Through the research from 51 patients (34 men, 17 women) suffered from serious burns (Classified according to the method of Bull and Fischer), who were treated in national institute of Burn (NIB). The results showed that: (1) the rate of patients, who have symptoms of hypercoagulation is rather high. Therefore, preventive treatment for disseminated-intravascular-coagulation (DIC) in seriously burnt patients is necessary. CM2 drug was cabaple of preventive treating hypercoagulation in seriously burnt patients.
Antithrombin III ; burns ; prevention & control

No abstract available.
Antithrombin III* ; Plasma* ; Pre-Eclampsia* ; Pregnancy*

Appropriate anticoagulation is essential for safe cardiopulmonary bypass (CPB). Two patients with infective endocarditis were scheduled for valve replacement. After an intravenous heparin injection for the CPB, the increases in the activated clotting time (ACT) in both patients were less than expected. Subsequent additional heparin administration failed to maintain a sufficient ACT for the CPB, and antithrombin III (AT III) tests during the CPB revealed low activities in both patients. Heparin resistance, due to consumption of circulating AT III as a result of infective endocarditis or prior heparinization, was postulated. While fresh frozen plasma (FFP) could not be timely administered in the first patient, ACT was successfully prolonged after the administration of FFP in the second. It is strongly suggested that adequate management of heparin resistance should be prepared for patients with infective endocarditis who require CPB.
Antithrombin III ; Antithrombin III Deficiency ; Cardiopulmonary Bypass* ; Endocarditis* ; Heparin* ; Humans ; Plasma

Appropriate anticoagulation is essential for safe cardiopulmonary bypass (CPB). Two patients with infective endocarditis were scheduled for valve replacement. After an intravenous heparin injection for the CPB, the increases in the activated clotting time (ACT) in both patients were less than expected. Subsequent additional heparin administration failed to maintain a sufficient ACT for the CPB, and antithrombin III (AT III) tests during the CPB revealed low activities in both patients. Heparin resistance, due to consumption of circulating AT III as a result of infective endocarditis or prior heparinization, was postulated. While fresh frozen plasma (FFP) could not be timely administered in the first patient, ACT was successfully prolonged after the administration of FFP in the second. It is strongly suggested that adequate management of heparin resistance should be prepared for patients with infective endocarditis who require CPB.
Antithrombin III ; Antithrombin III Deficiency ; Cardiopulmonary Bypass* ; Endocarditis* ; Heparin* ; Humans ; Plasma

Antithrombin III deficiency is an autosomal dominant disorder, which is manifested by recurrent venous thromboembolisms, such as: deep vein thrombosis and/or pulmonary embolism, but arterial embolisms are very rare. We report a case of a patient with hereditary antithrombin III deficiency, manifested by myocardial infarction and deep vein thrombosis.
Antithrombin III Deficiency* ; Antithrombin III* ; Embolism ; Humans ; Myocardial Infarction* ; Pulmonary Embolism ; Thromboembolism ; Venous Thrombosis*

OBJECTIVETo identify the antithrombin (AT) phenotype and gene mutation of a kindred with hereditary antithrombin deficiency.

METHODSPlasma AT activity and AT antigen level of the propositus and his kindred members were determined with chromogenic substrate method and immunoassay, respectively. All the seven exons and intron-exon boundaries of antithrombin gene were analyzed by PCR and direct sequencing of amplified PCR products from the propositus.

RESULTSThe propositus AT antigen level was normal but his AT activity was only 65% of normal value suggesting that he had type II AT deficiency. A heterozygous G13830A mutation in exon 6 resulting in Arg393His missense mutation in his AT polypeptide was identified in the propositus. The same phenotype and gene mutation were found in other 3 kindred members.

CONCLUSIONThe type II AT deficiency found in this kindred is caused by heterozygous G13830A mutation in AT gene.

Adult ; Antithrombin III ; genetics ; metabolism ; Antithrombin III Deficiency ; genetics ; Heterozygote ; Humans ; Male ; Mutation ; Pedigree

BACKGROUND: In the acute phase of myocardial infarction, the hemostatic mechanism is known to be activated. However, it remains unclear whether increased activity of the hemostatic mechanism is only a marker of the acute thrombotic episode or precedes its appearance. It is also inapparent whether a hypercoagulable state persist for a prolonged period after the apparent resolution of these disorders. METHODS: In a group of 23 patients with acute myocardial infarction who received fibrinolytic therapy with urokinase(group A) or tPA(group B), the plasma level of fibrinogen, antithrombin compared to those of the 10 normal controls. RESULTS: The plasme level of fibrinogen was significantly decreased in both group A and B before and 4 to 24 hours after thrombolytic therapy compared to that of normal controls. But it was increased 7 to 14 days after thrombolytic therapy. In a few of the patients, the plasma level of FDP and D-dimer were positive before thrombolytic therapy and in the most patients they were positive 4 hours after thrombolytic therapy. The plasma level of AT-III was significantly increased in both group A and B before thrombolytic therapy compared with that of normal controls, but, after thrombolytic therapy, there was no significant change in its level. CONCLUSIONS: In the patients with acute myocardial infarction, the thrombolysis occurred before thrombolytic therapy and it lasted for 24 hours after thrombolytic therapy.
Antithrombin III* ; Fibrinogen ; Humans ; Myocardial Infarction* ; Plasma ; Thrombolytic Therapy*

No abstract available.
Antithrombin III* ; Female ; Fibronectins* ; Hypertension, Pregnancy-Induced* ; Plasma* ; Pregnancy

OBJECTIVE: To define the abnormalities of coagulation system in cerebral infarction and the effect of aspirin. BACKGROUND: Toghi et al(1990,1993) suggested that the coagulation system was enhanced at all stages of cerebral infarction and long term use of antiplatelet medication in chronic stroke patients was effective in reducing the elevated coagulant proteins level. METHOD: We determined fibrinogen, antithrombin III (ATIII), thrombin-antithrombin III complex(TAT) in plasma from 40 stroke patients - 32 acute (<7days), 18 subacute (7-30days) and 32 chronic stage (>30days), and compared 14 patients receiving aspirin from acute stage with 10 patients not receiving aspirin. RESULT: The concentrations of fibrinogen and TAT were significantly elevated in acute and subacute stages, especially in subacute stage(P<0.01), whereas AT-III was decreased only in acute stage (P<0 05). Fibrinogen levels were significantly decreased in patients receiving aspirin than in patients not receiving aspirin during subacute stage (P<0.01). CONCLUSION: These results suggest that the coagulation system is enhanced during acute and subacute stages and early use of aspirin is effective in reducing the elevated fibrinogen in subacute stage.
Antithrombin III ; Aspirin ; Cerebral Infarction* ; Fibrinogen ; Humans ; Plasma ; Stroke

OBJECTIVETo identify the clinical phenotype and gene mutation in two kindreds with type I inherited antithrombin (AT) deficiency.

METHODSThe coagulation and anticoagulation testing and thrombophilia screening were used for phenotypic diagnosis and immunonephelometry and chromogenic assay for plasma level of AT antigen (AT:Ag) and AT activity (AT:A), respectively. All of the seven exons and intron-exon boundaries and untranslation regions of AT gene were amplified by PCR, and the PCR products analysis was by direct sequencing. The corresponding gene sites of the two family members and healthy individuals were detected according to the gene mutation sites.

RESULTSThe plasma levels of AT:Ag of proband 1 and proband 2 were 126 mg/L and 117 mg/L, and AT:A was 49% and 48%, respectively. Heterozygotic deletion of 3239-3240delCT in proband 1 and nonsense mutation 3206A-->T (K70Stop) in proband 2 were rchaacterized in exon 2 of AT gene. And some of their family members were also detected with the heterozygotic gene mutation.

CONCLUSIONType I inherited antithrombin deficiency of the two probands were caused by AT gene mutation 3239-3240delCT and 3206A-->T (K70Stop).

Antithrombin III Deficiency ; genetics ; Heterozygote ; Humans ; Mutation ; Pedigree ; Phenotype