Increased fibrin polymerization rate in patients with primary antiphospholipid syndrome and systemic lupus erythematosus

被引:12
作者
de Pablo, P
Ramirez, A
Cortina, E
de la Peña, A
Zamora, J
Izaguirre, R
Amigo, MC
机构
[1] Univ Nacl Autonoma Mexico, Inst Nacl Cardiol Ignacio Chavez, Dept Rheumatol, Mexico City 14080, DF, Mexico
[2] Inst Nacl Cardiol Ignacio Chavez, Dept Hematol, Mexico City, DF, Mexico
[3] Inst Nacl Cardiol Ignacio Chavez, Dept Endocrinol, Mexico City, DF, Mexico
关键词
fibrinogen; fibrin polymerization rate; antiphospholipid syndrome; systemic lupus erythematosus;
D O I
10.1177/107602960300900306
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The main event in blood coagulation is the thrombin-catalyzed conversion of fibrinogen into fibrin. This singular transformation of a soluble protein into an insoluble polymeric network occurs with faultless precision. Abnormalities of fibrin polymerization can lead to hemorragic and thrombotic disorders. Increased fibrinogen plasma concentration (Fg) and fibrin polymerization rate (FPR) could be additional risk factors associated with atherothrombosis in antiphospholipid syndrome (APS) and in systemic lupus erythematosus (SLE). Our objective was to investigate Fg and FPR in consecutive patients with APS and SLE. Thirty-nine patients and 31 age-and gender-matched healthy controls were studied. Sixteen patients had primary APS, 13 patients had SLE, and 10 patients had SLE plus APS. The mean of the FPR was significantly increased (0.2799 +/- 0.091) in patients with APS plus SLE as compared with the control group (0.2052 +/- 0.055) (p<0.05). Fg was higher in APS plus SLE (3.15 g/L +/- 0.43) and in primary APS (3.03 g/L +/- 0.29) than in controls (2.87 g/L +/- 0.49). Our results demonstrated an increased FPR in patients with APS plus SLE. This phenomenon could be an additional risk factor for thrombosis in these autoimmune diseases.
引用
收藏
页码:221 / 225
页数:5
相关论文
共 32 条
[1]  
Ames PRJ, 2000, J RHEUMATOL, V27, P1190
[2]  
Amrani D L, 1990, Blood Coagul Fibrinolysis, V1, P443, DOI 10.1097/00001721-199010000-00013
[3]   Antiphospholipid antibodies and the coagulation cascade [J].
Anglés-Cano, E ;
Guillin, MC .
RHEUMATIC DISEASE CLINICS OF NORTH AMERICA, 2001, 27 (03) :573-+
[4]   THE ANTIPHOSPHOLIPID SYNDROME - A SYNDROME IN EVOLUTION [J].
ASHERSON, RA ;
CERVERA, R .
ANNALS OF THE RHEUMATIC DISEASES, 1992, 51 (02) :147-150
[5]  
AWADA H, 1988, J LAB CLIN MED, V111, P229
[6]  
BALLEISEN L, 1985, THROMB HAEMOSTASIS, V54, P475
[7]  
CLAUSS A., 1957, ACTA HAEMATOL, V17, P237
[8]   CARDIOVASCULAR MANIFESTATIONS OF SYSTEMIC LUPUS-ERYTHEMATOSUS [J].
DOHERTY, NE ;
SIEGEL, RJ .
AMERICAN HEART JOURNAL, 1985, 110 (06) :1257-1265
[9]   FIBRINOGEN AS A CARDIOVASCULAR RISK FACTOR - A METAANALYSIS AND REVIEW OF THE LITERATURE [J].
ERNST, E ;
RESCH, KL .
ANNALS OF INTERNAL MEDICINE, 1993, 118 (12) :956-963
[10]   DOSE EFFECT RELATIONSHIP BETWEEN SMOKING AND BLOOD RHEOLOGY [J].
ERNST, E ;
MATRAI, A ;
SCHMOLZL, C ;
MAGYAROSY, I .
BRITISH JOURNAL OF HAEMATOLOGY, 1987, 65 (04) :485-487