The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.
📌 3 Key Takeaways
🎯
Objective & Hypothesis:To evaluate the role the coagulation and fibrinolysis abnormalities in the pathogenesis of ischemic stroke of undetermined etiology, we assayed plasma concentration of fibrinopeptide-A and thrombin-antithrombin III complex, both sensitive markers for thrombin activation and fibrin formation, and D-dimer, a marker of plasmin activity and fibrinolysis.
📊
Key Findings & Data:Hemostatic markers were measured in 32 patients with acute stroke and 20 patients with chronic stroke, and compared with 21 normal subjects.
💡
Conclusion & Impact:The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Fibrinoliz · İskemi · Trombin
Özet
To evaluate the role the coagulation and fibrinolysis abnormalities in the pathogenesis of ischemic stroke of undetermined etiology, we assayed plasma concentration of fibrinopeptide-A and thrombin-antithrombin III complex, both sensitive markers for thrombin activation and fibrin formation, and D-dimer, a marker of plasmin activity and fibrinolysis. Hemostatic markers were measured in 32 patients with acute stroke and 20 patients with chronic stroke, and compared with 21 normal subjects. Fibrinopeptid-A and thrombin-antithrombin III complex levels were not elevated significantly, whereas the D-dimer level was markedly raised in acute (p< 0.001) and chronic (p< 0.05) phases of ischemic stroke in comparison with the control group. Prolonged elevation of D-dimer concentration suggests that hemostatic abnormalities have a primary role in the pathogenesis of ischemic stroke. The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.
ULUTİN, T., SÖNMEZ, H., DOMANİÇ, N., İNCE, B., GÜREL, B. Ç., URAL, D., VURAL, A. V., HARMANCI, H., ÖZAYDIN, A., İNCE, E., SAYHAN, B. N., YILMAZ, Ş., KANIGÜR, G., KÖKOĞLU, E. (2002). Looking for our ten years results for coronary heart disease and ischemic stroke group for the standpoint of haemostasis. Turkish Journal of Hematology, Cilt: 19 - Sayı: 2, 255–263. https://ajindex.com/articles/412988
Fareed J, Bick RL, Hoppensteadt DA, Bermez EW. Molecular markers of hemostatic activation: Applications in the diagnosis of thrombosis and vascular and thrombotic disorders. Clin App Thromb Hemost 1995;l:87-102
Ulutin T, Sönmez H, Üçışık N, Süer S, Bayram Ç, Kökoğlu E, Sultuybek G. The molecular markers of hemostatic activation on coronary artery disease. Thrombosis Research 1997;88:329-32
Walenga JM, Fareed J, Messmore HL. Newer ave¬ nues in the monitoring of antithrombotic therapy: The role of automation. Semin Thromb Hemost 1983;9-.346-54. * 4. Messmore HL, Walenga JM, Fareed J. Molecular markers of platelet activation. Semin Thromb He- most 1983;9:354-78
Baver KA, Rosenberg RD. The pathophysiology of the prothrombotic state in humans: Insight gained from studies using markers of hemostatic system ac¬ tivation. Blood 1987;7O.343-50
Fareed J, Walenga JM. Changing trends in hemos¬tatic testing In: Oukda K (ed). Automation and New Technology in the Clinical Laboratory. Oxford: Oxford Press, 1990:203-10
Oida K, Maeda H, Naka T. Abnormal antithrombo-genic function on endothelial cells in diabetes melli-tus. In: King GL, Shigela Y, (eds). Endothelial Cell Dysfunction Diabetes. Japan: Churchill Livingstone; 1994:33-54
Süer S, Ulutin T, Sönmez H, Kökoğlu E, Üçışık N, Bayram Ç, Sultuybek G. Plazma Lp (a. and tPA-PAI- 1 complex levels in coronary heart disease. Thromb Res 1996;83:77-85
Loskutoff DJ, Sawdey M, Mimoro J. Type 1 plasmi- nogen activator inhibitor. Prog Hemostas Thromb 1988;9-.87-115
Kostner GM, Avogaro P, Lazzolato G, Marth E, Bitto- lo BG, Qunici GB. Lipoprotein(a) and the risk for myo- cardial infarction. Atherosclerosis 1981;38:51-61
Rhoads GG, Dahlen G, Berg K, Morton NE, Dan- nenberg AL. Lp(a) as a risk factor for myocardial in¬ farction. J Am Med Assoc 1986;256:2540-4
Loscalzo J, Weinfeld M, Fless GM, Scann AM. Li- poprotein (a), fibrinbinding and plasminogen activa¬ tion. Atherosclerosis 1990; 10:241-5
Balkuv-Ulutin Ş. Fibrinolytic system in atherosclero¬ sis. Semin Thromb Hemost 1986; 12:91-101
Hadden JM, Haris PI, Srai KSJ, Chapman D. Con- formational studies on human transferring. Biochem Soc Transact 1992;20:200
Stibler H, Borg S. Evidence of a reduced sialic acid content in serum transferring in male alcoholics. Al¬ cohol Clin Exp Res 1981;5:545
Mukhin DN, Tertov W, Kacharava AG, Orekhov AN. Desialylated lowdensity lipoproteins atherogenic lipoproteins occurring in blood of