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Arterial thrombosis

Two types of Protein S deficiency have been described. In type I deficiency there is tittle to no free Protein S but normal amounts of bound Protein S are present. In type II Protein S deficiency both free and bound Protein S are very low to absent. Deficiency of free Protein S is associated with venous and arterial thrombosis. [Pg.175]

Mousa SA, Bozarth JM, Edwards S et al (1998) Novel technetium 99m-labeled GPIIb/IIIa receptor antagonists as potential imaging agents for venous and arterial thrombosis. Coron Artery Dis 9 131-141... [Pg.147]

Junghans U, Seitz RJ, Wittsack HJ, Aulich A, Siebler M. Treatment of acute basilar artery thrombosis with a combination of systemic alteplase and tirofiban, a nonpeptide platelet glycoprotein Ilb/HIa inhibitor report of four cases. Radiology 2001 221 795-801. [Pg.116]

The ACCP Conference on Antithrombotic Therapy recommended against the use of aspirin as the primary method of VTE prophylaxis.2 Antiplatelet drugs clearly reduce the risk of coronary artery and cerebrovascular events in patients with arterial disease, but aspirin produces a very modest reduction in VTE following orthopedic surgeries of the lower extremities. The relative contribution of venous stasis in the pathogenesis of venous thrombosis compared with that of platelets in arterial thrombosis likely explains the reason for this difference. [Pg.141]

The most common adverse events reported with sirolimus are leukopenia (20%), thrombocytopenia (13% to 30%), and hyperlipidemia (38% to 57%).11,31 Other adverse effects include delayed wound healing, anemia, diarrhea, arthralgias, rash, and mouth ulcers. Sirolimus has an FDA black-box warning in newly transplanted liver and lung recipients.11 In liver transplant recipients, use of sirolimus immediately after transplant is associated with an increased risk of hepatic artery thrombosis, graft loss, and death. In lung transplant... [Pg.842]

Heparin-induced thrombocytopenia A clinical syndrome of IgG antibody production against the heparin-platelet factor 4 complex occurring in approximately 1% to 5% of patients exposed to either heparin or low-molecular-weight heparin. Heparin-induced thrombocytopenia results in excess production of thrombin, platelet aggregation, and thrombocytopenia (due to platelet clumping), often leading to venous and arterial thrombosis, amputation of extremities, and death. [Pg.1567]

Whereas (32 glycoprotein 1 ((J2-GPI) is the target of anticardiolipin antibodies, prothrombin is the antigen for most lupus anticoagulants. Both these antibodies are risk factors for both venous and arterial thrombosis. In addition, complications such as thrombocytopenia and recurrent miscarriages are manifestations of the so-called antiphospholipid syndrome (97). [Pg.156]

Radomski et al. [113] demonstrated that the CNTs were efficient in causing platelet aggregation both in vitro and in vivo, accelerating significantly the rate of development of carotid artery thrombosis in rats. Platelet aggregation was likely to result from MMP-dependent activation of GPIIb/IIa receptor. [Pg.194]

Stroke, hypertension, temporary vascular problem of many possible sites, retinal artery thrombosis Hemorrhagic or thrombotic stroke... [Pg.349]

Acute MI (myocardial infarction), 5 107 antianginal agents for, 5 110t and coronary arterial thrombosis, 5 170 Acute myelogenous leukemia (AML), and benzene exposure, 3 616 Acute oral toxicity... [Pg.15]

Yamazaki (Y2) detected increased Lp(a) and PA1 activity in patients with the antiphospholipid antibody syndrome with arterial thrombosis. [Pg.104]

Protein S The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors Villa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH]... [Pg.73]

Bourgain RH, Andries R, Braquet P. (1987). Effect of ginkgolide PAF-acether antagonists on arterial thrombosis. Adv Prostaglandin, Thromboxane, Leukotriene Res. 17B 815-17. [Pg.471]

A number of P3 position modified thrombin inhibitors exhibited oral bioavailability in rats and dogs, and were efficacious in a rat FeCl3-induced model of arterial thrombosis. Compoimds like 151 and the corresponding... [Pg.51]

Increased susceptibility to infection and the possible development of lymphoma may result from immunosuppression. Only physicians experienced in immunosuppressive therapy and management of renal transplant patients should use sirolimus. Manage patients receiving the drug in facilities equipped and staffed with adequate laboratory and supportive medical resources. The physician responsible for maintenance therapy should have complete information needed for the follow-up of the patient. Liver transplantation-excess mortality, graft loss, and hepatic artery thrombosis (HAT) The use of sirolimus in combination with tacrolimus was associated with excess mortality and graft loss in a study in de novo liver transplant recipients. Many of these patients had evidence of infection at or near the time of death. [Pg.1939]

Hepatic artery thrombosis In de novo liver transplant recipients, the use of sirolimus in combination with cyclosporine or tacrolimus was associated with an increase in P.1153... [Pg.1943]

Plasminogen, an inactive precursor, is activated to plasmin which as a protease is able to break down fibrin clots. The thrombolytic agents in use promote the conversion of plasminogen to plasmin at the site of a thrombus. Indications include post-myocardial infarction treatment. The thrombolytic must be administered within 6 hours for an optimal effect. Other indications are treatment of acute pulmonary thromboembolism, deep-vein thrombosis, acute arterial thrombosis and thromboembolism, as well as in the clearance of arteriovenous catheters and can-nulae. Agents are streptokinase, anistreplase, urokinase, alteplase, reteplase and tenecteplase. [Pg.374]

Arterial thrombosis. The formation of an aggregate of blood factors (thrombus), primarily platelets and fibrin, with entrapment of cellular elements in the arteries. Arthritis. Inflammation of a joint. [Pg.564]

Contraindications Abnormal vaginal bleeding, active arterial thrombosis, blood dys-crasias, estrogen-dependent cancer, known or suspected breast cancer, thrombophlebitis or thromboembolic disorders, thyroid dysfunction... [Pg.461]

Pulmonary embolism, deep vein thrombosis (DVT), arterial thrombosis and embolism (given within 7 days of onset) IV Infusion (1.5 million units diluted to 90 ml). Initially, 250,000 units infused over 30 min then, 100,000 units/hr for 24-72 hr for arterial thrombosis or embolism, and pulmonary embolism, 72 hr for DVT. Intra-arterial Infusion (1.5 million units diluted to 45 ml). Initially, 250,000 units infused over 30 min then 100,000 units/hr for maintenance. [Pg.1152]

It is indicated in acute myocardial infarction, pulmonary embolism, deep vein thrombosis, arterial thrombosis, acute thrombosis of central retinal vessels, extensive coronary emboli and severe iliofemoral thrombophlebitis. [Pg.246]

Activation of platelets is considered an essential process for arterial thrombosis. Thus, treatment with platelet-inhibiting... [Pg.768]

Aspirin decreases the incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with myocardial infarction, and thrombosis after coronary artery bypass grafting (see Chapter 34). [Pg.802]


See other pages where Arterial thrombosis is mentioned: [Pg.143]    [Pg.145]    [Pg.226]    [Pg.228]    [Pg.392]    [Pg.418]    [Pg.429]    [Pg.135]    [Pg.200]    [Pg.221]    [Pg.206]    [Pg.226]    [Pg.682]    [Pg.101]    [Pg.1943]    [Pg.137]    [Pg.284]    [Pg.244]    [Pg.262]    [Pg.295]    [Pg.53]    [Pg.443]    [Pg.443]    [Pg.768]   
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Acute arterial thrombosis

Arterial thrombosis assay

Arterial thrombosis, treatment

Artery thrombosis

Coronary arteries platelet thrombosis inhibition

Coronary artery thrombosis, treatment

Heparins arterial thrombosis

Peripheral arterial thrombosis, treatment

Platelet aggregation arterial thrombosis due

Platelet coronary artery thrombosis

Prostaglandins arterial thrombosis

Thrombosis

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