IMPAIRED HEMOSTATIC KINETICS AND ENDOTHELIAL FUNCTION IN BEHCETS-DISEASE

Citation
Ic. Haznedaroglu et al., IMPAIRED HEMOSTATIC KINETICS AND ENDOTHELIAL FUNCTION IN BEHCETS-DISEASE, Journal of internal medicine, 240(4), 1996, pp. 181-187
Citations number
23
Categorie Soggetti
Medicine, General & Internal
ISSN journal
09546820
Volume
240
Issue
4
Year of publication
1996
Pages
181 - 187
Database
ISI
SICI code
0954-6820(1996)240:4<181:IHKAEF>2.0.ZU;2-#
Abstract
Objectives. This study was planned to explore the alterations of endot helial functions in the prethrombotic state of Behcet's disease (BD) p atients. Design. Plasma levels of endothelial secretory markers, in vi vo molecular haemostatic and fibrinolytic parameters were cross-sectio nally determined in the study group. Setting and subjects. In our tert iary referral centre, 30 (13 men, 17 women) ED patients, mean age 31+/ -7 years, and 15 (eight men, seven women) healthy volunteers, mean age 26+/-9 years, were eligible for inclusion in the study after obtainin g their written consents. Interventions. All plasma samples for the as says of haemostatic parameters were obtained before and after an endot helial stimulant, desmopressin acetate (DDAVP). Results. We have shown that in the procoagulant phase of ED patients: (1) basal thrombomodul in concentrations are increased and could not be provoked by DDAVP inf usion; (2) both thromboxane B2 and 6-keto prostaglandin F1 alpha incre ments occur concurrently; (3) in vivo coagulation markers are elevated and raised plasmin-alpha(2) antiplasmin complex indicates a subclinic al concomitant fibrinolysis; (4) the fibrinolytic process is conveyed in a somewhat complex manner in which plasminogen activator binding ki netics might be also altered, Conclusions. Endothelial cell injury, au gmented thrombotic risk with compensatory excessive fibrinolysis and a lterations in endothelial cell receptor-fibrinolytic marker relations might take place in the pathogenesis and thereby modulate the natural course of haemostatic processes of ED.