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Частота и факторы риска тромбоэмболических осложнений у пациентов с воспалительными заболеваниями кишечника
Частота и факторы риска тромбоэмболических осложнений у пациентов с воспалительными заболеваниями кишечника
Лищинская А.А., Князев О.В., Каграманова А.В., Дудина Г.А., Сабельникова Е.А., Ли И.А., Носкова К.К., Бодунова Н.А., Парфенов А.И. Частота и факторы риска тромбоэмболических осложнений у пациентов с воспалительными заболеваниями кишечника. Терапевтический архив. 2022;94(2):172–179.
DOI: 10.26442/00403660.2022.02.201367
DOI: 10.26442/00403660.2022.02.201367
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Аннотация
Обоснование. Воспалительные заболевания кишечника (ВЗК) характеризуются хроническим иммунным воспалением слизистой оболочки и/или толщи стенки кишки, а также сопровождаются нарушениями со стороны свертывающей системы крови, часто с развитием гиперкоагуляционного состояния.
Цель. Выявить частоту тромбоэмболических осложнений (ТЭО) у больных ВЗК и установить влияние приобретенных и наследственных факторов гиперкоагуляции, способствующих развитию ТЭО.
Материалы и методы. Проведена оценка клинического состояния 1238 больных ВЗК, находившихся на лечении в 2019 г. Из них 748 больных язвенным колитом (ЯК) и 490 больных болезнью Крона (БК). Среди больных ЯК мужчин 369 (49,3%), женщин – 379 (50,7%). У 10,1% пациентов с ЯК имели место клинически значимые ТЭО. Среди пациентов с БК мужчин 227 (46,3%), женщин – 263 (53,7%). У 7,3% пациентов с БК имелись клинически значимые ТЭО.
Результаты. В общей сложности у 112 (9,0%) из 1238 пациентов с ВЗК выявлены клинически значимые ТЭО, потребовавшие терапии антикоагулянтами. Среди пациентов с ЯК (n=748) у 76 (10,2%) выявлены клинически значимые ТЭО. Среди пациентов с БК (n=490) у 36 (7,3%) выявлены ТЭО. Из 112 больных ВЗК с клинически значимыми ТЭО у 45 (40,2%) выявлены генетические полиморфизмы, которые повышают сродство к фибриногену, увеличивают способность тромбоцитов к агрегации, способствуют снижению активности ферментов фолатного цикла, в том числе метилентетрагидрофолатредуктазы, что может проявляться умеренным повышением уровня гомоцистеина. Из 45 пациентов с ВЗК, имеющих клинически значимые ТЭО, обусловленные наследственными факторами, 30 (66,6%) больных страдали ЯК, 15 (33,7%) больных – БК (относительный риск 1,038; 95% доверительный интервал 0,746–1,444; χ2=0,049; р=0,83921). Кроме того, 67 (59,8%) пациентов с ВЗК, у которых отмечались клинически значимые ТЭО, не имели генетических полиморфизмов, приводящих к гиперкоагуляции.
Заключение. На основании проведенного анализа мы можем сделать заключение о том, что такие факторы риска развития ТЭО, как статус курильщика, длительный постельный режим, прием гормональных контрацептивов, варикозное расширение вен нижних конечностей, высокая активность заболевания, терапия глюкокортикостероидами, протяженность поражения кишки у больных ВЗК, генетические факторы тромбофилии, должны учитываться врачами-гастроэнтерологами при лечении больных ЯК и БК. Наследственный фактор гиперкоагуляции в равной степени влияет на развитие ТЭО у больных как ЯК, так и БК.
Ключевые слова: болезнь Крона, воспалительные заболевания кишечника, тромбоэмболические осложнения, язвенный колит
Aim. To identify the frequency of thromboembolic complications (TEC) in IBD patients and to determine the influence of acquired and inherited hypercoagulation factors that contribute to the development of TEС.
Materials and methods. The clinical status of 1,238 IBD patients who were treated in 2019 was evaluated. Of these, 748 patients with ulcerative colitis (UC) and 490 patients with Crohn's disease (CD). Among UC patients, there were 369 (49.3%) men and 379 (50.7%) women. In 10.1% of patients with UC, there were clinically significant feasibility studies. There were 227 (46.3%) men and 263 (53.7%) women among patients with CD; 7.3% of patients with CD had clinically significant feasibility studies.
Results. In general 112 (9.0%) of 1,238 IBD patients had clinically significant feasibility studies. Among patients with UC (n=748), 76 (10.2%) showed clinically significant feasibility studies. Among patients with CD (n=490), 36 (7.3%) had a feasibility study. Of 112 IBD patients with clinically significant TEC, 45 (40.2%) had genetic polymorphisms that increase affinity for fibrinogen, increase platelet aggregation, and contribute to a decrease in the activity of folate cycle enzymes, including methylenetetrahydrofolate reductase, which may be manifested by a moderate increase in homocysteine levels. Of the 45 IBD patients with clinically significant TEC due to inherited factors, 30 (66.6%) patients had UC, 15 (33.7%) patients had CD (hazard ratio 1.038, 95% confidence interval 0.746–1.444; χ2=0.049; p=0.83921); 67 (59.8%) patients with IBD who had clinically significant TEC did not have genetic polymorphisms leading to hypercoagulation.
Conclusion. Based on the analysis, we can conclude that such risk factors for the development of TEC as the status of a smoker, long bed rest, taking hormonal contraceptives, varicose veins of the lower extremities, high activity of the disease, glucocorticoids therapy, the extent of intestinal damage in patients with IBD, genetic factors, should be taken into account by gastroenterologists in the treatment of patients with UC and CD. The hereditary factor of hypercoagulation equally affects the development of TEC, both in patients with UC and CD.
Keywords: Crohn's disease, inflammatory bowel disease, thromboembolic complications, ulcerative colitis
Цель. Выявить частоту тромбоэмболических осложнений (ТЭО) у больных ВЗК и установить влияние приобретенных и наследственных факторов гиперкоагуляции, способствующих развитию ТЭО.
Материалы и методы. Проведена оценка клинического состояния 1238 больных ВЗК, находившихся на лечении в 2019 г. Из них 748 больных язвенным колитом (ЯК) и 490 больных болезнью Крона (БК). Среди больных ЯК мужчин 369 (49,3%), женщин – 379 (50,7%). У 10,1% пациентов с ЯК имели место клинически значимые ТЭО. Среди пациентов с БК мужчин 227 (46,3%), женщин – 263 (53,7%). У 7,3% пациентов с БК имелись клинически значимые ТЭО.
Результаты. В общей сложности у 112 (9,0%) из 1238 пациентов с ВЗК выявлены клинически значимые ТЭО, потребовавшие терапии антикоагулянтами. Среди пациентов с ЯК (n=748) у 76 (10,2%) выявлены клинически значимые ТЭО. Среди пациентов с БК (n=490) у 36 (7,3%) выявлены ТЭО. Из 112 больных ВЗК с клинически значимыми ТЭО у 45 (40,2%) выявлены генетические полиморфизмы, которые повышают сродство к фибриногену, увеличивают способность тромбоцитов к агрегации, способствуют снижению активности ферментов фолатного цикла, в том числе метилентетрагидрофолатредуктазы, что может проявляться умеренным повышением уровня гомоцистеина. Из 45 пациентов с ВЗК, имеющих клинически значимые ТЭО, обусловленные наследственными факторами, 30 (66,6%) больных страдали ЯК, 15 (33,7%) больных – БК (относительный риск 1,038; 95% доверительный интервал 0,746–1,444; χ2=0,049; р=0,83921). Кроме того, 67 (59,8%) пациентов с ВЗК, у которых отмечались клинически значимые ТЭО, не имели генетических полиморфизмов, приводящих к гиперкоагуляции.
Заключение. На основании проведенного анализа мы можем сделать заключение о том, что такие факторы риска развития ТЭО, как статус курильщика, длительный постельный режим, прием гормональных контрацептивов, варикозное расширение вен нижних конечностей, высокая активность заболевания, терапия глюкокортикостероидами, протяженность поражения кишки у больных ВЗК, генетические факторы тромбофилии, должны учитываться врачами-гастроэнтерологами при лечении больных ЯК и БК. Наследственный фактор гиперкоагуляции в равной степени влияет на развитие ТЭО у больных как ЯК, так и БК.
Ключевые слова: болезнь Крона, воспалительные заболевания кишечника, тромбоэмболические осложнения, язвенный колит
________________________________________________
Aim. To identify the frequency of thromboembolic complications (TEC) in IBD patients and to determine the influence of acquired and inherited hypercoagulation factors that contribute to the development of TEС.
Materials and methods. The clinical status of 1,238 IBD patients who were treated in 2019 was evaluated. Of these, 748 patients with ulcerative colitis (UC) and 490 patients with Crohn's disease (CD). Among UC patients, there were 369 (49.3%) men and 379 (50.7%) women. In 10.1% of patients with UC, there were clinically significant feasibility studies. There were 227 (46.3%) men and 263 (53.7%) women among patients with CD; 7.3% of patients with CD had clinically significant feasibility studies.
Results. In general 112 (9.0%) of 1,238 IBD patients had clinically significant feasibility studies. Among patients with UC (n=748), 76 (10.2%) showed clinically significant feasibility studies. Among patients with CD (n=490), 36 (7.3%) had a feasibility study. Of 112 IBD patients with clinically significant TEC, 45 (40.2%) had genetic polymorphisms that increase affinity for fibrinogen, increase platelet aggregation, and contribute to a decrease in the activity of folate cycle enzymes, including methylenetetrahydrofolate reductase, which may be manifested by a moderate increase in homocysteine levels. Of the 45 IBD patients with clinically significant TEC due to inherited factors, 30 (66.6%) patients had UC, 15 (33.7%) patients had CD (hazard ratio 1.038, 95% confidence interval 0.746–1.444; χ2=0.049; p=0.83921); 67 (59.8%) patients with IBD who had clinically significant TEC did not have genetic polymorphisms leading to hypercoagulation.
Conclusion. Based on the analysis, we can conclude that such risk factors for the development of TEC as the status of a smoker, long bed rest, taking hormonal contraceptives, varicose veins of the lower extremities, high activity of the disease, glucocorticoids therapy, the extent of intestinal damage in patients with IBD, genetic factors, should be taken into account by gastroenterologists in the treatment of patients with UC and CD. The hereditary factor of hypercoagulation equally affects the development of TEC, both in patients with UC and CD.
Keywords: Crohn's disease, inflammatory bowel disease, thromboembolic complications, ulcerative colitis
Полный текст
Список литературы
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DOI:10.1111/j.1572-0241.2006.00943.x.
3. Suárez Ferrer C, Vera Mendoza MI, Amo San Román L, et al. Risk of thromboembolic phenomena in patients with inflammatory bowel disease. Gastroenterol Hepatol. 2012;35:634-9. DOI:10.1016/j.gastrohep.2012.07.003
4. Twig G, Zandman-Goddard G, Szyper-Kravitz M, Shoenfeld Y. Systemic thromboembolism in inflammatory bowel disease: Mechanisms and clinical applications. Ann N Y Acad Sci. 2005;1051:166-73. DOI:10.1196/annals.1361.058
5. Grip O, Svensson PJ, Lindgren S. Inflammatory bowel disease promotes venous thrombosis earlier in life. Scand J Gastroenterol. 2000;35:619-23.
6. Sloan WP Jr, Bargen JA, Gage RP. Life histories of patients with chronic ulcerative colitis: A review of 2,000 cases. Gastroenterology. 1950;16:25-38.
7. Edwards FC, Truelove SC. The course and prognosis of ulcerative colitis III complications. Gut. 1964;5:1-22.
8. Talbot RW, Heppell J, Dozois RR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc. 1986;61:140-5.
9. Bernstein CN, Blanchard JF, Houston DS, Wajda A. The incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory bowel disease: A population-based cohort study. Thromb Haemost. 2001;85:430-4.
10. Yuhara H, Steinmaus C, Corley D, et al. Meta-analysis: the risk of venous thromboembolism in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013;37:953-62. DOI:10.1111/apt.12294
11. Grainge MJ, West J, Card TR. Venous thromboembolism during active disease and remission in inflammatory bowel disease: a cohort study. Lancet. 2010;375:657-63. DOI:10.1016/S0140-6736(09)61963-2
12. Horsted F, West J, Grainge MJ. Risk of venous thromboembolism in patients with cancer: a systematic review and meta-analysis. PLoS Med. 2012;9:1001275. DOI:10.1371/journal.pmed.1001275
13. Solem CA, Loftus EV, Tremaine WJ, Sandborn WJ. Venous thromboembolism in inflammatory bowel disease. Am J Gastroenterol. 2004;99:97-101.
DOI:10.1046/j.1572-0241.2003.04026
14. Koutroubakis IE. Therapy insight: Vascular complications in patients with inflammatory bowel disease. Nat Clin Pract Gastroenterol Hepatol. 2005;2:266-72. DOI:10.1038/ncpgasthep0190
15. Lijfering WM, Rosendaal FR, Cannegieter SC. Risk factors for venous thrombosis – current understanding from an epidemiological point of view. Br J Haematol. 2010;149:824. DOI:10.1111/j.1365-2141.2010.08206.x
16. Spina L, Saibeni S, Battaglioli T, et al. Thrombosis in inflammatory bowel diseases: role of inherited thrombophilia. Am J Gastroenterol. 2005;100:2036-4116.
DOI:10.1111/j.1572-0241.2005.42029
17. Nguyen GC, Bernstein CN, Bitton A, et al. Consensus statements on the risk, prevention, and treatment of venous thromboembolism in inflammatory bowel disease: Canadian Association of Gastroenterology. Gastroenterology. 2014;146:835-48. DOI:10.1053/j.gastro.2014.01.042
18. Alkim H, Koksal AR, Boga S, et al. Etiopathogenesis, Prevention, and treatment of thromboembolism in inflammatory bowel disease. Clin Appl Thromb Hemost. 2017;23(6):501-10. DOI:10.1177/1076029616632906
19. Ivashkin VT, Shelygin YuA, Belousova EA, et al. Draft Clinical guidelines for the diagnosis and treatment of ulcerative colitis. Coloproctology. 2019;18(4):7-36 (in Russian). DOI:10.33878/2073-7556-2019-18-4-7-36
20. Harvey RF, Bradshaw JM. A simple index of Crohn’s-disease activity. Lancet. 1980;315(8167):514.
21. Russian clinical guidelines for the diagnosis, treatment and prevention of venous thromboembolic complications (VTEO). Phlebology. 2017;4(2):44-6 (in Russian).
22. Kuznetsova BA. Laboratornye metody issledovaniia sistemy svertyvaniia krovi. Pod red. IN Bokareva; RATGPSS im. A. Shmidta. Moscow: Minzdravsotsrazvitiia RF, 2011 (in Russian).
23. Stomenskaia IS, Kostrova OIu, Struchko GIu, Timofeeva NIu. Thromboelastometry is a method. I.S. Stomenskaya, et al. Medical Almanac. 2017;2:96-8 (in Russian).
24. Magro F, Soares JB, Fernandes D. Venous thrombosis and prothrombotic factors in inflammatory bowel disease. World J Gastroenterol. 2014;20:4857-72. DOI:10.3748/wjg.v20.i17.4857
25. Algahtani FH, Farag YMK, Aljebreen AM, et al. Thromboembolic events in patients with inflammatory bowel disease. Saudi J Gastroenterol. 2016;22(6):423-7.
DOI:10.4103/1319-3767.195558
26. Galstyan GM, Polevodova OA, Gavrish AYu, et al. Thrombotic complications in patients with hemophilia. Terapevticheskii Arkhiv (Ter. Arkh.). 2017;89(7):76-84 (in Russian). DOI:10.17116/terarkh201789776-84
27. Schreiber S, Howaldt S, Schnoor M, et al. Recombinant erythropoietin for the treatment of anemia in inflammatory bowel disease. N Engl J Med. 1996;334:619-23.
28. Jelkmann W. Proinflammatory cytokines lowering erythropoietin production. J Interferon Cytokine Res. 1998;18:555-9.
29. Kyrle PA, Minar E, Hirschl M, et al. High plasma levels of factor VIII and the risk of recurrent venous thromboembolism. N Engl J Med. 2000;343:457-62. DOI:10.1056/NEJM200008173430702
30. Chiarantini E, Valanzano R, Liotta AA. Hemostatic abnormalities in inflammatory bowel disease. Thromb Res. 1996;82:137-46.
31. Chamouard P, Grunebaum L, Wiesel ML, et al. Prothrombin fragment 1+2 and thrombin-antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases. Eur J Gastroenterol Hepatol. 1995;7:1183-8.
32. Heits F, Stahl M, Ludwig D, et al. Elevated serum thrombopoietin and interleukin-6 concentrations in thrombocytosis associated with inflammatory bowel disease. J Interferon Cytokine Res. 1999;19:757-60.
33. Sands BE, Bank S, Sninsky CA, et al. Preliminary evaluation of safety and activity of recombinant human interleukin-11 in patients with active Crohn’s disease. Gastroenterology. 1999;117:58-64.
34. Centers for Disease Control and Prevention (CDC). Venous thromboembolism in adult hospitalizations – United States, 2007–2009. MMWR Morb Mortal Wkly Rep. 2012;61:401-4.
35. Faye AS, Hung KW, Cheng K, et al. Minor hematochezia decreases use of venous thromboembolism prophylaxis in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2019;26(9):1394-400. DOI:10.1093/ibd/izz269; PMID: 31689354
36. Yuhara H, Steinmaus C, Corley D, et al. Meta-analysis: the risk of venous thromboembolism in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013;37(10):953-62. DOI:10.1111/apt.1229
37. Nguyen GC, Sam J. Rising prevalence of venous thromboembolism and its impact on mortality among hospitalized inflammatory bowel disease patients. Am J Gastroenterol. 2008;103(9):2272-80. DOI:10.1111/j.15720241.2008.02052.x
2. Danese S, Papa A, Saibeni S, et al. Inflammation and coagulation in inflammatory bowel disease: The clot thickens. Am J Gastroenterol. 2007;102:174-86.
DOI:10.1111/j.1572-0241.2006.00943.x.
3. Suárez Ferrer C, Vera Mendoza MI, Amo San Román L, et al. Risk of thromboembolic phenomena in patients with inflammatory bowel disease. Gastroenterol Hepatol. 2012;35:634-9. DOI:10.1016/j.gastrohep.2012.07.003
4. Twig G, Zandman-Goddard G, Szyper-Kravitz M, Shoenfeld Y. Systemic thromboembolism in inflammatory bowel disease: Mechanisms and clinical applications. Ann N Y Acad Sci. 2005;1051:166-73. DOI:10.1196/annals.1361.058
5. Grip O, Svensson PJ, Lindgren S. Inflammatory bowel disease promotes venous thrombosis earlier in life. Scand J Gastroenterol. 2000;35:619-23.
6. Sloan WP Jr, Bargen JA, Gage RP. Life histories of patients with chronic ulcerative colitis: A review of 2,000 cases. Gastroenterology. 1950;16:25-38.
7. Edwards FC, Truelove SC. The course and prognosis of ulcerative colitis III complications. Gut. 1964;5:1-22.
8. Talbot RW, Heppell J, Dozois RR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc. 1986;61:140-5.
9. Bernstein CN, Blanchard JF, Houston DS, Wajda A. The incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory bowel disease: A population-based cohort study. Thromb Haemost. 2001;85:430-4.
10. Yuhara H, Steinmaus C, Corley D, et al. Meta-analysis: the risk of venous thromboembolism in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013;37:953-62. DOI:10.1111/apt.12294
11. Grainge MJ, West J, Card TR. Venous thromboembolism during active disease and remission in inflammatory bowel disease: a cohort study. Lancet. 2010;375:657-63. DOI:10.1016/S0140-6736(09)61963-2
12. Horsted F, West J, Grainge MJ. Risk of venous thromboembolism in patients with cancer: a systematic review and meta-analysis. PLoS Med. 2012;9:1001275. DOI:10.1371/journal.pmed.1001275
13. Solem CA, Loftus EV, Tremaine WJ, Sandborn WJ. Venous thromboembolism in inflammatory bowel disease. Am J Gastroenterol. 2004;99:97-101.
DOI:10.1046/j.1572-0241.2003.04026
14. Koutroubakis IE. Therapy insight: Vascular complications in patients with inflammatory bowel disease. Nat Clin Pract Gastroenterol Hepatol. 2005;2:266-72. DOI:10.1038/ncpgasthep0190
15. Lijfering WM, Rosendaal FR, Cannegieter SC. Risk factors for venous thrombosis – current understanding from an epidemiological point of view. Br J Haematol. 2010;149:824. DOI:10.1111/j.1365-2141.2010.08206.x
16. Spina L, Saibeni S, Battaglioli T, et al. Thrombosis in inflammatory bowel diseases: role of inherited thrombophilia. Am J Gastroenterol. 2005;100:2036-4116.
DOI:10.1111/j.1572-0241.2005.42029
17. Nguyen GC, Bernstein CN, Bitton A, et al. Consensus statements on the risk, prevention, and treatment of venous thromboembolism in inflammatory bowel disease: Canadian Association of Gastroenterology. Gastroenterology. 2014;146:835-48. DOI:10.1053/j.gastro.2014.01.042
18. Alkim H, Koksal AR, Boga S, et al. Etiopathogenesis, Prevention, and treatment of thromboembolism in inflammatory bowel disease. Clin Appl Thromb Hemost. 2017;23(6):501-10. DOI:10.1177/1076029616632906
19. Ивашкин В.Т., Шелыгин Ю.А., Белоусова Е.А., и др. Проект клинических рекомендаций по диагностике и лечению язвенного колита. Колопроктология. 2019;18(4):7-36 [Ivashkin VT, Shelygin YuA, Belousova EA, et al. Draft Clinical guidelines for the diagnosis and treatment of ulcerative colitis. Coloproctology. 2019;18(4):7-36 (in Russian)]. DOI:10.33878/2073-7556-2019-18-4-7-36
20. Harvey RF, Bradshaw JM. A simple index of Crohn’s-disease activity. Lancet. 1980;315(8167):514.
21. Российские клинические рекомендации по диагностике, лечению и профилактике венозных тромбоэмболических осложнений (ВТЭО). Флебология. 2017;4(2):44-6 [Russian clinical guidelines for the diagnosis, treatment and prevention of venous thromboembolic complications (VTEO). Phlebology. 2017;4(2):44-6 (in Russian)].
22. Кузнецова Б.А. Лабораторные методы исследования системы свертывания крови. Под ред. И.Н. Бокарева; РАТГПСС им. А. Шмидта. М.: Минздравсоцразвития РФ, 2011 [Kuznetsova BA. Laboratornye metody issledovaniia sistemy svertyvaniia krovi. Pod red. IN Bokareva; RATGPSS im. A. Shmidta. Moscow: Minzdravsotsrazvitiia RF, 2011 (in Russian)].
23. Cтоменская И.С., Кострова О.Ю., Стручко Г.Ю., Тимофеева Н.Ю. Тромбоэластометрия – метод лабораторной диагностики нарушений системы гемостаза. Мед. альманах. 2017;2:96-8 [Stomenskaia IS, Kostrova OIu, Struchko GIu, Timofeeva NIu. Thromboelastometry is a method. I.S. Stomenskaya, et al. Medical Almanac. 2017;2:96-8 (in Russian)].
24. Magro F, Soares JB, Fernandes D. Venous thrombosis and prothrombotic factors in inflammatory bowel disease. World J Gastroenterol. 2014;20:4857-72. DOI:10.3748/wjg.v20.i17.4857
25. Algahtani FH, Farag YMK, Aljebreen AM, et al. Thromboembolic events in patients with inflammatory bowel disease. Saudi J Gastroenterol. 2016;22(6):423-7.
DOI:10.4103/1319-3767.195558
26. Галстян Г.М., Полеводова О.А., Гавриш А.Ю., и др. Тромботические осложнения у больных гемофилией. Терапевтический архив. 2017;89(7):76-84 [Galstyan GM, Polevodova OA, Gavrish AYu, et al. Thrombotic complications in patients with hemophilia. Terapevticheskii Arkhiv (Ter. Arkh.). 2017;89(7):76-84 (in Russian)].
DOI:10.17116/terarkh201789776-84
27. Schreiber S, Howaldt S, Schnoor M, et al. Recombinant erythropoietin for the treatment of anemia in inflammatory bowel disease. N Engl J Med. 1996;334:619-23.
28. Jelkmann W. Proinflammatory cytokines lowering erythropoietin production. J Interferon Cytokine Res. 1998;18:555-9.
29. Kyrle PA, Minar E, Hirschl M, et al. High plasma levels of factor VIII and the risk of recurrent venous thromboembolism. N Engl J Med. 2000;343:457-62. DOI:10.1056/NEJM200008173430702
30. Chiarantini E, Valanzano R, Liotta AA. Hemostatic abnormalities in inflammatory bowel disease. Thromb Res. 1996;82:137-46.
31. Chamouard P, Grunebaum L, Wiesel ML, et al. Prothrombin fragment 1+2 and thrombin-antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases. Eur J Gastroenterol Hepatol. 1995;7:1183-8.
32. Heits F, Stahl M, Ludwig D, et al. Elevated serum thrombopoietin and interleukin-6 concentrations in thrombocytosis associated with inflammatory bowel disease. J Interferon Cytokine Res. 1999;19:757-60.
33. Sands BE, Bank S, Sninsky CA, et al. Preliminary evaluation of safety and activity of recombinant human interleukin-11 in patients with active Crohn’s disease. Gastroenterology. 1999;117:58-64.
34. Centers for Disease Control and Prevention (CDC). Venous thromboembolism in adult hospitalizations – United States, 2007–2009. MMWR Morb Mortal Wkly Rep. 2012;61:401-4.
35. Faye AS, Hung KW, Cheng K, et al. Minor hematochezia decreases use of venous thromboembolism prophylaxis in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2019;26(9):1394-400. DOI:10.1093/ibd/izz269; PMID: 31689354
36. Yuhara H, Steinmaus C, Corley D, et al. Meta-analysis: the risk of venous thromboembolism in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013;37(10):953-62. DOI:10.1111/apt.1229
37. Nguyen GC, Sam J. Rising prevalence of venous thromboembolism and its impact on mortality among hospitalized inflammatory bowel disease patients. Am J Gastroenterol. 2008;103(9):2272-80. DOI:10.1111/j.15720241.2008.02052.x
________________________________________________
2. Danese S, Papa A, Saibeni S, et al. Inflammation and coagulation in inflammatory bowel disease: The clot thickens. Am J Gastroenterol. 2007;102:174-86.
DOI:10.1111/j.1572-0241.2006.00943.x.
3. Suárez Ferrer C, Vera Mendoza MI, Amo San Román L, et al. Risk of thromboembolic phenomena in patients with inflammatory bowel disease. Gastroenterol Hepatol. 2012;35:634-9. DOI:10.1016/j.gastrohep.2012.07.003
4. Twig G, Zandman-Goddard G, Szyper-Kravitz M, Shoenfeld Y. Systemic thromboembolism in inflammatory bowel disease: Mechanisms and clinical applications. Ann N Y Acad Sci. 2005;1051:166-73. DOI:10.1196/annals.1361.058
5. Grip O, Svensson PJ, Lindgren S. Inflammatory bowel disease promotes venous thrombosis earlier in life. Scand J Gastroenterol. 2000;35:619-23.
6. Sloan WP Jr, Bargen JA, Gage RP. Life histories of patients with chronic ulcerative colitis: A review of 2,000 cases. Gastroenterology. 1950;16:25-38.
7. Edwards FC, Truelove SC. The course and prognosis of ulcerative colitis III complications. Gut. 1964;5:1-22.
8. Talbot RW, Heppell J, Dozois RR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc. 1986;61:140-5.
9. Bernstein CN, Blanchard JF, Houston DS, Wajda A. The incidence of deep venous thrombosis and pulmonary embolism among patients with inflammatory bowel disease: A population-based cohort study. Thromb Haemost. 2001;85:430-4.
10. Yuhara H, Steinmaus C, Corley D, et al. Meta-analysis: the risk of venous thromboembolism in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013;37:953-62. DOI:10.1111/apt.12294
11. Grainge MJ, West J, Card TR. Venous thromboembolism during active disease and remission in inflammatory bowel disease: a cohort study. Lancet. 2010;375:657-63. DOI:10.1016/S0140-6736(09)61963-2
12. Horsted F, West J, Grainge MJ. Risk of venous thromboembolism in patients with cancer: a systematic review and meta-analysis. PLoS Med. 2012;9:1001275. DOI:10.1371/journal.pmed.1001275
13. Solem CA, Loftus EV, Tremaine WJ, Sandborn WJ. Venous thromboembolism in inflammatory bowel disease. Am J Gastroenterol. 2004;99:97-101.
DOI:10.1046/j.1572-0241.2003.04026
14. Koutroubakis IE. Therapy insight: Vascular complications in patients with inflammatory bowel disease. Nat Clin Pract Gastroenterol Hepatol. 2005;2:266-72. DOI:10.1038/ncpgasthep0190
15. Lijfering WM, Rosendaal FR, Cannegieter SC. Risk factors for venous thrombosis – current understanding from an epidemiological point of view. Br J Haematol. 2010;149:824. DOI:10.1111/j.1365-2141.2010.08206.x
16. Spina L, Saibeni S, Battaglioli T, et al. Thrombosis in inflammatory bowel diseases: role of inherited thrombophilia. Am J Gastroenterol. 2005;100:2036-4116.
DOI:10.1111/j.1572-0241.2005.42029
17. Nguyen GC, Bernstein CN, Bitton A, et al. Consensus statements on the risk, prevention, and treatment of venous thromboembolism in inflammatory bowel disease: Canadian Association of Gastroenterology. Gastroenterology. 2014;146:835-48. DOI:10.1053/j.gastro.2014.01.042
18. Alkim H, Koksal AR, Boga S, et al. Etiopathogenesis, Prevention, and treatment of thromboembolism in inflammatory bowel disease. Clin Appl Thromb Hemost. 2017;23(6):501-10. DOI:10.1177/1076029616632906
19. Ivashkin VT, Shelygin YuA, Belousova EA, et al. Draft Clinical guidelines for the diagnosis and treatment of ulcerative colitis. Coloproctology. 2019;18(4):7-36 (in Russian). DOI:10.33878/2073-7556-2019-18-4-7-36
20. Harvey RF, Bradshaw JM. A simple index of Crohn’s-disease activity. Lancet. 1980;315(8167):514.
21. Russian clinical guidelines for the diagnosis, treatment and prevention of venous thromboembolic complications (VTEO). Phlebology. 2017;4(2):44-6 (in Russian).
22. Kuznetsova BA. Laboratornye metody issledovaniia sistemy svertyvaniia krovi. Pod red. IN Bokareva; RATGPSS im. A. Shmidta. Moscow: Minzdravsotsrazvitiia RF, 2011 (in Russian).
23. Stomenskaia IS, Kostrova OIu, Struchko GIu, Timofeeva NIu. Thromboelastometry is a method. I.S. Stomenskaya, et al. Medical Almanac. 2017;2:96-8 (in Russian).
24. Magro F, Soares JB, Fernandes D. Venous thrombosis and prothrombotic factors in inflammatory bowel disease. World J Gastroenterol. 2014;20:4857-72. DOI:10.3748/wjg.v20.i17.4857
25. Algahtani FH, Farag YMK, Aljebreen AM, et al. Thromboembolic events in patients with inflammatory bowel disease. Saudi J Gastroenterol. 2016;22(6):423-7.
DOI:10.4103/1319-3767.195558
26. Galstyan GM, Polevodova OA, Gavrish AYu, et al. Thrombotic complications in patients with hemophilia. Terapevticheskii Arkhiv (Ter. Arkh.). 2017;89(7):76-84 (in Russian). DOI:10.17116/terarkh201789776-84
27. Schreiber S, Howaldt S, Schnoor M, et al. Recombinant erythropoietin for the treatment of anemia in inflammatory bowel disease. N Engl J Med. 1996;334:619-23.
28. Jelkmann W. Proinflammatory cytokines lowering erythropoietin production. J Interferon Cytokine Res. 1998;18:555-9.
29. Kyrle PA, Minar E, Hirschl M, et al. High plasma levels of factor VIII and the risk of recurrent venous thromboembolism. N Engl J Med. 2000;343:457-62. DOI:10.1056/NEJM200008173430702
30. Chiarantini E, Valanzano R, Liotta AA. Hemostatic abnormalities in inflammatory bowel disease. Thromb Res. 1996;82:137-46.
31. Chamouard P, Grunebaum L, Wiesel ML, et al. Prothrombin fragment 1+2 and thrombin-antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases. Eur J Gastroenterol Hepatol. 1995;7:1183-8.
32. Heits F, Stahl M, Ludwig D, et al. Elevated serum thrombopoietin and interleukin-6 concentrations in thrombocytosis associated with inflammatory bowel disease. J Interferon Cytokine Res. 1999;19:757-60.
33. Sands BE, Bank S, Sninsky CA, et al. Preliminary evaluation of safety and activity of recombinant human interleukin-11 in patients with active Crohn’s disease. Gastroenterology. 1999;117:58-64.
34. Centers for Disease Control and Prevention (CDC). Venous thromboembolism in adult hospitalizations – United States, 2007–2009. MMWR Morb Mortal Wkly Rep. 2012;61:401-4.
35. Faye AS, Hung KW, Cheng K, et al. Minor hematochezia decreases use of venous thromboembolism prophylaxis in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2019;26(9):1394-400. DOI:10.1093/ibd/izz269; PMID: 31689354
36. Yuhara H, Steinmaus C, Corley D, et al. Meta-analysis: the risk of venous thromboembolism in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2013;37(10):953-62. DOI:10.1111/apt.1229
37. Nguyen GC, Sam J. Rising prevalence of venous thromboembolism and its impact on mortality among hospitalized inflammatory bowel disease patients. Am J Gastroenterol. 2008;103(9):2272-80. DOI:10.1111/j.15720241.2008.02052.x
Авторы
А.А. Лищинская1, О.В. Князев*1–3, А.В. Каграманова1, Г.А. Дудина1, Е.А. Сабельникова1, И.А. Ли1, К.К. Носкова1, Н.А. Бодунова1, А.И. Парфенов1
1 ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы, Москва, Россия;
2 ФГБУ «Национальный медицинский исследовательский центр колопроктологии им. А.Н. Рыжих» Минздрава России, Москва, Россия;
3 ГБУ «Научно-исследовательский институт организации здравоохранения и медицинского менеджмента» Департамента здравоохранения г. Москвы, Москва, Россия
*oleg7@bk.ru
1 Loginov Moscow Clinical Scientific Center, Moscow, Russia;
2 Ryzhykh National Medical Research Centre for Coloproctology, Moscow, Russia;
3 Research Institute of Health Organization and Medical Management, Moscow, Russia
*oleg7@bk.ru
1 ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы, Москва, Россия;
2 ФГБУ «Национальный медицинский исследовательский центр колопроктологии им. А.Н. Рыжих» Минздрава России, Москва, Россия;
3 ГБУ «Научно-исследовательский институт организации здравоохранения и медицинского менеджмента» Департамента здравоохранения г. Москвы, Москва, Россия
*oleg7@bk.ru
________________________________________________
1 Loginov Moscow Clinical Scientific Center, Moscow, Russia;
2 Ryzhykh National Medical Research Centre for Coloproctology, Moscow, Russia;
3 Research Institute of Health Organization and Medical Management, Moscow, Russia
*oleg7@bk.ru
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