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Воспаление и легочная гипертензия у пациентов с хронической обструктивной болезнью легких
Воспаление и легочная гипертензия у пациентов с хронической обструктивной болезнью легких
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Аннотация
Цель исследования: определение профиля провоспалительных циктокинов у пациентов с легочной гипертензией на фоне хронической обструктивной болезни легких (ХОБЛ).
Материалы и методы: в исследование включен 51 пациент, из них с ХОБЛ – 11 больных и группа здоровых лиц (13 человек). В данной работе сделан акцент на ЛГ у пациентов с ХОБЛ в сравнении с контролем. Определяли высокочувствительный С-реактивный белок (СРБ), интерлейкины (ИЛ) ИЛ-1, 6, фактор некроза опухоли-α (ФНО-α) и sCD40L.
Результаты: уровень СРБ достоверно выше (р<0,05) в группе ХОБЛ (5,6±1,2 мг/л) по сравнению со здоровыми (0,5±0,1 мг/л). Концентрации ИЛ-1b у больных ХОБЛ были сопоставимы со здоровыми (2,3±0,6 пкг/мл против 2,4±0,2 пкг/мл). Уровень ФНО-α и ИЛ-6 ниже нормы у пациентов с ХОБЛ по сравнению со здоровыми.
Заключение: особенности характеристики воспалительного процесса при ассоциированных формах ЛГ (тенденция к увеличению уровня фракталкина при ХОБЛ) можно использовать с целью дифференциальной диагностики ЛГ.
Ключевые слова: легочная гипертензия, хроническая обструктивная болезнь легких, патогенез, лечение, воспаление, фенотип, цитокины, фракталкин.
Material and methods: 51 patients with PH were included in clinical study from them with chronic obstructive pulmonary disease (COPD) – 11 patients and group of 13 healthy persons. High sensitivity C-reactive protein (hsCRP), interleukin (IL)-1, 6, 8, TNF-α and sCD40L were evaluated.
Results: the C-reactive protein (hsCRP) level is authentic above (р<0,05) in COPD group (5,6±1,2 mg/l) in comparison with healthy group (0,5±0,1 mg/l). The concentration of IL-1b is similarly in COPD group and healthy group (2,3±0,6 pkg/ml vs 2,4±0,2 pkg/ml).
Conclusion: features of inflammatory characteristic COPD can be used for the purpose of differential diagnostics of pulmonary hypertension.
Key words: pulmonary hypertension, chronic obstructive pulmonary disease, pathogenesis, treatment, inflammation, phenotype, interleukin, fractalkine.
Материалы и методы: в исследование включен 51 пациент, из них с ХОБЛ – 11 больных и группа здоровых лиц (13 человек). В данной работе сделан акцент на ЛГ у пациентов с ХОБЛ в сравнении с контролем. Определяли высокочувствительный С-реактивный белок (СРБ), интерлейкины (ИЛ) ИЛ-1, 6, фактор некроза опухоли-α (ФНО-α) и sCD40L.
Результаты: уровень СРБ достоверно выше (р<0,05) в группе ХОБЛ (5,6±1,2 мг/л) по сравнению со здоровыми (0,5±0,1 мг/л). Концентрации ИЛ-1b у больных ХОБЛ были сопоставимы со здоровыми (2,3±0,6 пкг/мл против 2,4±0,2 пкг/мл). Уровень ФНО-α и ИЛ-6 ниже нормы у пациентов с ХОБЛ по сравнению со здоровыми.
Заключение: особенности характеристики воспалительного процесса при ассоциированных формах ЛГ (тенденция к увеличению уровня фракталкина при ХОБЛ) можно использовать с целью дифференциальной диагностики ЛГ.
Ключевые слова: легочная гипертензия, хроническая обструктивная болезнь легких, патогенез, лечение, воспаление, фенотип, цитокины, фракталкин.
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Material and methods: 51 patients with PH were included in clinical study from them with chronic obstructive pulmonary disease (COPD) – 11 patients and group of 13 healthy persons. High sensitivity C-reactive protein (hsCRP), interleukin (IL)-1, 6, 8, TNF-α and sCD40L were evaluated.
Results: the C-reactive protein (hsCRP) level is authentic above (р<0,05) in COPD group (5,6±1,2 mg/l) in comparison with healthy group (0,5±0,1 mg/l). The concentration of IL-1b is similarly in COPD group and healthy group (2,3±0,6 pkg/ml vs 2,4±0,2 pkg/ml).
Conclusion: features of inflammatory characteristic COPD can be used for the purpose of differential diagnostics of pulmonary hypertension.
Key words: pulmonary hypertension, chronic obstructive pulmonary disease, pathogenesis, treatment, inflammation, phenotype, interleukin, fractalkine.
Полный текст
Список литературы
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2. Рекомендации ВНОК по диагностике и лечению легочной гипертензии. Кардиоваскул. терапия и профилактика. 2007; 6 (6). Прил. 2.
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9. Jais X, Launay D, Yaici A et al. Immunosuppressive therapy in lupus- and mixed connective tissue disease-associated pulmonary arterial hypertension: a retrospective analysis of twenty-three cases. Arthritis Rheum 2008; 58 (2): 521–31.
10. Lagrand WK, Visser CA, Hermens WT et al C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon? Circulation 1999; 100: 96–102.
11. Lakoski SG, Cushman M, Palmas W et al The relationship between blood pressure and C-reactive protein in the Multi-Ethnic Study of Atherosclerosis (MESA). J Am Coll Cardiol 2005; 46: 1869–74.
12. Patel AR, Hurst JR, Wedzicha JA. The potential value of biomarkers in diagnosis and staging of COPD and exacerbations. Semin Respir Crit Care Med 2010; 31 (3): 267–75.
13. Joppa P, Petrasova D, Stancak B et al. Systemic inflammation in patients with COPD and pulmonary hypertension. Chest 2006; 130 (2): 326–33.
14. Venugopal SK, Devaraj S, Yuhanna I et al Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation 2002; 106: 1439–41.
15. Verma S, Li SH, Badiwala MV et al Endothelin antagonism and interleukin-6 inhibition attenuate the proatherogenic effects of C-reactive protein. Circulation 2002; 105: 1890–96.
16. Humbert M, Monti G, Brenot F et al. Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension. Am J Respir Crit Care Med 1995; 151 (5): 1628–31.
17. Heresi G, Dweik R. Biomarkers in pulmonary hypertension. PVRI review 2010; 2 (1): 12–16.
18. Peacock AJ, Murphy NF, McMurray JJ et al. An epidemiological study of pulmonary arterial hypertension. Eur Respir J 2007; 30 (1): 104–9.
19. Thabut G, Dauriat G, Stern JB et al. Pulmonary hemodynamics in advanced COPD candidates for lung volume reduction surgery or lung transplantation. Chest 2005; 127 (5): 1531–6.
20. Hoeper MM, Mayer E, Simonneau G et al. Chronic thromboembolic pulmonary hypertension. Circulation 2006; 113 (16): 2011–20.
21. Humbert M, Sitbon O, Chaouat A et al. Pulmonary arterial hypertension in France: results from a national registry. Am J Respir Crit Care Med 2006; 173 (9): 1023–30.
22. Dorfmuller P, Perros F, Balabanian K et al Inflammation in pulmonary arterial hypertension. Eur Respir J 2003; 22: 358–63.
23. Rich S, Dantzker DR, Ayres SM et al Primary pulmonary hypertension: a national prospective study. Ann Intern Med 1987; 107: 216–23.
24. Amany R. Seraga, Sahar M et al. Regulated upon activation, normal T-cell expressed and secreted chemokine and interleukin-6 in rheumatic pulmonary hypertension, targets for therapeutic decisions. Eur J Cardiothorac Surg 2010; 37: 853–58.
25. Tuder RM, Groves B, Badesch DB et al. Exuberant endothelial cell growth and element of inammation are present in plexiform lesions of pulmonary hypertension. Am J Pathol 1994; 144: 275–85.
26. Fong AM, Robinson LA, Streeber DA et al. Fractalkine and CX3CR1 mediate a novel mechanism of leukocyte capture, firm adhesion, and activation under physiologic flow. J Exp Med 1998; 188: 1413.
27. Garcia GE, Xia Y, Chen S et al. NF-kappaB-dependent fractalkine induction in rat aortic endothelial cells stimulated by IL-1beta, TNF-alpha, and LPS. J Leukoc Biol 2000; 67 (4): 577–84.
28. Ludwig A, Berkhout T, Moores K et al. Fractalkine is expressed by smooth muscle cells in response to IFN-gamma and TNF-alpha and is modulated by metalloproteinase activity. J Immunol 2002; 168 (2): 604–12.
29. Moon SO, Kim W, Sung MJ et al. Resveratrol suppresses tumor necrosis factor-alpha-induced fractalkine expression in endothelial cells. Mol Pharmacol 2006; 70 (1): 112–9.
30. Wang XX, Zhang FR, Shang YP et al. Transplantation of autologous endothelial progenitor cells may be beneficial in patients with idiopathic pulmonary arterial hypertension: a pilot randomized controlled trial. J Am Coll Cardiol 2007; 49.
2. Рекомендации ВНОК по диагностике и лечению легочной гипертензии. Кардиоваскул. терапия и профилактика. 2007; 6 (6). Прил. 2.
3. Клячкина И.Л. Муколитические препараты при продуктивном кашле у больных хронической обструктивной болезнью легких. Cons. Med. 2007; 9 (3).
4. Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. (Based on the April 1998 NHLBI/WHO Workshop). National Institutes of Health, National Heart. Lung and Blood Institute. April 2001 (Updated 2003).
5. Белоусов Ю.Б., Омельяновский В.В. Клиническая фармакология болезней органов дыхания у детей. Рук-во для врачей. М., 1996; с. 176.
6. Principi N, Zavattini G. Possibility of interaction among antibiotics and mucolytics in children. Int J Pharm Res 1986; 6 (5) 369–72.
7. Humbert M, Morrell NW, Archer SL et al. Cellular and molecular patho-biology of pulmonary arterial hypertension. J Am Coll Cardiol 2004; 43: S13–24.
8. Sanchez O, Sitbon O, Jaïs X et al. Immunosuppressive therapy in connective tissue diseases-associated pulmonary arterial hypertension. Chest 2006; 130 (1): 182–9.
9. Jais X, Launay D, Yaici A et al. Immunosuppressive therapy in lupus- and mixed connective tissue disease-associated pulmonary arterial hypertension: a retrospective analysis of twenty-three cases. Arthritis Rheum 2008; 58 (2): 521–31.
10. Lagrand WK, Visser CA, Hermens WT et al C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon? Circulation 1999; 100: 96–102.
11. Lakoski SG, Cushman M, Palmas W et al The relationship between blood pressure and C-reactive protein in the Multi-Ethnic Study of Atherosclerosis (MESA). J Am Coll Cardiol 2005; 46: 1869–74.
12. Patel AR, Hurst JR, Wedzicha JA. The potential value of biomarkers in diagnosis and staging of COPD and exacerbations. Semin Respir Crit Care Med 2010; 31 (3): 267–75.
13. Joppa P, Petrasova D, Stancak B et al. Systemic inflammation in patients with COPD and pulmonary hypertension. Chest 2006; 130 (2): 326–33.
14. Venugopal SK, Devaraj S, Yuhanna I et al Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation 2002; 106: 1439–41.
15. Verma S, Li SH, Badiwala MV et al Endothelin antagonism and interleukin-6 inhibition attenuate the proatherogenic effects of C-reactive protein. Circulation 2002; 105: 1890–96.
16. Humbert M, Monti G, Brenot F et al. Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension. Am J Respir Crit Care Med 1995; 151 (5): 1628–31.
17. Heresi G, Dweik R. Biomarkers in pulmonary hypertension. PVRI review 2010; 2 (1): 12–16.
18. Peacock AJ, Murphy NF, McMurray JJ et al. An epidemiological study of pulmonary arterial hypertension. Eur Respir J 2007; 30 (1): 104–9.
19. Thabut G, Dauriat G, Stern JB et al. Pulmonary hemodynamics in advanced COPD candidates for lung volume reduction surgery or lung transplantation. Chest 2005; 127 (5): 1531–6.
20. Hoeper MM, Mayer E, Simonneau G et al. Chronic thromboembolic pulmonary hypertension. Circulation 2006; 113 (16): 2011–20.
21. Humbert M, Sitbon O, Chaouat A et al. Pulmonary arterial hypertension in France: results from a national registry. Am J Respir Crit Care Med 2006; 173 (9): 1023–30.
22. Dorfmuller P, Perros F, Balabanian K et al Inflammation in pulmonary arterial hypertension. Eur Respir J 2003; 22: 358–63.
23. Rich S, Dantzker DR, Ayres SM et al Primary pulmonary hypertension: a national prospective study. Ann Intern Med 1987; 107: 216–23.
24. Amany R. Seraga, Sahar M et al. Regulated upon activation, normal T-cell expressed and secreted chemokine and interleukin-6 in rheumatic pulmonary hypertension, targets for therapeutic decisions. Eur J Cardiothorac Surg 2010; 37: 853–58.
25. Tuder RM, Groves B, Badesch DB et al. Exuberant endothelial cell growth and element of inammation are present in plexiform lesions of pulmonary hypertension. Am J Pathol 1994; 144: 275–85.
26. Fong AM, Robinson LA, Streeber DA et al. Fractalkine and CX3CR1 mediate a novel mechanism of leukocyte capture, firm adhesion, and activation under physiologic flow. J Exp Med 1998; 188: 1413.
27. Garcia GE, Xia Y, Chen S et al. NF-kappaB-dependent fractalkine induction in rat aortic endothelial cells stimulated by IL-1beta, TNF-alpha, and LPS. J Leukoc Biol 2000; 67 (4): 577–84.
28. Ludwig A, Berkhout T, Moores K et al. Fractalkine is expressed by smooth muscle cells in response to IFN-gamma and TNF-alpha and is modulated by metalloproteinase activity. J Immunol 2002; 168 (2): 604–12.
29. Moon SO, Kim W, Sung MJ et al. Resveratrol suppresses tumor necrosis factor-alpha-induced fractalkine expression in endothelial cells. Mol Pharmacol 2006; 70 (1): 112–9.
30. Wang XX, Zhang FR, Shang YP et al. Transplantation of autologous endothelial progenitor cells may be beneficial in patients with idiopathic pulmonary arterial hypertension: a pilot randomized controlled trial. J Am Coll Cardiol 2007; 49.
Авторы
С.Н.Наконечников, И.Е.Чазова, Т.В.Мартынюк, Л.Г.Ратова, А.В.Рвачева, К.А.Зыков, В.П.Масенко
1 НИИ клинической кардиологии им. А.Л.Мясникова, Москва;
2 ФГУ РКНПК Минздравсоцразвития РФ, Москва
1 НИИ клинической кардиологии им. А.Л.Мясникова, Москва;
2 ФГУ РКНПК Минздравсоцразвития РФ, Москва
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