(Stroke. 1998;29:1755-1758.)
© 1998 American Heart Association, Inc.
Antiphospholipid-Protein Antibodies and Ischemic Stroke
Not Just Cardiolipin Any More
David Tanne, MD;
Douglas A. Triplett, MD, FACP, FCAP;
Steven R. Levine, MD
From the Center for Stroke Research, Department of Neurology, Henry Ford
Hospital and Health Sciences Center, Detroit, Mich (D.T., S.R.L.) and the
Midwest Hemostasis and Thrombosis Laboratories, Ball Memorial Hospital,
Muncie, Ind (D.A.T.). Dr Tanne is currently at the Department of Neurology,
Chaim Sheba Medical Center, Tel Hashomer, Israel.
Correspondence to Steven R. Levine, MD, Director, WSU/Detroit Medical Center Stroke Program, WSU School of Medicine, University Health Center 6E, 4201 St Antoine, Detroit, MI 48201.
Key Words: antibodies, anticardiolipin antibodies, antiphospholipid cerebral ischemia
Within the past decade, cerebral infarction in as
many as 40% of patients was not found to have a determined cause based
on NINCDS Stroke Data Bank criteria.1 With
improved understanding of the complex pathogenic processes leading to
ischemic stroke and refined imaging and diagnostic
tests, underlying potential causes are more often recognized. Yet, the
etiology of ischemic stroke in a discouragingly large number of
patients continues to elude clinicians.
Antiphospholipid antibodies (aPL) are a heterogeneous
family of autoantibodies associated with a clinical syndrome
characterized by thrombo-occlusive events. Anticardiolipin antibodies
(aCL), detected by standard enzyme-linked immunosorbent assay (ELISA),
and the lupus anticoagulant (LA), which prolongs
phospholipid-dependent coagulation assays, are conventional assays for
aPL and the ones currently best characterized and
standardized.2 3 There is partial concordance
between the 2 assays. The preponderance of evidence indicates, however,
that LA assay is more specific for patients at risk for thromboembolic
events.4 In contrast, the aCL assay is more
sensitive but nonspecific and could be found also in various contexts
ranging from health to certain medications, malignancies, and
infectious diseases. aCL have been identified in approximately 10% of
unselected patients with first ischemic
stroke.5 The isotype mainly implicated in
thrombosis is IgG, more specifically subtype
IgG2.6 Recent data suggest
that the presence of high titers of aCL immunoreactivity, mainly IgG
isotype but possibly also IgM, correlates with an increased risk of
thrombosis.7 8 9 Generally, titers of IgG aCL
implicated are >40 GPL, although this is a somewhat arbitrary cutoff
point and is dependent on . . . [Full Text of this Article]
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