Search J Rheum

Advanced Search

Home

Current Issue

Archives

Guidelines for Authors

Classified Ads

Links

Subscriptions

Subscriber Registration

Guidelines for Website Users

JRheum Update Service

Contact Info

Gene Polymorphisms of Tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 in Patients with Antiphospholipid Antibodies

SHINSUKE YASUDA, AKITO TSUTSUMI, TATSUYA ATSUMI, MARIA L. BERTOLACCINI, KENJI ICHIKAWA, MUNTHER A. KHAMASHTA, GRAHAM R.V. HUGHES, and TAKAO KOIKE

ABSTRACT.

Objective.
Impaired fibrinolytical outcomes may be one of the pathogenic factors for thrombotic events in patients with antiphospholipid antibodies (aPL). We investigated the consequences of the gene polymorphisms of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) in patients positive for aPL.

Methods. Seventy-seven Japanese and 82 British patients with aPL were examined for Alu-repeat insertion (I)/deletion (D) polymorphism of the tPA gene by polymerase chain reaction (PCR), and 4G/5G polymorphism in the PAI-1 promoter gene by site-directed mutagenesis-PCR and restriction fragment length polymorphism analysis. Correlations between these polymorphisms and clinical symptoms of antiphospholipid syndrome (APS) (arterial thrombosis, venous thrombosis, miscarriage) were analyzed.

Results. Significant differences in the allele frequencies of these genes did not exist between patients and controls. There was no significant correlation between these gene polymorphisms and clinical symptoms of APS in patients with aPL.

Conclusion. Polymorphisms of the tPA or PAI-1 genes probably do not significantly influence the risk of arterial thrombosis, venous thrombosis, or pregnancy morbidity in patients with aPL. (J Rheumatol 2002;29:1192-7)

Key Indexing Terms:

FIBRINOLYSIS
GENOME
PATHOGENESIS
ANTIPHOSPHOLIPID ANTIBODY SYNDROME
THROMBOSIS


From Department of Medicine II, Hokkaido University School of Medicine, Sapporo, Japan; and Lupus Research Unit, The Rayne Institute, St. Thomas' Hospital, London, UK.

S. Yasuda, MD, PhD; A. Tsutsumi, MD, PhD; T. Atsumi, MD, PhD; M.L. Bertolaccini, MD; K. Ichikawa, MD, PhD, Department of Medicine II, Hokkaido University School of Medicine; M.A. Khamashta, MD, PhD; G.R.V. Hughes, MD, FRCP, Lupus Research Unit, The Rayne Institute; T. Koike, MD, PhD, Department of Medicine II, Hokkaido University School of Medicine.

Address reprint requests to Dr. T. Koike, Department of Medicine II, Hokkaido University School of Medicine, Kita 15, Nishi 7, Kita-ku, Sapporo 060-8638, Japan. E-mail: tkoike@med.hokudai.ac.jp

Submitted April 12, 2001; revision accepted December 18, 2001.




Return to June 2002 Table of Contents



© 2002. The Journal of Rheumatology Publishing Company Limited.
All rights reserved.