Hemostasis and fibrinolysis in patients with intermittent claudication: effects of prostaglandin E1

Citation
C. Weiss et al., Hemostasis and fibrinolysis in patients with intermittent claudication: effects of prostaglandin E1, PROS LEUK E, 63(5), 2000, pp. 271-277
Citations number
25
Categorie Soggetti
Cell & Developmental Biology
Journal title
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
ISSN journal
09523278 → ACNP
Volume
63
Issue
5
Year of publication
2000
Pages
271 - 277
Database
ISI
SICI code
0952-3278(200011)63:5<271:HAFIPW>2.0.ZU;2-R
Abstract
There is evidence that the coagulation system is activated in patients with peripheral arterial occlusive disease (PAOD). The beneficial effects of th e vasoactive drug prostaglandin E1 (PGE1) may rely in part on the modulatio n of the coagulation system. The study was designed to evaluate the effects of PGE1 on hemostatic and fibrinolytic variables in patients with intermit tent claudication. Therefore molecular markers of thrombin (prothrombin fragment 1+2, PTF 1+2; thrombin-antithrombin III complexes, TAT) and fibrin formation (fibrinopep tide A, FPA) and markers of the fibrinolytic activity (fibrin degradation p roducts, D-dimers) were determined before and immediately after the first P GE1 dose (60 mug in 100 ml NaCl over 2 h i.v) as well as after 4 weeks of d aily infusion therapy in 12 PAOD patients and in eight control patients bef ore and after a single placebo infusion. Plasma levels of PTF1+2,TAT, FPA a nd D-dimers tended to decrease after the initial dose of PGE1. Infusion the rapy with PGE1 for 4 weeks led to a decrease of all hemostatic and fibrinol ytic parameters with most pronounced changes for PFT1 +2, D-dimers and plas minogen activator inhibitor-1 decreasing by 11% (P < 0.05), 20% (P < 0.05), and 7% (P < 0.05), respectively. These variables remained unchanged in con trols with placebo infusion. In summary, infusion therapy with PGE1 in patients with PAOD reduces thromb in formation and results in a decrease of fibrin degradation. PGE1 may thus reduce fibrin deposition involved in the pathogenesis of atherosclerosis. (C) 2000 Harcourt Publishers Ltd.