valve Failure and their Modification by Daflon 500 mg. Eur
J Vasc Endovasc Surg 2008; 35; 102–10.
16. Management of chronic venous disorders of the lower limbs. Guidelines acoording to scientific evidence. Int Angiology 2014; 33 (2): 1–208.
Авторы
С.В.Сапелкин*1,2, А.О.Баскаева2
1 ФГБУ Институт хирургии им. А.В.Вишневского Минздрава России. 117997, Россия, Москва, ул. Большая Серпуховская, д. 27;
2 ФГБУ Поликлиника №5 УДП РФ. 119121, Россия, Москва, ул. Плющиха, д. 14
*sapelkin@ixv.ru
________________________________________________
S.V.Sapelkin*1,2, A.O.Baskaeva2
1 A.V.Vishnevsky Institute of Surgery of the Ministry of Health of the Russian Federation. 117997, Russian Federation, Moscow, ul. Bol'shaia Serpukhovskaia, d. 27;
2 Out-Patient Сlinic №5 of Administration of the President of Russian Federation. 119121, Russian Federation, Moscow, ul. Pliushchikha, d. 14
*sapelkin@ixv.ru