This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Ames, P R J Articles by Brancaccio, V Search for Related Content PubMed PubMed Citation Articles by Ames, P R J Articles by Brancaccio, V Social Bookmarking                         What's this?

Antioxidant susceptibility of pathogenic pathways in subjects with antiphospholipid antibodies: a pilot study

75 Canterbury House, Royal Street, London SE1 7EH, UK. Tel: / 44 207 9289211; pames{at}rayne.umds.ac.uk

C Tommasino

Chemical Pathology, S Gennaro Hospital, Naples, Italy

J Alves

Autoimmune Disease Unit, Curry Cabral Hospital, Lisbon, Portugal

J D Morrow

Department of Medicine, Vanderbilt University, Nashville, TN, USA

L Iannaccone

Coagulation Unit, Cardarelli Hospital, Naples, Italy

G Fossati

Chemical Pathology, S Gennaro Hospital, Naples, Italy

S Caruso

F Caccavo

Chemical Pathology, Cardarelli Hospital, Naples, Italy

V Brancaccio

Coagulation Unit, Cardarelli Hospital, Naples, Italy

The pathogenesis of antiphospholipid antibody (aPL) related thrombosis is multifactorial and includes, amongst others, enhanced coagulation activation measured as prothrombin fragment 1 / 2 (F1 / 2), elevated plasma levels of von Willebrand factor (vWF), plasminogen activator inhibitor (PAI) and endothelin-l (ET-1) as well as heightened thromboxane generation and lipid peroxidation. To evaluate the antioxidant susceptibility of some of the above pathways, probucol (500 mg/d orally, a cholesterol lowering agent bearing antioxidant properties) was administered for a three week period to 14 subjects with aPL and to seven healthy controls. At baseline aPL participants showed higher plasma levels of vWF (P ‘ 0.006), ET-1 (P ‘ 0.0002) and enhanced urinary excretion of 11-dehydro-thromboxane-B₂ (TXB₂)(P ‘ 0.0004), F2-isoprostanes (marker of lipid peroxidation) (P ‘ 0.02) and albumin (P ‘ 0.04) than controls. In the aPL group baseline IgG anticardiolipin (aCL) titre positively related with urinary TXB₂ (r² ‘ 0.43, P ‘ 0.01) and inversely with urinary NO_x (r² ‘ÿ0.6, P ‘ 0.005) whereas urinary NO^x and TXB² were negatively correlated (r² ‘ÿ0.42, P ‘ 0.01). After the treatment period significant decreases from baseline values were noted for PAI (P ‘ 0.01), ET-1 (P ‘ 0.006), TXB² (P ‘ 0.02), F2-isoprostanes (P ‘ 0.01) and albuminuria (P ‘ 0.01) in aPL participants but not in controls. These pilot data support oxidative sensitive mechanisms and a potential role for antioxidant treatment in the pathogenesis of aPL induced vasculopathy.

Key Words: antiphospholipid antibodies • oxidation • atherosclerosis • microalbuminuria

Lupus, Vol. 9, No. 9, 688-695 (2000)
DOI: 10.1191/096120300677692516


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				E Matsuura and L. Lopez Autoimmune-mediated atherothrombosis Lupus, October 1, 2008; 17(10): 879 - 888. [Abstract] [PDF]

				J. Delgado Alves, L. J. Mason, P. R. J. Ames, P. P. Chen, J. Rauch, J. S. Levine, R. Subang, and D. A. Isenberg Antiphospholipid antibodies are associated with enhanced oxidative stress, decreased plasma nitric oxide and paraoxonase activity in an experimental mouse model Rheumatology, October 1, 2005; 44(10): 1238 - 1244. [Abstract] [Full Text] [PDF]

				J D. Alves, E L Radway-Bright, S Lee, B Grima, J Hothersall, C T Ravirajan, and D A Isenberg Antiphospholipid antibodies are induced by in vitro fertilization and correlate with paraoxonase activity and total antioxidant capacity of plasma in infertile women Lupus, May 1, 2005; 14(5): 373 - 380. [Abstract] [PDF]