Antithrombin Iii Deficiency
Mostrando 13-21 de 21 artigos, teses e dissertações.
-
13. Acute myeloid leukaemia in a patient with congenital antithrombin III deficiency.
-
14. Abnormal antithrombin III with defective serine protease binding (antithrombin III "Denver").
A hereditary (three family members) deficiency of antithrombin III (AT-III) in which AT-III antigen (AT-III ag) is normal in spite of low heparin cofactor and antithrombin activity is described. Plasma levels were: AT-III ag, 0.92-0.96 U/ml; AT-III heparin cofactor activity, 0.54-0.62 U/ml; progressive antithrombin activity index, 0.13-0.18; anti-Xa activity
-
15. Antithrombin III tours gene: identification of a point mutation leading to an arginine----cysteine replacement in a silent deficiency.
-
16. Relation between antithrombin III and clinical and serological parameters in systemic lupus erythematosus.
The increased frequency of thromboembolic events in patients with systemic lupus erythematosus (SLE) has been attributed to reduced or dysfunctional antithrombin III (At-III). We analysed At-III values, measured by three different assay techniques, in SLE patients, patients with rheumatoid arthritis, and normal and hospitalised controls. In addition, attempt
-
17. Deficiency of protein C in congenital thrombotic disease.
A family with a history of recurring thrombosis was studied to determine if a plasma protein deficiency could account for the observed disease. Protein C levels in plasma were determined immunologically using the Laurell rocket technique. The propositus, his father, and his paternal uncle, who are severely affected, had 38-49% of normal levels of protein C a
-
18. Potentially prothrombotic abnormalities of coagulation in benign intracranial hypertension.
OBJECTIVE: Benign intracranial hypertension (BIH) may be caused by intracranial venous sinus thrombosis. Cerebral angiograms may, however, be normal in patients with BIH that are associated with conditions with an increased risk of venous thrombosis. This raises the possibility that unrecognised non-occlusive venous thrombus might impede CSF drainage. This s
-
19. Bleeding diathesis coincident with chronic myelomonocytic leukaemia.
Two important haematological problems were found in an otherwise healthy 78 year old man: chronic myelomonocytic leukaemia; and a complex, acquired, hyperfibrinolytic bleeding disorder characterized by prolonged coagulation times, deficiency of coagulation factors V, X, and XI, anti-thrombin III and proteins C and S, with high concentrations of circulating t
-
20. Congenital Deficiency of α2-Plasmin Inhibitor Associated with Severe Hemorrhagic Tendency *
α2-Plasmin inhibitor (α2PI) is a recently characterized, fast-reacting plasmin inhibitor in human plasma that appears to play an important role in regulation of in vivo fibrinolysis. We report here a case of complete deficiency of α2PI in man. The patient, a 25-yr-old Japanese man, had a life-long severe bleeding tendency (hemarthrosis and excessive bleed
-
21. Met 358 to Arg mutation of alpha 1-antitrypsin associated with protein C deficiency in a patient with mild bleeding tendency.
The molecular defect responsible for a dramatic prolongation of all standard clotting tests discovered in a 15-yr-old boy has been identified. Initial investigations revealed the presence of an activated Factor X (Factor Xa) and thrombin inhibitor which copurified with alpha 1-antitrypsin (alpha 1-AT), thereby suggesting the occurrence of an alpha 1-AT varia