Anticardiolipin Antibodies and Hypercoagulability
Authors: Anjay Anand
Journal: Annals of Internal Medicine (1993)

Letters15 June 1993Anticardiolipin Antibodies and HypercoagulabilityAnjay Anand, MDAnjay Anand, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-118-12-199306150-00019 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Ginsburg and colleagues [1] are to be commended on their long-term study showing the enhanced risk posed by anticardiolipin antibodies for deep venous thrombosis and pulmonary embolism in healthy adult men. Although their mechanism of action is unknown, the anticardiolipin antibodies lead to a hypercoagulable state not only in systemic lupus erythematosus but also in the absence of disease.The investigators found that low-dose aspirin was not protective and that thrombosis recurred despite therapeutic anticoagulation. A recent study [2] evaluating thrombosis in patients with antiphospholipid antibodies found that recurrence rates during no treatment; aspirin; and low-, intermediate-, and high-intensity warfarin therapy (international normalized ratios [INRs] < 1.9; 2.0 to 2.9; and > 3.0, respectively) were 0.19, 0.32, 0.57, 0.07 (P = 0.12), and 0.00 (P < 0.001) per patient-year, respectively. Although this study found no benefit with aspirin, it did find significant to complete protection when intermediate- to high-intensity warfarin was used as a prophylactic agent [2]. When a decision to treat is made (for example, when high-titer anticardiolipin antibodies are associated with episodes of thrombosis), an INR of 3.0 should be set and reduced if a bleeding risk is perceived. Indefinite anticoagulation may prove useful in reliable patients with recurrent thrombotic episodes.Another issue of interest is the apparent absence of thrombotic risk in patients who develop anticardiolipin antibodies in the presence of the human immunodeficiency virus (HIV) [3], other infectious processes [4], or chlorpromazine therapy [5]. This suggests that these antibodies are heterogeneous in structure or function, or both, and that different antibodies recognize and react with distinct epitopes, depending on the structural array of phospholipids. Further analysis of anticardiolipin antibodies may provide clues both to the pathogenesis of the coagulation abnormalities and to better mechanisms of prevention.References1. Ginsburg KS, Liang MH, Newcomer L, Goldhaber SZ, Schur PH, Hennekens CH, et al. Anticardiolipin antibodies and the risk for ischemic stroke and venous thrombosis. Ann Intern Med. 1992; 117: 997-1002. Google Scholar2. Rosove MH, Brewer PM. Antiphospholipid thrombosis: clinical course after the first thrombotic event in 70 patients. Ann Intern Med. 1992; 117:303-8. Google Scholar3. Stimmler MM, Quismorio FP Jr, McGehee WG, Boylen T, Sharma OP. Anticardiolipin antibodies in acquired immunodeficiency syndrome. Arch Intern Med. 1989; 149:1833-5. Google Scholar4. Santiago MB, Cossermelli WA, Tuma MF, Pinto MN, Oliviera RM. Anticardiolipin antibodies in patients with infectious diseases. Clin Rheumatol. 1989; 8:23-8. Google Scholar5. Canoso RT, de Oliviera RM. Chlorpromazine-induced anticardiolipin antibodies and lupus anticoagulant: absence of thrombosis. Am J Hematol. 1988; 27:272-5. Google Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 June 1993Volume 118, Issue 12Page: 986-987KeywordsAntibodiesAspirinHemorrhageInternational normalized ratioLupus erythematosusPathogenesisPhospholipidsPulmonary embolismSystemic lupus erythematosusThrombosis ePublished: 15 August 2000 Issue Published: 15 June 1993 Copyright & PermissionsCopyright © 1993 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...