Cognitive Deficits in Patients With Antiphospholipid Syndrome

Tektonidou, Maria G.; Varsou, Natassa; Kotoulas, Grigorios; Antoniou, Anna; Moutsopoulos, Haralampos Μ.

doi:10.1001/archinte.166.20.2278

Cited by 117 publications

(44 citation statements)

References 22 publications

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“…Although scant, studies in primary APS have reported a high predominance of cognitive deficits involving attention and verbal fluency [12,13]. In addition, several authors reported the occurrence of chronic or recurrent ischemic events affecting small or large cerebral vessels and leading to multi-infarct dementia [1].…”

Section: The Current Clinical Spectrum Of Anti-phospholipid Syndromementioning

confidence: 99%

Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers

et al. 2014

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The clinical spectrum of the anti-phospholipid syndrome (APS) is not limited to vascular thrombosis or miscarriages but includes additional manifestations that cannot be explained solely by a thrombophilic state. Anti-cardiolipin, anti-beta2 glycoprotein I (anti-β2GPI) and lupus anticoagulant (LA) assays are not only the formal diagnostic and classification laboratory tools but also parameters to stratify the risk to develop the clinical manifestations of the syndrome. In particular, anti-β2GPI antibodies reacting with an immunodominant epitope on domain I of the molecule were reported as the prevalent specificity in APS patients, correlating with a more aggressive clinical picture. Several laboratory assays to improve the diagnostic and predictive power of the standard tests have been proposed. Plates coated with the phosphatidylserine-prothrombin complex for detecting antibodies represent a promising laboratory tool correlating with LA and with clinical manifestations. Anti-phospholipid antibodies can be found in patients with full-blown APS, in those with thrombotic events or obstetric complications only or in asymptomatic carriers. An inflammatory second hit is required to increase the presence of β2GPI in vascular tissues, eventually triggering thrombosis. Post-transcriptional modifications of circulating β2GPI, different epitope specificities or diverse anti-β2GPI antibody-induced cell signaling have all been suggested to affect the clinical manifestations and/or to modulate their occurrence.

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Section: The Current Clinical Spectrum Of Anti-phospholipid Syndromementioning

confidence: 99%

Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers

et al. 2014

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“…White matter disease is a marker of small vessel disease and increases with aging and cumulative burden of cerebrovascular risk factors(12, 18). Additionally, chronic inflammatory diseases such as lupus erythematous may trigger white matter disease without these cerebrovascular risk factors(29, 30). …”

Section: Discussionmentioning

confidence: 99%

COX-2 rs20417 Polymorphism Is Associated with Stroke and White Matter Disease

Oliveira‐Filho

Ornellas

Zhang

et al. 2015

Journal of Stroke and Cerebrovascular Diseases

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Goals To investigate the effect of COX-2 polymorphism and its product, prostaglandin-E2 (PGE2), on stroke risk in an endemic area for Chagas disease. In a separate cohort, to investigate the effect of COX-2 polymorphisms on the total burden of cerebral white matter disease. Methods Cases were outpatients with ischemic stroke; controls were stroke-free subjects from two outpatient clinics (heart failure and caregivers of a movement disorders clinic). We extracted DNA from total blood to investigate the rs20417 COX-2 polymorphism. Serologic tests (ELISA) were performed to confirm T. cruzi infection and to quantify PGE2 levels. In the Boston cohort, white matter hyperintensity volume (WMHv) was quantified on the admission brain MRIs of subjects with ischemic stroke, who also donated DNA for the COX-2 gene region analysis. Findings We studied 44 patients with stroke and 96 controls (46 with heart failure and 50 caregivers) in the Brazilian cohort; and 788 stroke patients (302 cardioembolic, 486 non-cardioembolic) in the Boston cohort. In the Brazilian cohort, rs20417 polymorphism was associated with both stroke (p=5x10−6) and decreased PGE2 levels (p=4x10−5); similarly, Chagas was associated with stroke (p=4x10−3) and decreased PGE2 levels (p=7x10−3). In the Boston cohort, rs20417 polymorphism was associated with increased WMHv among non-cardioembolic (p=0.037), but not among cardioembolic stroke patients. Conclusions Variation in COX-2 gene is associated with both symptomatic and silent brain cerebrovascular disease. This candidate gene region should be tested in population-based samples.

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“…Prior studies’ limitations may be addressed by research using brain tissue with definitive identification of infarcts, including microscopic infarcts, which elude identification by currently available neuroimaging technology [12, 22]. Case reports with brain tissue data showed perivascular inflammation and amyloid-β deposition in vessels, while others found changes suggestive of a non-inflammatory vasculopathy [23].…”

Section: Discussionmentioning

confidence: 99%

Antiphospholipid Antibodies, Brain Infarcts, and Cognitive and Motor Decline in Aging (ABICMA): Design of a Community-Based, Longitudinal, Clinical-Pathological Study

et al. 2012

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The overall goal of the Antiphospholipid Antibodies, Brain Infarcts, and Cognitive and Motor Decline in Aging study is to test the hypothesis that antiphospholipid antibodies (aPL) are associated with an increased risk of pathologically proven brain infarcts and are related to cognitive and motor decline in aging. Putative biologic mechanisms underlying the association of aPL with infarcts and the relation of aPL with clinical outcomes of cognitive and motor impairment, including vascular and other processes, will be examined. The design of this longitudinal, clinical-pathologic study involves quantifying four aPL assays, and relating these to brain infarcts, and to cognitive and motor decline. Vascular mechanisms assessed using antemortem magnetic resonance neuroimaging and postmortem neuropathology, as well as nonvascular mechanisms of inflammation and blood-brain barrier permeability alterations will be examined as plausible mediators of the relation of aPL to cognitive and motor impairment. We will take advantage of antemortem biological specimens (longitudinally collected sera and plasma from which aPL, annexins, C-reactive protein, and matrix metalloproteinases will be quantified), and clinical, neuroimaging, and postmortem neuropathologic data from about 800 elderly, community-dwelling women and men who have agreed to brain autopsy at the time of death, participating in one of two ongoing studies of aging: the Religious Orders Study and the Memory and Aging Project.

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Cognitive Deficits in Patients With Antiphospholipid Syndrome

Cited by 117 publications

References 22 publications

Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers

Antiphospholipid syndrome in 2014: more clinical manifestations, novel pathogenic players and emerging biomarkers

COX-2 rs20417 Polymorphism Is Associated with Stroke and White Matter Disease

Antiphospholipid Antibodies, Brain Infarcts, and Cognitive and Motor Decline in Aging (ABICMA): Design of a Community-Based, Longitudinal, Clinical-Pathological Study

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