Venous thromboembolism, factor V Leiden, and methylenetetrahydrofolate reductase in a sickle cell anemia patient

被引:13
作者
Koren, A [1 ]
Zalman, L
Levin, C
Abu Hana, M
Mader, R
Shalev, S
机构
[1] Haemek Med Ctr, Pediat Dept B, IL-18101 Afula, Israel
[2] Haemek Med Ctr, Pediat Hematol Unit, IL-18101 Afula, Israel
[3] Technion Israel Inst Technol, Baruch Rappaport Sch Med, Haifa, Israel
[4] Haemek Med Ctr, Hematol Lab, Afula, Israel
[5] Haemek Med Ctr, Unit Med Genet, Afula, Israel
关键词
activated protein C resistance; factor V Leiden; methylenetetrahydrofolate reductase (MTHFR); sickle cell anemia; thromboembolism;
D O I
10.1080/088800199277047
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Vaso-occlusive crisis is the most common cause of morbidity in patients with sickle cell anemia (SCA). Central nervous system involvement that leads to hemiplegia is the most frequent neurological complication in those patients. Peripheral deep venous thromboembolism was not reported in SCA patients. Activated protein C resistance is associated with an increased risk of thrombophilia. The authors report an SCA patient with recurrent cerebrovascular accident and deep venous thrombosis. Activated protein C resistance due to factor V Leiden heterozygous and heterozygocity for the methylenetetrahydrofolate reductase were diagnosed and suspected to be the risk factors that contribute to the development of the deep vein thrombosis in this SCA patient.
引用
收藏
页码:469 / 472
页数:4
相关论文
共 13 条
[1]   FACTOR-8 (ANTIHAEMOPHILIC FACTOR) ACTIVITY IN SICKLE-CELL ANAEMIA [J].
ABILDGAARD, CF ;
SIMONE, JV ;
SCHULMAN, I .
BRITISH JOURNAL OF HAEMATOLOGY, 1967, 13 (01) :19-+
[2]  
ADRAGNA NC, 1994, BLOOD, V83, P553
[3]   FAMILIAL THROMBOPHILIA DUE TO A PREVIOUSLY UNRECOGNIZED MECHANISM CHARACTERIZED BY POOR ANTICOAGULANT RESPONSE TO ACTIVATED PROTEIN-C - PREDICTION OF A COFACTOR TO ACTIVATED PROTEIN-C [J].
DAHLBACK, B ;
CARLSSON, M ;
SVENSSON, PJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (03) :1004-1008
[4]  
DAngelo A, 1997, BLOOD, V90, P1
[5]   ABNORMAL ADHERENCE OF SICKLE ERYTHROCYTES TO CULTURED VASCULAR ENDOTHELIUM - POSSIBLE MECHANISM FOR MICRO-VASCULAR OCCLUSION IN SICKLE-CELL DISEASE [J].
HEBBEL, RP ;
YAMADA, O ;
MOLDOW, CF ;
JACOB, HS ;
WHITE, JG ;
EATON, JW .
JOURNAL OF CLINICAL INVESTIGATION, 1980, 65 (01) :154-160
[6]   VENOUS THROMBOSIS DUE TO POOR ANTICOAGULANT RESPONSE TO ACTIVATED PROTEIN-C - LEIDEN THROMBOPHILIA STUDY [J].
KOSTER, T ;
ROSENDAAL, FR ;
DERONDE, H ;
BRIET, E ;
VANDENBROUCKE, JP ;
BERTINA, RM .
LANCET, 1993, 342 (8886-7) :1503-1506
[7]  
POWARS DR, 1978, BIOCH CLIN ASPECTS H, P151
[8]   ROLE OF COAGULATION SYSTEM IN PATHOPHYSIOLOGY OF SICKLE-CELL DISEASE [J].
RICKLES, FR ;
OLEARY, DS .
ARCHIVES OF INTERNAL MEDICINE, 1974, 133 (04) :635-641
[9]   MUTATION IN THE GENE CODING FOR COAGULATION-FACTOR-V AND THE RISK OF MYOCARDIAL-INFARCTION, STROKE, AND VENOUS THROMBOSIS IN APPARENTLY HEALTHY-MEN [J].
RIDKER, PM ;
HENNEKENS, CH ;
LINDPAINTER, K ;
STAMPFER, MJ ;
EISENBERG, PR ;
MILETICH, JP .
NEW ENGLAND JOURNAL OF MEDICINE, 1995, 332 (14) :912-917
[10]  
SERJEANT GR, 1985, SICKLE CELL DIS, P233