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Accelerated globulin deficiency

Deficiencies in the accelerated globulin and the serum prothrombin conversion factor may be acquired. The accelerated globulin deficiency occurs in severe hepatic disease, acute leukemia, postoperative states, radiation injury, after isotope administration, and in late stages of cancer. Deficiencies of the serum thrombin conversion factors also occur in advanced liver disease, but they develop as well when anticoagulants are administered. [Pg.407]

Proaccelerin Accelerator Globulin (Ac-G) V Factor V deficiency, (parahemophilia) Increased risk for thrombosis (Factor V Leiden) Extremely rare 7-10 0.025 Liver, megakaryocytes, endothelial cells 11-15 FA5 HUMAN... [Pg.843]

Deficiencies in other factors, such as the plasma thromboplastin antecedent, the accelerator globulin, and the serum prothrombin conversion factor have all been described. The deficiencies lead to various forms of hemophilia. The severity of degree of bleeding episodes is much less marked than in classical hemophilia. These deficiencies are usually congenital, transmitted by sex-linked dominant or recessive or by autosomal dominant genes. The manifestations of these deficiencies are usually referred to as hemophilioid states c, d, a, and b, respectively. The major characteristics of these various types of congenital hemophilioid states are summarized in Table 7-4. [Pg.407]


See other pages where Accelerated globulin deficiency is mentioned: [Pg.412]    [Pg.412]    [Pg.118]    [Pg.616]   
See also in sourсe #XX -- [ Pg.407 ]




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