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2013 | 85 | 11 | 630-637
Tytuł artykułu

Selected factors of fibrinolysis in the Buerger’s disease

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Thrombangiitis obliterans (TAO marked by coexistence of thrombotic and inflammatory changes of neurovascular tract has evoked a considerable dispute concerning pathogenesis of this disease. The aim of the study was to define the level of activation of fibirinolitic system in course of TAO disease by means of determination its basic constituents as well as to examine the essence of level of fibrinolysis disorders in pathogenesis and development of this disease. Material and methods. Fifty patients with thrombangiitis obliterans (TAO), 30 patients with peripheral occlusive disease - PAOD (ASO) and 20 healthy volunteers (K) have been subjected to the examination. We determined the activity some factors of fibrinolysis: t-PA, PAI-1, PAP, plasminogen, α2-antiplasminogen, D-dimmer as well as euglobulin lysis time. The analysis comprised 7 features and 8 factors of variability: a membership to a group of patients, sex, age, smoking, aggravation of the disease within last 3 months, occurrence of Raynaud’s symptom, a degree of ischemia according to Fontaine, time the disease lasted. Results. The significant differences between the average were checked by means of t-Student test or variance analysis (ANOVA) and co-relation rate r (Pearson). We concluded that the average value of PAI-1 in the group TAO was significantly higher than in comparison with ASO group. The increased values were revealed in case of 76 % of patients. The euglobulin lysis time was vitally extended in case of 60% of patients in ASO group. In all three groups higher levels of α2-antiplasmin were detected in case of elderly patients compared to the younger ones. Conclusions. The obtained results allow us to ascertain the state of potentially weakened fibrinolysis in case of patients with Buerger’s disease as well as with PAOD.
Słowa kluczowe
Wydawca

Rocznik
Tom
85
Numer
11
Strony
630-637
Opis fizyczny
Daty
wydano
2013-11-01
online
2013-12-31
Twórcy
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
autor
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
  • Department of Vascular Surgery and Angiology, Medical University in Lublin
Bibliografia
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  • 2. Majewski W, Marszałek A, Staniszewski R et al.: Clinical and morphological aspects of Buerger’s disease. Int Angiol 1997; 16: 239.
  • 3. D isdier P, Granel B, Serratrice J, Constans et al.: Cannabis arterities revisited- ten new case reports. Angiology 2001; 52: 505.
  • 4. Disdier P, Swiader L, Jouglard J et al: Cannabis- induced arteritis vs. Leo Buerger disease. Nosologic discussion apropos of two new cases. Presse Med 1999; 28: 71.
  • 5. Schneider F, Abdoucheli-Baudot N, Tassart M et al: Cannabis and tobacco: cofactors favoring juvenile obliterative arteriopathy. J Mal Vasc 2000; 25: 388.
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  • 8. Wysokiński WE , Kwiatkowska W, Masłowski L: Buerger’s disease in two brothers: iliac artery occlusion by thrombangiitis obliterans- case reports. Angiology 1998; 49(5): 409.[Crossref]
  • 9. Kobayashi M, Ito M, Nakagawa A et al: Immunohistochemical analysis of arterial wall cellular infiltration in Buerger’s disease (endarteritis obliterans). J Vasc Surg 1999; 29(3): 451.[Crossref]
  • 10. Łopaciuk S: Zatory i zakrzepy. PZWL, Warszawa 1996; 2002.
  • 11. W roński J, Zubilewicz T, Terlecki P et al.: The function of chosen factors of coagulation and fibrinolysis in the pathogenesis of thrombangiitis obliterans. Acta Angiologica 1998; 4; 3/4: 81
  • 12. W oller T, Lawall H, Amann B et al: Comparison of haemostatic parameters in arterial and venous blood from patients with pripheral arterial occlusive disease. Vasa 1999; 28: 10.
  • 13. Van der Bom JG , Bots ML, Haverkate F et al: Fibrinolytic activity in peripheral atherosclerosis in the eldery. Thromb Haemost 1999; 81: 275.
  • 14. Figueras J, Monastrio Y, Lidon RM et al.: Thrombin formation and fibrinolytic activity in patients with myocardial infarction or unstable angina: in-hospital course relationship with recurrent angina at rest. J Am Coll Cardiol 2000; 36: 2044.
  • 15. Blann A, Dobrotova M, Kubisz P et al.: Von Willebrand factor, soluble P-selectin, tissue plasminogen activator and plasminogen activator inhibitor in atherosclerosis. Thromb Haemost 1995; 74: 626.[PubMed]
  • 16. Falkenberg M, Tjarnstrom J, Ortenwall P et al.: Localization of fibrinolytic activators and inhibitors in normal and atherosclerotic vessels. Thromb Haemost 1996; 75: 933.[PubMed]
  • 17. Gleerup G, Winther K: Decreased fibrinolytic activity and increased platelet function in hypertension. Possible influenze of calcium antagonism. Am J Hypertens 1991; 4: 168.
  • 18. Juhan-Vague, Alessi M, Vague P: Thronbogenic and fibrinolytic factors and cardiovascular risk in non-insulin-dependent diabetes mellitus. Ann Med 1996; 28: 371.[Crossref]
  • 19. Kazuyuki S, Fumiharu M, Hiroshi S et al.: Impaired fibrinolysis early after percutaneous transluminal coronary angioplasty is associated with restenosis. American Heart Journal 1996; 131: 1.
  • 20. Guzowski A, Kłoczko J, Głowiński S et al.: Comparison of fibrinolytic activity after varicose vein surgery of one and both limbs. Acta Angiologica 1997; 3: 25.
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_2478_pjs-2013-0095
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