Нарушения в системе гемостаза при эндогенном гиперкортицизме и метаболическом синдроме

Длительная гиперкортизолемия сопровождается множественными дефектами регуляции различных обменов веществ. Вместе с метаболическими эффектами глюкокортикоиды оказывают действие непосредственно на сосудистую стенку, влияя на ее ремоделирование и ангиогенез. Синдром эндогенного гиперкортицизма характеризуется достаточно разно­образными нарушениями системы гемостаза с тенденцией к гиперкоагуляции. Изменения метаболических и гемостатических показателей в активной стадии заболевания длительное время не нормализуются в стадии ремиссии, в связи с чем сохраняется риск развития атеросклероза, атеротромбоза и тромбоэмболических осложнений, что обусловливает необходимость последующей медикаментозной их коррекции. По данным зарубежной литературы, тромбоэмболические осложнения являются основной причиной смертности у данных больных и встречаются в 4 раза чаще, чем в популяции.

гиперкортицизм, метаболический синдром, гемостаз, тромбоэмболические осложнения

1. Нейроэндокринология. Клинические очерки. Под ред. Е.И. Маровой. Ярославль: ДИА-пресс 1999: 81-144.

2. Pivonello R., Faggiano A., Lombardi G., Colao A. The metabolic syndrome and cardiovascular risk in Cushing's syndrome. Endocrin Metab Clin North Am 2005; 34: 2: 327-339.

3. Colao A., Pivonello R., Spiezia S. et al. Persistence of increased cardiovascular risk in patients with Cushing's disease after five years of successful cure. J Clin Endocrinol Metab 1999; 84: 8: 2664-2662.

4. Erbil Y., Ademoglu E., Ozbey N. et al. Evaluation of the cardiovascular risk in patients with subclinical Cushing syndrome before and after surgery. World J Surg 2006; 30: 9: 1665-1671.

5. Marek J., Hána V., Krsek M. How corticoids, growth hormone and oestrogens influence lipids and atherosclerosis. Vnitr Lek 2007; 53: 4: 386-390.

6. Pivonello R., De Martino M.C., De Leo M. et al. Cushing's syndrome: aftermath of the cure. Arq Bras Endocrin Metab 2007; 51: 8: 1381-1381.

7. Tsuiki M., Tanabe A., Takagi S. et al. Cardiovascular risks and their long-term clinical outcome in patients with subclinical Cushing's syndrome. Endocr J 2008; 55: 4: 737-745.

8. Albiger N., Testa R.M., Almoto B. et al. Patients with Cushing's syndrome have increased intimal media thickness at different vascular levels: comparison with a population matched for similar cardiovascular risk factors. Horm Metab Res 2006; 38: 6: 405-410.

9. Dovio A., Allasino B., Palmas E. et al. Increased osteoprotegerin levels in Cushing's syndrome are associated with an adverse cardiovascular risk profile. J Clin Endocrin Metab 2007; 92: 5: 1803-1888.

10. Faggiano A., Pivonello R., Spiezia S et al. Cardiovascular risk factors and common carotid artery caliber and stiffness in patients with Cushing's disease during active disease and 1 year after disease remission. J Clin Endocrinol Metab 2003; 88(6): 2527-33

11. Mancini T., Kola B., Mantero F. et al. High cardiovascular risk in patients with Cushing's syndrome according to 1999 WHO/ISH guidelines. Clin Endocrinol (Oxf) 2004; 61: 6: 768-777.

12. Tauchmanovà L., Rossi R., Biondi B. et al. Patients with subclinical Cushing's syndrome due to adrenal adenoma have increased cardiovascular risk. J Clin Endocrin Metab 2002; 87: 11: 4872-4878.

13. Whitworth J.A., Williamson P.M., Mangos G., Kelly J.J. Cardiovascular consequences of cortisol excess. Vasc Health Risk Manag 2005; 1: 4: 291-299.

14. Corrado E., Muratori I., Tantillo R. et al. Relationship between endothelial dysfunction, intima media thickness and cardiovascular risk factors in asymptomatic subjects. Int Angiol 2005; 24: 1: 52-58.

15. Zacharieva S., Atanassova I., Nachev E. et al. Markers of vascular function in hypertension due to Cushing's syndrome. Horm Metab Res 2005; 37: 1: 36-39.

16. Ermetici F., Malavazos A.E., Corbetta S. et al. Soluble adhesion molecules levels in patients with Cushing's syndrome before and after cure. J Endocrinol Invest. 2008; 31: 5: 389-392.

17. Dentali F., Romualdi E., Ageno W. The metabolic syndrome and the risk of thrombosis. Haematologica 2007; 92(3): 297-299

18. Kakafika A.I., Liberopoulos E.N., Karagiannis A. et al. Dyslipidaemia, hypercoagulability and the metabolic syndrome. Curr Vasc Pharmacol 2006; 4: 3: 175-183.

19. Semple P.L., Laws E.R. Jr. Complications in a contemporary series of patients who underwent transsphenoidal surgery for Cushing's disease. J Neurosurg 1999; 91: 2: 175-179.

20. Small M., Lowe G.D., Forbes C.D., Thomson J.A. Thromboembolic complications in Cushing's syndrome. Clin Endocrinol (Oxf) 1983; 19: 4: 503-511.

21. Sjöberg H.E., Blombäck M., Granberg P.O. Thromboembolic complications, heparin treatment in increase in coagulation factors in Cushing's syndrome. Acta Med Scand 1976; 199: 1-2: 95-98.

22. Boscaro M., Sonino N., Scarda A. et al. Anticoagulant prophylaxis markedly reduces thromboembolic complications in Cushing's syndrome. J Clin Endocrin Metab 2002; 87: 8: 3662-3666.

23. Долгов В.В., Свирин П.В. Лабораторная диагностика нарушений гемостаза. М-Тверь: Триада 2005: 44-49, 59-64.

24. Фред Дж. Шиффман. Патофизиология системы крови. Пер. с англ. под ред. акад. Ю.В. Наточина. Ст-Петербург: Невский диалект 2001; 191-214, 253-269.

25. Лупинская З.А. Эндотелий сосудов - основной регулятор местного кровотока. Вестн КРСУ 2003; 7

26. Ambrosi B., Sartorio A., Pizzocaro A. et al. Evaluation of haemostatic and fibrinolytic markers in patients with Cushing's syndrome and in patients with adrenal incidentaloma. Exp Clin Endocrinol Diabetes 2000; 108: 4: 294-298.

27. Patrassi G.M., Sartori M.T., Viero M.L. et al. The fibrinolytic potential in patients with Cushing's disease: a clue to their hypercoagulable state. Blood Coagul Fibrinolysis 1992; 3: 6: 789-793.

28. Casonato A., Daidone V., Sartorello F. et al. Polymorphisms in von Willebrand factor gene promoter influence the glucocorticoid-induced increase in von Willebrand factor: the lesson learned from Cushing syndrome. Br J Haematol 2008; 140: 2: 230-235.

29. Dal Bo Zanon R., Fornasiero L., Boscaro M. et al. Increased factor VIII associated activities in Cushing's syndrome: a probable hypercoagulable state. Thromb Haemost 1982; 47: 2: 116-117.

30. Dal Bo Zanon R., Fornasiero L., Boscaro M. et al. Clotting changes in Cushing's syndrome: elevated factor VIII activity. Folia Haematol Int Mag Klin Morphol Blutforsch 1983; 110: 2: 268-277.

31. Fatti L.M., Bottasso B., Invitti C. et al. Markers of activation of coagulation and fibrinolysis in patients with Cushing's syndrome. J Endocrinol Invest 2000; 23: 3: 145-150.

32. Kirilov G., Tomova A., Dakovska L. et al. Eur J Endocrinol. Elevated plasma endothelin as an additional cardiovascular risk factor in patients with Cushing's syndrome. 2003; 149: 6: 549-553.

33. Kristo C., Ueland T., Godang K. et al. Biochemical markers for cardiovascular risk following treatment in endogenous Cushing's syndrome. J Endocrinol Invest 2008; 31: 5: 400-405.

34. Casonato A., Pontara E., Boscaro M. et al. Abnormalities of von Willebrand factor are also part of the prothrombotic state of Cushing's syndrome. Blood Coagul Fibrinol 1999; 10: 3: 145-151.

35. Prázný M., Jezková J., Horová E. et al. Impaired microvascular reactivity and endothelial function in patients with Cushing's syndrome: influence of arterial hypertension. Physiol Res 2008; 57: 1: 13-22.

36. Halleux C.M., Declerck P.J., Tran S.L. et al. Hormonal control of lasminogen activator inhibitor-1 gene expression and production in human adipose tissue: stimulation by glucocorticoids and inhibition by catecholamines. J Clin Endocrinol Metab 1999; 84: 11: 4097-4105.

37. Morange P.E., Aubert J., Peiretti F. et al. Glucocorticoids and insulin promote plasminogen activator inhibitor 1 production by human adipose tissue. Diabetes 1999; 48: 4: 890-895.

38. Lordelo R.A., Mancini M.C., Cercato C., Halpern A. Hormonal axes in obesity: cause or effect? Arq Bras Endocrinol Metabol 2007; 51: 1: 34-41.

39. Walker B.R. Cortisol-cause and cure for metabolic syndrome? Diabet Med 2006; 23: 12: 1281-1288.

40. Iwasaki Y., Takayasu S., Nishiyama M. et al. Is the metabolic syndrome an intracellular Cushing state? Effects of multiple humoral factors on the transcriptional activity of the hepatic glucocorticoid-activating enzyme (11beta-hydroxysteroid dehydrogenase type 1) gene. Mol Cell Endocrinol 2008; 285: 1-2: 10-8.

41. Góth M., Hubina E., Korbonits M. Correlations between the hypothalamo-pituitary-adrenal axis and the metabolic syndrome Orv Hetil 2005; 146: 2: 51-55.

42. Morton N.M., Densmore V., Wamil M. et al. A polygenic model of the metabolic syndrome with reduced circulating and intra-adipose glucocorticoid action. Diabetes 2005; 54: 12: 3371-3378.

43. Alessi M.C., Juhan-Vague I. Metabolic syndrome, hemostasis and thrombosis. Thromb Haemost. 2008; 99: 6: 995-1000.

44. Kohler H.P. Insulin resistance syndrome: interaction with coagulation and fibrinolysis. Swiss Med Wkly 2002; 132: 19-20: 241-252.

45. Nieuwdorp M., Stroes E.S., Meijers J.C., Büller H. Hypercoagulability in the metabolic syndrome. Curr Opin Pharmacol 2005; 5: 2: 155-159.

46. Palomo I., Alarcón M., Moore-Carrasco R., Argilés J.M. Hemostasis alterations in metabolic syndrome (review). Int J Mol Med 2006; 18: 5: 969-974.

47. Skurk T., Hauner H. Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1. Int J Obes Relat Metab Disord 2004; 28: 11: 1357-1364.

48. Van Guilder G.P., Hoetzer G.L., Greiner J.J. et al. Metabolic syndrome and endothelial fibrinolytic capacity in obese adults. Am J Physiol Regul Integr Comp Physiol 2008; 294: 1: R39-44.