Problems of haemostatic disorders in metabolic syndrome

Czech version

Authors: P. Galajda; M. Mokáň
Authors‘ workplace: I. interná klinika Jesseniovej lekárskej fakulty UK a MFN Martin, Slovenská republika, prednosta prof. MUDr. Marián Mokáň, DrSc., FRCP Edin
Published in: Vnitř Lék 2009; 55(Suppl 1)(Supplementum 1): 88-93

Overview

Metabolic syndrome (MS) is defined as cluster of independent risk factors of coronary heart disease (CHD) and type 2 diabetes mellitus (DM2) including glucose metabolism disorders associated with insulin resistance, central obesity, dyslipidaemia with increasing of triglyceride levels and decreasing of high density lipoprotein levels and arterial hypertension. There are differences in prediction of CHD and DM2 risk among recommendations for diagnostic criteria of MS according to WHO (1999), NCEP-ATPIII (2001), ACE/AACE (2003), AHA/NHBLI (2004) and IDF (2005). New risk factors include markers of low grade inflammatory reaction, endothelial dysfunction and hypofibrinolytic state. Inflammatory parameters (C‑reactive protein, fibrinogen) and endothelial markers (von Willebrand factor) are more important for prediction of CHD risk, while PAI‑1 as marker of fibrinolytic disturbance is independent risk factor for DM2 development.

Key words:
metabolic syndrome – low grade inflammatory reaction – endothelial dysfunction – plasminogen activator inhibitor type 1

Sources

1. Galajda P. Metabolický syndróm. In: Mokáň M, Martinka E, Galajda P (eds). Diabetes mellitus a vybrané metabolické ochorenia. Martin: P+M 2008: 685–698.

2. Alberti KGM, Zimmet FZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus: provinsional report of a WHO consultation. Diabet Med 1998; 15: 539–553.

3. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA 2001; 285: 2486–2497.

4. Bloomgarden ZT. American Association of Clinical Endocrinologists (AACE) consensus conference on insulin resistance syndrome: 25–26 august 2002, Washington, DC. Diabetes Care 2003; 26: 1297–1303.

5. Grundy SM, Brewer HB Jr, Cleeman JI et al. Definition of metabolic syndrome. Report of the National Heart, Lung and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition. Circulation 2004; 109: 433–438.

6. International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome (April 14 2005). Available from: www.idf.org/webdata/docs/Metab_syndrome_def.pdf.

7. Tkáč I, Klimeš I, Krahulec B et al. Diagnóza a možnosti liečebného ovplyvnenia metabolického syndrómu. Vyjadrenie stanoviska panelu expertov odborných spoločností. Interná medicína 2005; 5: 239–242.

8. Ford ES, Giles WH. A comparison of the prevalence of the metabolic syndrome using two proposed definitions. Diabetes Care 2003; 26: 575–581.

9. Reaven GM. Role of insulin resistance in human disease (syndrome X): an expanded definition. Annu Rev Med 1993; 44: 121–131.

10. Reaven GM. Syndrome X – past, present, and future. In: Draznin B, Rizza R (eds). Clinical Research in Diabetes and Obesity. Totowa, NJ: Humana Press, Inc 1998: 357–382.

11. Lewis GF, Carpentier A, Adeli K et al. Disordered fat storage and mobilization in the pathogenesis of insulin resistance and type 2 diabetes. Endocr Rev 2002; 23: 201–229.

12. Fernández-Real JM, Ricart W. Insulin resistance and inflammation in an evolutionary perspectives: the contribution of cytokine genotype/phenotype to thriftiness. Diabetologia 1999; 42: 1367–1374.

13. Permana PA, Menge C, Reaven PD. Macrophage-secreted factors induce adipocyte inflammation and insulin resistance. Biochem Biophys Res Commun 2006; 341: 507–514.

14. Yudkin JS, Kumari M, Humphries SE et al. Inflammation, obesity, stress and coronary heart disease: is interleukin‑6 the link? Atherosclerosis 2000; 148: 209–214.

15. Galajda P, Mokáň M. Poruchy hemostázy a diabetes mellitus. Martin: Prokonzult 2001: 1–255.

16. Haffner SM. The metabolic syndrome: Inflammation, diabetes mellitus and cardiovascular disease. Am J Cardiol 2006; 97 (Suppl 2A): 3A–11A.

17. Yudkin JS, Stehouwer CD, Emeis JJ et al. C‑reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999; 19: 972–978.

18. Lowe GD. Circulating inflammatory markers and risk of cardiovascular and non‑cardiovascular disease. J Thromb Haemost 2005; 3: 1618–1627.

19. Graham I, Atar D, Borch-Johnsen K et al. European guidelines on cardiovascular disease prevention in clinical practice: executive summary. Eur Heart J 2007; 28: 2375–2414.

20. Festa A, D’Agostino R Jr, Tracy RP et al. Elevated levels of acute-phase proteins and plasminogen activator inhibitor-1 predict the development of type 2 diabetes: the Insulin Resistance Atherosclerosis Study. Diabetes 2002; 51: 1131–1137.

21. Hanley AJ, Karter AJ, Festa A et al. Factor analysis of metabolic syndrome using directly measured insulin sensitivity. The Insulin Resistance Atherosclerosis Study. Diabetes 2002; 51: 2642–2647.

22. Remková A. Protrombotický stav ako súčasť metabolického syndrómu. Vnitř Lék 2005; 51: 1120–1125.

23. Fibrinogen Studies Collaboration: Collaborative meta‑analysis of prospective observational studies of plasma fibrinogen and cardiovascular disease. Eur J Cardiovasc Prev Rehabil 2004; 11: 9–17.

24. Calles-Escandon J, Cipolla M. Diabetes and endothelial dysfunction: A clinical perspective. Endocr Rev 2001; 22: 36–52.

25. Charles MA, Morange P, Eschwège E et al. Effect of weight change and metformin on fibrinolysis and the von Willebrand factor in obese nondiabetic subjects: the BIGPRO1 Study. Biguanides and the prevention of the risk of obesity. Diabetes Care 1998; 21: 1967–1972.

26. Mertens I, Van Gaal LF. Obesity, haemostasis and fibrinolytic system. Obes Rev 2002; 3: 85–101.

27. Sakkinen PA, Wahl P, Cushman M et al. Clustering of procoagulation, inflammation and fibrinolysis variables with metabolic factors in insulin resistance syndrome. Am J Epidemiol 2000; 152: 897–907.

28. Lijnen HR, Alessi MC, Van Hoef B et al. On the role of plasminogen activator inhibitor-1 in adipose tissue development and insulin resistance in mice. J Thromb Haemost 2005; 3: 1174–1179.

29. Bouchard L, Mauriège P, Vohl MC et al. Plasminogen activator inhibitor-1 polymorphisms are associated with obesity and fat distribution in the Quebeck Family Study: evidence of interactions with menopause. Menopause 2005; 12: 136–143.

30. Vaughan DE. PAI‑1 and atherothrombosis. J Thromb Haemost 2005; 3: 1879–1883.

31. Colwell JA, Nesto RW. The platelets in diabetes. Focus on prevention of ischemic events. Diabetes Care 2003; 26: 2181–2188.

32. Pearson TA, Blair SN, Daniels SR et al. AHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 update. Consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases (AHA Scientific Statement). Circulation 2002; 106: 388–391.

33. Colwell JA, American Diabetes Association. Aspirin therapy in diabetes. Diabetes Care 2003; 26 (Suppl 1): S87–S88.

34. Sacco M, Pellegrini F, Roncaglioni MC et al. PPP Collaborative Group. Primary prevention of cardiovascular events with low‑dose aspirin and vitamin E in type 2 diabetic patients. Results of the primary prevention project (PPP) trial. Diabetes Care 2003; 26: 3264–3272.

35. de Gaetano G, Collaborative Group of the Primary Prevention Project. Low‑dose aspirin and vitamin E in people at cardiovascular risk: a randomised trial in general practice. Lancet 2001; 357: 89–95.

36. Kubisz P, Mištuna D, Staško J et al. Poruchy krvných doštičiek. In: Malý J, Pecka M(eds). Trombóza a hemostáza. Hradec Králové: HK Credit 2007: 16.