Antiphospholipid Antibodies: A Critique of Their Heterogeneity and Hegemony

H, Reyes; Dearing, Linda; Shoenfeld, Yehuda; Peter, James B.

doi:10.1055/s-2007-1001893

Cited by 28 publications

(17 citation statements)

References 45 publications

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“…1,17,18 Antiphospholipid antibodies have also been detected in malignancies, infections, and drug ingestion; in these conditions, aPL antibodies have not appeared to increase the risk for thrombosis. 16,19 Drugs that have been reported to induce aPL antibody production include procainamide, phenothiazine, quinidine, and hydralazine.…”

Section: Discussionmentioning

confidence: 99%

“…Currently, they are detected by either ELISA, with anionic phospholipids used as the antigens (eg, anticardiolipin antibodies, antiphosphatidylserine antibodies), or by the ability to prolong coagulation time in a phospholipid-dependent assay (lupus coagulant). 1,2 Antiphospholipid (aPL) antibodies are an element of the antiphospholipid syndrome, a condition characterized by arterial and venous thrombosis, recurrent fetal loss, and thrombocytopenia in the presence of aPL antibodies. 3 There also appears to be an association between aPL antibodies and ischemic events even in the absence of the other features of the syndrome.…”

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confidence: 99%

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Seasonal Distribution of Antiphospholipid Antibodies

Luong

Rand

et al. 2001

Stroke

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Background and Purpose-The purpose of this study was to determine if there was a seasonal variation in antiphospholipid antibody (aPL) titers and whether this variation differed between stroke cases and control subjects. Methods-IgG and IgM anticardiolipin and antiphosphatidyl serine antibody titers were obtained on serum samples from 884 stroke patients and 1024 control subjects over a 7-year period. Temporal distributions by month of blood draw were evaluated. Results-Marked seasonal differences in the proportion of positive titers were found for control subjects, but no seasonal variability among patients was noted. In control subjects, positive titers occurred less frequently in the summer months, mirroring the seasonal trends seen in respiratory track infections and rheumatic fever. Conclusions-Our data suggest some aPL antibodies arise from different origins in patients and control subjects. The seasonality observed in the apparently normal population may be related to antibodies of infectious origin and is consistent with the reported lack of association with thrombosis of infection-related antibodies. (Stroke. 2001;32:1707-1711.)

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Seasonal Distribution of Antiphospholipid Antibodies

Luong

Rand

et al. 2001

Stroke

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“…11,18 Of interest, biologic falsepositive tests for syphilis are seen in up to 40% of patients with systemic lupus; the number increases to 90% in patients with systemic lupus plus the LA. 19,23,28 An abnormality often (theoretically) exists in the phospholipid-dependent coagulation reactions, including the prothrombin time, the activated partial thromboplastin time (aPTT), and the Russell's viper venom time (dRVVT), as the lupus anticoagulant is not directed against a specific factor, but to phospholipids. The inhibitor usually does not exert an increasing effect with prolonged incubation with normal plasma, and thus this simple screen can often be used to distinguish the lupus inhibitor from inhibitors that neutralize specific clotting factors.…”

Section: Lupus Anticoagulants and Thrombosismentioning

confidence: 99%

Antiphospholipid Syndrome and Thrombosis

Bick¹,

Baker²

1999

Semin Thromb Hemost

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Antiphospholipid antibodies [such as anticardiolipin antibodies (ACLA)] are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The most common thrombotic events associated with ACLA are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome) or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). Type V patients are those with antiphospholipid antibodies and fetal wastage syndrome. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of ACLA in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through VI) should be defined, if possible, as this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with ACLA, patients with primary lupus anticoagulant thrombosis syndrome usually suffer venous thrombosis. Because the activated partial thromboplastin time (aPTT) is unreliable in patients with lupus anticoagulant (prolonged in only about 40 to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests including ELISA for ACLA, the dRVVT for lupus anticoagulant, hexagonal phospholipid neutralization procedure, and B-2-GP-I (IgG, IgA, and IgM) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If these are negative, in the appropriate clinical setting, subgroups should also be assessed. Finally, most patients with antiphospholipid thrombosis syndrome will fail warfarin therapy and, except for retinal vascular thrombosis, most will fail antiplatelet therapy, thus it is of major importance to make this diagnosis in order that patients can be treated with the most effective therapy for secondary prevention, low-molecular weight heparin (LMWH) or unfractionated heparin (UHF) in most instances.

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“…Antibodies to annexin-V, also referred to as placental anticoagulant protein [130], may be of particular importance in patients with RMS, but additional studies are needed. Two studies have shown that immunoglobulin fractions of antiphospholipid antibody or B-2-GP-I decrease trophoblastic annexin-V [130 -132], but several studies have suggested this anti-annexin-V activity is limited to the antiphosphatidlyserine subgroup antibody idiotype [133,134]. Two studies, however, have failed to demonstrate abnormalities of annexin-V in patients with antiphospholipid syndrome who miscarry and concluded that it may play no role in RMS [135,136].…”

Section: Anticardiolipins and Obstetric Syndromesmentioning

confidence: 99%