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Thrombotic complications

Calcification, and possibly sclerosis, of the aortic and mitral valves may be a cause of embolism of calcific or complicating thrombotic material. However, these degenerative disorders of heart valves are so common, particularly in the elderly, that it has been very difficult to associate them causally with stroke (Boon et al. 1996). [Pg.65]

While VTE may initially cause few or no symptoms, the first overt manifestation of the disease may be sudden death.2 Death from PE can occur within minutes, before effective treatment can be given. In addition to the symptoms produced by the acute event, the long-term sequelae of VTE such as the post-thrombotic syndrome (PTS a complication of VTE occurring due to damage to the vein caused by a blood... [Pg.134]

PCCs contain the vitamin K-dependent factors II, VII, IX, and X. These agents represent another attempt to bypass the factor at which the antibody is directed (see Fig. 64-2). However, PCCs carry the risk of serious thrombotic complications. Porcine factor VIII is most useful when the inhibitor titer is less than 50 BU (see Fig. 64-2 for dose and frequency). Owing to its similarity to human factor VIII, porcine factor VIII participates in the coagulation cascade. However, most inhibitors have very weak neutralizing activity against it. Porcine factor VIII is a third-line agent (only after factor Vila and a PCC have failed) owing to a 15% incidence of cross-reactivity.15... [Pg.991]

EHEC are the pathogenic subgroup of Stx-producing E. coli (STEC). Acute hemorrhagic colitis has been associated mainly with the 0157 H7 serotype. This serotype has been responsible for larger outbreaks of infection, has higher rates of complications, and appears to be more pathogenic than non-EHEC STEC strains. The spectrum of disease associated with E. coli 0157 H7 includes bloody diarrhea, which is seen in as many as 95% of patients, nonbloody diarrhea, hemolytic-uremic syndrome (HUS), and thrombotic thrombocytopenic purpura. [Pg.1121]

Pathological findings frequently observed in organs of patients who have died of sepsis include disseminated intravascular coagulation (DIC), manifested as diffuse thrombotic occlusions in the entire microvascular system, associated with alterations in the hemostatic mechanism and clinical signs of hemorrhagic diathesis. Many observations indicate that DIC contributes to the major symptoms of the systemic inflammatory response syndrome (SIRS), which frequently complicate sepsis (HI, H2, H3, T6). [Pg.76]

Monreal M, Davant E. Thrombotic complications of central venous catheters in cancer patients. Acta Haematol 2001 106(l-2) 69-72. [Pg.41]

In an effort to overcome the lack of solubility, poor penetration across the blood-brain barrier and decreased delivery of conventional systemic agents by a compromised intratumoral blood supply, several studies have evaluated various combinations of BCNU alone or with other agents delivered intraarterally. Unfortunately, response rates and median survival times observed in patients treated with intraarterial chemotherapy have not been significantly different than those seen in patients treated with standard intravenous nitrosurea-containing regimens, while increased rates of toxicity such as leukoen-cephalopathy, retinal injury, edema, myelosuppression, sepsis, and thrombotic complications have been noted (40-46). [Pg.140]

Epoprostenol is the natural occurring prostacyclin which is formed in vascular endothelial cells. It increases cyclic AMP in the thrombocyte and is a strong platelet aggregation inhibitor. It is used to prevent thrombotic complications during hemodialysis when heparin is contraindicated. As its duration of action is no longer than 30 minutes it has to be given as an intravenous infusion. [Pg.373]

Epoetin alfa Agonist of erythropoietin receptors expressed by red cell progenitors Stimulates erythroid proliferation and differentiation, and induces the release of reticulocytes from the bone marrow Treatment of anemia, especially anemia associated with chronic renal failure, HIV infection, cancer, and prematurity prevention of the need for transfusion in patients undergoing certain types of elective surgery IV or SC administration 1-3 times per week Toxicity Hypertension, thrombotic complications, and, very rarely, pure red cell aplasia to reduce the risk of serious CV events, hemoglobin levels should be maintained < 12 g/dL... [Pg.749]

There has been an anecdotal report of thrombosis in a girl taking estrogens in addition to older evidence that they can reduce antithrombin activity, which could indeed raise the risk of thrombotic complications (207). [Pg.190]

Early epidemiological data on the recurrence of thrombosis (44) indicated something of an inherited predisposition, and others found a low content of fibrinolytic activators in the vessel wall of women who 6-12 months earlier had experienced a thrombotic complication while using oral contraceptives (45) high doses of estrogen affected the concentrations of such activators (46). However, such lesions are apparently not exclusive to users of oral contraceptives (SEDA-8,360) and examination of the vessel wall is not of predictive value in determining risk. [Pg.217]

Nojima, J., Kuratsune, H., Suehisa, E., Futsukaichi, Y., Yamanishi, H., Machii, T., Iwatani, Y., and Y. Kanakura, 2001, Association between the prevalence of antibodies to beta(2)-glycoprotein I, prothrombin, protein C, protein S, and annexin V in patients with systemic lupus erythematosus and thrombotic and thrombocytopenic complications. Clin Chem. 47(6) 1008-15. [Pg.24]

The most common adverse effects of erythropoietin are associated with a rapid increase in hematocrit and hemoglobin and include hypertension and thrombotic complications. These difficulties can be minimized by raising the hematocrit and hemoglobin slowly and by adequately monitoring and treating hypertension. Allergic reactions have been infrequent and mild. [Pg.754]

Dignat-George F, Camoin-Jau L, Sabatier F, et al. Endothelial microparticles A potential contribution to the thrombotic complications of the antiphospholipid syndrome. Thromb Haemost 2004 91 667-673. [Pg.155]

Deficiency of antithrombin predisposes the patient to thrombotic complications. Antithrombin deficiencies can be the result of low protein levels or due to functionally abnormal molecules. Low protein levels can be brought about by reduced synthesis or an increased turnover of the molecule, Functional deficiencies can be brought about by mutations in either the reactive site or heparin binding sites, A number of such mutations have been documented (81,86,87),... [Pg.6]

Twenty-five percent ofthrombophilic patients develop thrombosis at unusual sites resulting in cerebral venous thrombosis, mesenteric vein thrombosis, hepatic venous thrombosis, retinal vein thrombosis, purpura fulminans, splenic vein thrombosis, portal vein thrombosis, renal vein thrombosis, or axillary vein thrombosis. The thrombotic disorders may involve inflammatory factors that contribute to the vascular deficit. In addition, embolic events also play a role in the development of these thrombotic complications. [Pg.17]

Some patients with acute myocardial infarction (AMI) are found to have HIT antibodies career state of HIT antibodies regardless of previous heparin usage. In those patients, early-onset HIT has been observed, which occurs within a very short period after UFH administration during PCI even if it is the initial exposure to UFH (10). Once HIT antibodies are generated after the exposure to UFH, the antibodies do not disappear for approximately 100 days after the cessation of UFH. If UFH intervention is resumed while the antibodies remain, HIT may readily develop as rapid-onset type of HIT (II). Thrombotic complications are highly anticipated following the abrupt onset of HIT in patients who have been exposed recently to UFH. [Pg.95]

Optimal stent implantation and new antiplatelet therapy have reduced the thrombotic complication after stent implantation, dramatically. However, thrombosis remains a challenge in some lesions and patient subgroups. As an initial and unavoidable event during stent implantation, thrombosis and platelet activation are also involved in the development of neointimal hyperplasia. Stents coated with heparin and other antithrombotic drugs have been demonstrated to decrease thrombotic complications, although their effect on neointimal hyperplasia remains uncertain. As heparin is attached to the stent surface, we divide thromboresistant stents as heparin-coated stents and drug-eluting thromboresistant stents. [Pg.249]

Drug-eluting stents to reduce thrombotic complication have also been evaluated (Table 2). It is known that a final common pathway for platelet aggregation exists. Platelet aggregation is... [Pg.249]


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See also in sourсe #XX -- [ Pg.145 ]




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Complicance

Complicating

Complications

Heparins thrombotic complications

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