Semin Respir Crit Care Med 1998; 19(1): 3-11
DOI: 10.1055/s-2007-1009378
Copyright © 1998 by Thieme Medical Publishers, Inc.

The Endovascular Compartment

David D'Cruz* , Munther A. Khamashta , Graham RV. Hughes
  • *The Bone and Joint Research Unit, The Royal London Hospital, London, and
  • †Lupus Research Unit, The Rayne Institute, St. Thomas' Hospital, London, United Kingdom
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Publication History

Publication Date:
20 March 2008 (online)

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Abstract

Autoimmune endothelial damage or activation offers an attractive explanation for some of the clinical manifestations of pulmonary disease. Endothelial cells may for example be involved by antibodies directed against the endothelium and/or by cellular immunity. Alternatively, vascular and organ damage may be caused by thrombosis associated with antiphospholipid antibodies. These heterogenous prothrombotic antibodies include the confusingly named lupus anticoagulant as well as antibodies reacting with negatively charged phospholipids which include cardiolipin. In this article, we have focused on endothelial cell immunopathology, antiphospholipid antibodies and their relationship to clinical problems such as thrombosis, thromboembolic disease and pulmonary hypertension.