Antiphospholipid antibodies and platelets

Jong, Ann De; Ziboh, Vincent A.; Robbins, Dick L.

doi:10.1007/s11926-000-0085-8

Cited by 10 publications

(9 citation statements)

References 38 publications

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“…In vivo and in vitro studies demonstrate that aPL activate endothelial cells and platelets and contribute to thrombosis and tissue injury (Pierangeli et al, 1999; DeJong et al, 2000). A major antigen recognized by aPL is beta2 glycoprotein 1, a member of the complement control protein superfamily (Giannakopoulos, 2007; Shi et al, 1993).…”

Section: Complement Activation On Platelets In Autoimmune Disordersmentioning

confidence: 99%

Complement activation on platelets: Implications for vascular inflammation and thrombosis

Peerschke

Yin

Ghebrehiwet

2010

Molecular Immunology

211

153

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Platelets participate in a variety of responses of the blood to injury. An emerging body of evidence suggests that these cells express an intrinsic capacity to interact with and trigger both classical and alternative pathways of complement. This activity requires cell activation with biochemical agonists and/or shear stress, and is associated with the expression of P-selectin, gC1qR, and chondroitin sulfate. Platelet mediated complement activation measurably increases soluble inflammatory mediators (C3a and C5a). Platelets may also serve as targets of classical complement activation in autoimmune conditions such as antiphospholipid syndromes (APS) and immune thrombocytopenia purpura (ITP). Retrospective correlation with clinical data suggests that enhanced platelet associated complement activation correlates with increased arterial thrombotic events in patients with lupus erythematosus and APS, and evidence of enhanced platelet clearance from the circulation in patients with ITP. Taken together, these data support a role for platelet mediated complement activation in vascular inflammation and thrombosis.

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Section: Complement Activation On Platelets In Autoimmune Disordersmentioning

confidence: 99%

Complement activation on platelets: Implications for vascular inflammation and thrombosis

Peerschke

Yin

Ghebrehiwet

2010

Molecular Immunology

211

153

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“…These antibodies can bind directly to platelet surfaces (4)(5)(6)(7). Recent compelling data presented by Holers et al show that in vivo complement activation is required for aPL-induced fetal loss and growth retardation (8).…”

mentioning

confidence: 99%

Platelet C4d is highly specific for systemic lupus erythematosus

Navrátil

Manzi

Kao

et al. 2006

Arthritis & Rheumatism

100

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Objective. Complement-activation product C4d is deposited on normal erythrocytes, while abnormal levels have been observed on the surface of erythrocytes of patients with systemic lupus erythematosus (SLE). This study examines whether C4d also deposits on human platelet surfaces, and whether platelet-bound C4d may provide a biomarker for SLE.Methods. We conducted a cross-sectional study of 105 patients with SLE, 115 patients with other diseases, and 100 healthy controls. Levels of C4d on the surface of platelets were examined by flow cytometry and scanning confocal microscopy. Statistical analyses were performed to determine the clinical variables associated with platelet C4d.Results. Abnormal levels of platelet C4d were found to be highly specific for SLE. Platelet C4d was detected in 18% of patients with SLE, being 100% specific for a diagnosis of SLE compared with healthy controls and 98% specific for SLE compared with patients with other diseases (P < 0.0001). In addition, platelet C4d was significantly associated with positivity for lupus anticoagulant (P < 0.0001) and anticardiolipin antibodies of the IgG (P ‫؍‬ 0.035) or the IgM (P ‫؍‬ 0.016) isotype. Platelet C4d was also significantly associated with SLE disease activity according to the SLE Disease Activity Index (P ‫؍‬ 0.039), low serum C4 (P ‫؍‬ 0.046), an elevated erythrocyte sedimentation rate (P ‫؍‬ 0.006), and abnormal levels of C4d on erythrocytes (P < 0.0001).Conclusion. This observation suggests that platelet-bound C4d may be a useful biomarker for SLE and may be a clue to the pathogenic mechanisms responsible for the myriad thrombotic and vascular complications of lupus associated with antiphospholipid antibodies.

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“…The aCL testing methods appeared to be sensitive for antiphospholipid antibodies in that aCL testing failed to identify only 9.5% of individuals with other evidence (positive LA testing) of antiphospholipid antibodies. However, because positive LA test results often are considered to be of greater clinical importance than positive aCL test results, [2][3][4][5] it is important to test for both LA and aCL. Evaluation of our aCL testing methods, subsequent to this study, suggested a possible oversensitivity of IgM testing, especially for low-titer or weakly positive antibodies.…”

Section: Discussionmentioning

confidence: 99%

“…L upus anticoagulants (LA) and anticardiolipin antibodies (aCL) are associated with an increased risk of venous and arterial thrombotic events, recurrent fetal loss, and thrombocytopenia. [1][2][3][4][5] Other clinical manifestations include livedo reticularis, 6,7 superficial thrombophlebitis, 8 leg ulcers, 8 cardiac valvular disease, [9][10][11] migraine headache, 12,13 and chorea. [14][15][16] Lupus anticoagulants or aCL (or both) occur in primary antiphospholipid antibody syndrome 15 and in other diseases, especially systemic lupus erythematosus (SLE).…”

mentioning

confidence: 99%