Diagnosis and treatment of the coagulopathies

被引:2
作者
Esnaola-Rojas, MM [1 ]
机构
[1] Hosp Frances, Ctr Neurol Tratamiento & Rehabil, Buenos Aires, DF, Argentina
关键词
cerebrovascular event; coagulopathy; hypercoagulability; primary antiphospholipid syndrome; risk factors;
D O I
10.33588/rn.2912.99349
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction. Approximately 5% of all cerebrovascular events (CVE), and 10% of those occurring in young patients, are due to hematological disorders. Hypercoagulability states are related to CVE in young patients, deep vein thrombosis, recurrent thromboses, pulmonary embolism, a family history of thrombosis and unusual venous and arterial thromboses. Development. The conditions related to increased risk of thrombosis are: the congenital thrombophilias due to deficiency of protein C, protein S or antithrombin III, resistance to protein C activated by Leiden's factor V-cofactor of protein C with genetic mutation-; the primary antiphospholipid syndrome with anticardiolipin antibodies and lupus inhibitor; platelet disorders, deficit of heparin cofactor II, deficit of plasminogen and plasminogen tissue activator (t-PA) and increase in the inhibitor of plasminogen tissue activator (PAI-I); alterations in factors of coagulation such as deficits of factor VII and factor XIII, mutation of prothrombin 20210-->A, increase in factor VIII: Hyperfibrinogenemia and hyperhomocysteinemia are also independent risk factors for CVE. Conclusion. The patients, especially young patients, with recurrent thrombosis or thrombosis of unknown origin should be assessed seeking clinical and serological signs of the primary antiphospholipid syndrome or other coagulopathies. A Although we still have no results of controlled prospective studies regarding these conditions, long term anticoagulation is recommended on the findings of small-scale retrospective studies [REV NEUROL 1999, 29: 1290-300].
引用
收藏
页码:1290 / 1300
页数:11
相关论文
共 38 条
[1]  
Akhtar MS, 1998, AM J CLIN PATHOL, V109, P387
[2]   Plasma homocysteine and cardiovascular disease mortality [J].
Alfthan, G ;
Aro, A ;
Gey, KF .
LANCET, 1997, 349 (9049) :397-397
[3]  
Ames PRJ, 1998, THROMB HAEMOSTASIS, V79, P46
[5]  
Bentolila S, 1997, STROKE, V28, P1846
[6]   HETEROZYGOSITY FOR HOMOCYSTINURIA IN PREMATURE PERIPHERAL AND CEREBRAL OCCLUSIVE ARTERIAL-DISEASE [J].
BOERS, GHJ ;
SMALS, AGH ;
TRIJBELS, FJM ;
FOWLER, B ;
BAKKEREN, JAJM ;
SCHOONDERWALDT, HC ;
KLEIJER, WJ ;
KLOPPENBORG, PWC .
NEW ENGLAND JOURNAL OF MEDICINE, 1985, 313 (12) :709-715
[7]   The antiphospholipid/cofactor syndromes: A primary variant with antibodies to beta 2-glycoprotein-I but no antibodies detectable in standard antiphospholipid assays [J].
Cabral, AR ;
Amigo, MC ;
Cabiedes, J ;
AlarconSegovia, D .
AMERICAN JOURNAL OF MEDICINE, 1996, 101 (05) :472-481
[8]   Cerebral venous thrombosis and anticardiolipin antibodies [J].
Carhuapoma, JR ;
Mitsias, P ;
Levine, SR .
STROKE, 1997, 28 (12) :2363-2369
[9]   Factor XIII Val 34 Leu - A novel association with primary intracerebral hemorrhage [J].
Catto, AJ ;
Kohler, HP ;
Bannan, S ;
Stickland, M ;
Carter, A ;
Grant, PJ .
STROKE, 1998, 29 (04) :813-816
[10]   Pseudo-homozygous activated protein C resistance due to coinheritance of heterozygous factor V Leiden mutation and type I factor V deficiency. Variable expression when analyzed by different activated protein C resistance functional assays [J].
Delahousse, B ;
Iochmann, S ;
Pouplard, C ;
Fimbel, B ;
Charbonnier, B ;
Gruel, Y .
BLOOD COAGULATION & FIBRINOLYSIS, 1997, 8 (08) :503-509