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(Stroke. 2001;32:1699.)
© 2001 American Heart Association, Inc.

Editorial

2001: A Prospective, Seasonal Odyssey Into Antiphospholipid Protein Antibodies

Steven R. Levine, MD Bradley S. Jacobs, MD

From the Stroke Program, Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan.

Correspondence and reprint requests to Steven R. Levine, MD, Stroke Program, Department of Neurology UHC 8C, WSU School of Medicine, 4201 St. Antoine, Detroit, MI 48201-2153. E-mail slevine@med.wayne.edu

The human immune response is highly complex, dictated by incompletely understood genetic and environmental factors, and it appears to be important in contributing to several forms of cerebrovascular disease. Antiphospholipid-protein antibodies (aPL) have been implicated in immune-mediated clotting in both arterial and venous beds¹ and are considered to be the most common hematological condition associated with ischemic stroke. However, given the vast number of conditions associated with aPL production, including systemic lupus erythematosus, HIV, syphilis, other infections, malignancy, immunizations, and medications, it is clear that aPL are quite a heterogeneous family of immunoglobulins that vary in specificity, isotype, subclass, titer, and associated mechanisms of action. aPL may also be seen in otherwise healthy individuals. Thus, there has been great difficulty is sorting out the potentially important aPL from the nonspecific immune system "noise." A major breakthrough in the field came in 1990 when 3 groups identified the need for a cooperative phospholipid binding protein in order to detect most, but not all, aPL antibodies.^2–4 Based on limited data, it has been suggested that infection-related aPL may be less pathogenic and that these aPL do not require a cofactor (apolipoprotein H, also called ß₂ glycoprotein-1 [ß₂GP1]) for their detection with ELISA. ß₂GP1 is a cationic plasma glycoprotein with a molecular mass of 50 kDa and a plasma concentration of 200 µg/mL. Cofactor-dependent aPL may allow identification of a more specific group of antibodies involved in thrombo-occlusive disease.¹ These differences in aPL may also contribute to the lack of consistent . . . [Full Text of this Article]