Antiphospholipid syndrome: pathogenesis and a window of treatment opportunities in the future

Mehdi, Ali A; Uthman, Imad; Khamashta, Munther A.

doi:10.1111/j.1365-2362.2010.02281.x

Cited by 41 publications

(32 citation statements)

References 94 publications

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“…Such antiHsp60-induced endothelial damage would constitute the "first hit" and would favor the recruitment of aPL by exposing phosphatidylserine, a negatively charged phospholipid that interacts with phospholipid-binding proteins. Antiphospholipid antibody binding to phospholipid-binding protein on the endothelial cell membrane (the "second hit") could promote a prothrombotic environment and predispose to arterial vascular events (38).…”

Section: Discussionmentioning

confidence: 99%

Association of autoantibodies to heat‐shock protein 60 with arterial vascular events in patients with antiphospholipid antibodies

Dieudé¹,

Correa²,

Neville³

et al. 2011

Arthritis & Rheumatism

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Objective. Anti-heat shock protein 60 autoantibodies (anti-Hsp60) are associated with cardiovascular disease and are known to affect endothelial cells in vitro, and we have recently shown that anti-Hsp60 promote thrombosis in a murine model of arterial injury. Based on those findings, we undertook the present study to investigate the hypothesis that the presence of antiHsp60, alone or in combination with other thrombogenic risk factors, is associated with an elevated risk of vascular events.Methods. The study population was derived from 3 ongoing cohort studies: 2 independent systemic lupus erythematosus (SLE) registries and 1 cohort comprising SLE patients and non-SLE patients. Data from a total of 402 participants were captured; 199 of these participants had had confirmed vascular events (arterial vascular events in 102, venous vascular events in 76, and both arterial and venous vascular events in 21). Anti-Hsp60 were detected by enzyme-linked immunoassay, and association with vascular events was assessed by regression analysis. Conclusion. We demonstrate that anti-Hsp60 are associated with an increased risk of arterial vascular events, but not venous vascular events, in aPL-positive individuals. These data suggest that anti-Hsp60 may serve as a useful biomarker to distinguish risk of arterial and venous vascular events in patients with aPL. Results. Multiple regression analysis revealed

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Section: Discussionmentioning

confidence: 99%

Association of autoantibodies to heat‐shock protein 60 with arterial vascular events in patients with antiphospholipid antibodies

Dieudé¹,

Correa²,

Neville³

et al. 2011

Arthritis & Rheumatism

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“…On the other hand, prevalence of secondary APS is highest in patients with SLE, so it can be assumed that SLE represents an inflammatory basis for APS. Additionally, experimental models suggest significant role of complement system and inflammation in APS pathogenesis, which is similar to SLE pathogenesis [49][50][51]. New data indicate role of vitamin D in SLE pathogenesis and also very current are researches of vitamin D role in APS [52].…”

Section: Is Antiphospholipid Syndrome a Systemic Autoimmune Disorder?mentioning

confidence: 88%

Systemic Lupus Erythematosus and Antiphospholipid Syndrome

Plavšić¹,

Mišković²,

Rašković

et al. 2014

Open Access Maced J Med Sci

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Antiphospholipid syndrome is an autoimmune disorder defined as association of vascular thrombosis and/or pregnancy complications with presence of antiphospholipid antibodies (lupus anticoagulant, anticardiolipin and anti-β2 glycoprotein I). It is the most common cause of acquired thrombophilia, and can occur as an independent entity or in relation with other diseases, especially systemic lupus erythematosus. Presence of antiphospholipid syndrome in systemic lupus erythematosus is additional vaso occlusive factor in already present inflammation, bringing further risk for thrombotic events. Clinical and serological manifestations of antiphospholipid syndrome and systemic lupus erythematosus are very similar, so possible connection for these two autoimmune disorders is assumed.

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“…The major target antigen of autoimmune α-CL is a neo-epitope on the phospholipid-binding protein β2-glycoprotein-1 (β2GPI) that appears consequent to its binding to phospholipids (Galli et al, 1990;Viard et al, 1992). The pathogenicity of α-CL is thought to be related to its ability to interfere with the regulatory function of β2GPI in prevention of the initiation of coagulation (Shoenfeld, 2003;Mehdi et al, 2010).…”

Section: Anti-cardiolipin (α-Cl)mentioning

confidence: 99%