Plasminogen activator inhibitor-1 (PAI-1) polymorphisms in patients with obstructive sleep apnoea

被引:13
作者
Barceló, A
Llompart, E
Barbé, F
Morlá, M
Vila, M
Agustí, AGN
机构
[1] Hosp Univ Son Dureta, Serv Pneumol, Palma de Mallorca 07014, Spain
[2] Hosp Univ Son Dureta, Serv Anal Clin, Palma de Mallorca, Spain
[3] Hosp Univ Son Dureta, Unitat Invest REUNI, Palma de Mallorca, Spain
关键词
apnoea; cardiovascular; fibrinolysis; genetics;
D O I
10.1053/rmed.2001.1239
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cardiovascular diseases are frequent among patients with the obstructive sleep apnoea syndrome (OSAS). The aetiopathogenesis of this association is unclear. Type I plasminogen activator inhibitor (PAI-I) is one of the primary regulators of the fibrinolytic system. A reported association between PAI-I activity and an insertion/deletion polymorphism (4G/5G) in the promoter region of the PAI-I gene suggests a critical role for this genomic region in the pathogenesis of several cardiovascular diseases, In this study, we determined the prevalence of this polymorphism in patients with OSAS and in healthy control subjects. The 4G/5G polymorphism in the promoter region of the PAI-I gene was determined in 78 male patients with severe OSAS (56 +/- 2 apnoeas per hour) and in 70 healthy male, non-smoker volunteers of similar age, without personal or familial history of cardiovascular disease. The frequency of the 4G/4G, 4G/5G and 5G/5G genotypes in patients with OSAS (18%, 62%, 19%, respectively) was not significantly different from that seen in healthy subjects (16%, 60%, 24% P=NS). These results show that the distribution of the 4G/5G polymorphism in the promoter region of the PAI-I gene in patients with OSAS is similar to that observed in healthy subjects, This observation suggests that the PAI-I polymorphism has no relationship with the increased risk of cardiovascular diseases seen in patients with OSAS. (C) 2002 Elsevier Science Ltd.
引用
收藏
页码:193 / 196
页数:4
相关论文
共 21 条
[1]   Abnormal lipid peroxidation in patients with sleep apnoea [J].
Barceló, A ;
Miralles, C ;
Barbé, F ;
Vila, M ;
Pons, S ;
Augustí, AGN .
EUROPEAN RESPIRATORY JOURNAL, 2000, 16 (04) :644-647
[2]  
Catto AJ, 1997, THROMB HAEMOSTASIS, V77, P730
[3]  
DAWSON SJ, 1993, J BIOL CHEM, V268, P10739
[4]   POSSIBLE ATHEROGENIC EFFECTS OF HYPOXIA DURING OBSTRUCTIVE SLEEP-APNEA [J].
DEAN, RT ;
WILCOX, I .
SLEEP, 1993, 16 (08) :S15-S22
[5]   ALLELE-SPECIFIC INCREASE IN BASAL TRANSCRIPTION OF THE PLASMINOGEN-ACTIVATOR INHIBITOR-1 GENE IS ASSOCIATED WITH MYOCARDIAL-INFARCTION [J].
ERIKSSON, P ;
KALLIN, B ;
VANTHOOFT, FM ;
BAVENHOLM, P ;
HAMSTEN, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (06) :1851-1855
[6]   THE RELATIONSHIP BETWEEN SYSTEMIC HYPERTENSION AND OBSTRUCTIVE SLEEP-APNEA - FACTS AND THEORY [J].
FLETCHER, EC .
AMERICAN JOURNAL OF MEDICINE, 1995, 98 (02) :118-128
[7]  
HAMSTEN A, 1987, LANCET, V2, P3
[8]   The link between sleep apnea and cardiovascular disease - Time to target the nonsleepy sleep apneics? [J].
Hedner, J ;
Grote, L .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2001, 163 (01) :5-6
[9]  
Hedner J.A., 1994, Sleep and Breathing, P823
[10]   ASSOCIATION OF SLEEP-APNEA WITH MYOCARDIAL-INFARCTION IN MEN [J].
HUNG, J ;
WHITFORD, EG ;
PARSONS, RW ;
HILLMAN, DR .
LANCET, 1990, 336 (8710) :261-264