Venous thromboembolism concentrate

Despite the variations that are found, the overall conclusion is that oral contraceptives cause an increase in coagulation factors I (fibrinogen), II, VII, IX, X, and XII, and a reduction in antithrombin III concentrations, which would be expected to predispose to venous thromboembolism, especially if not counterbalanced by an increase either in fibrinolytic activity or of other inhibitory proteins of the coagulation, such as protein C (70). 

The effect of continuously administered low-dose 17-beta-estradiol (E2) + norethisterone acetate (NETA) on coagulation and fibrinolytic factors has been studied in 120 menopausal women, using two dosage variations (1 mg of E2 with 0.25 mg or 0.5 mg of NETA) compared with placebo over a year (53). In either dose, the combination significantly lowered plasma concentrations of factor VII, fibrinogen, antithrombin, and plasminogen activator inhibitor-1 (PAI-1) compared with placebo. These changes appear favorable, since they may lead to increased fibrinolytic activity and could reduce the risk of coronary heart disease. However, antithrombin activity was also reduced, which may increase the risk of venous thromboembolism. 

An extensive literature review has provided a useful assessment of the benefit to harm balance of raloxifene (20). The findings were reassuring. One large fracture prevention trial provided the best evidence that raloxifene 60 mg/day for 3 years reduced the relative risk of vertebral fractures by 30-50% in women with prevalent fractures or osteoporosis. The extraskeletal effects of raloxifene include a reduction in total cholesterol and low density lipoprotein cholesterol concentrations. Raloxifene was not associated with endometrial hyperplasia, and there was a 72% reduction in the incidence of invasive breast cancer. Adverse events associated with raloxifene included an increase in the absolute risk of venous thromboembolism and increased risks of hot... 

Deficiencies of methionine adenosyltransferase, cystathionine 8-synthase, and cystathionine )/-lyase have been described. The first leads to hypermethioninemia but no other clinical abnormality. The second leads to hypermethioninemia, hyperhomocysteinemia, and homo-cystinuria. The disorder is transmitted as an autosomal recessive trait. Its clinical manifestations may include skeletal abnormalities, mental retardation, ectopia lentis (lens dislocation), malar flush, and susceptibility to arterial and venous thromboembolism. Some patients show reduction in plasma methionine and homocysteine concentrations and in urinary homocysteine excretion after large doses of pyridoxine. Homocystinuria can also result from a deficiency of cobalamin (vitamin B12) or folate metabolism. The third, an autosomal recessive trait, leads to cystathioninuria and no other characteristic clinical abnormality. 

Cardiovascular The main adverse effect of prothrombin complex concentrates is a risk of thrombosis, as patients taking oral anticoagulants have prothrombotic susceptibility factors [31, 33 ]. Reported thromboembolic complications include ischemic stroke, venous thromboembolism (venous thrombosis or pulmonary embolism), myocardial infarction, and disseminated intravascular coagulation [32 ]. 

High Hey concentration is an independent risk factor for coronary artery disease, stroke, peripheral vascular atherosclerosis, and for arterial and venous thromboembolism, although the mechanisms for this effect remain poorly understood. The association between cognitive function and risk of death from stroke suggests that cerebrovascular disease is an important cause of declining cognitive function. 

Thromboembolic complications developed in two of 81 patients with Von Willebrand disease treated with a high-purity factor VlllWon Willebrand factor (VWF) concentrate (10). Four cases of venous thrombosis were reported in patients with Von Willebrand disease treated with an intermediate-purity factor VIII/VWF concentrate. Use of pure VWF concentrate without increased factor VlllrC is preferable (11). 

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