Antiphospholipid Syndrome

Schössler, W

doi:10.1159/000024425

Cited by 26 publications

(15 citation statements)

References 24 publications

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“…Cerebrovascular disease in young patients without significant risk factors should raise suspicion for APS. In two reports, aPL were found in 25 and 20 per cent of patients with stroke of unclear aetiology, under the age of 45 and 50, respectively 4 5…”

Section: Discussionmentioning

confidence: 98%

Cerebral embolism from libman-sacks endocarditis

et al. 2011

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Libman-Sacks endocarditis consists of aseptic valvular abnormalities, associated with systemic lupus erythematosus and antiphospholipid syndrome. Embolic ischaemic stroke is a possible clinical presentation. The authors present the case of a woman in her fourth decade who developed central facial palsy after several transient ischaemic attacks with visual loss. Cerebral imaging revealed multiple small ischaemic lesions in the right hemisphere. The transoesophagic echocardiogram showed mitral vegetations and she tested positive for antiphospholipid antibodies. She underwent mitral valve replacement for a mechanical prosthesis due to extensive valvular damage and started anticoagulation. The valve's microbiological exams were negative establishing the diagnosis of libman-sacks endocarditis. Endocarditis should be suspected with sequential cerebral ischaemia in patients of all ages. Valvular surgery is the mainstay of treatment in recurrent embolic events. Association with antiphospholipid antibodies is common yet a poor-known fact. The patient is currently asymptomatic on warfarin and aspirin, with a normal functioning mitral prosthesis.

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Section: Discussionmentioning

confidence: 98%

Cerebral embolism from libman-sacks endocarditis

et al. 2011

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“…[58] Autoantibodies detected by the lupus anticoagulant assay are mostly directed to either b 2--glycoprotein-1 or to prothrombin. [50] The average frequency of these antibodies in SLE is 44% for anticardiolipin antibodies and 34% for lupus anticoagulant. [57] Antiphospholipid antibodies have been reported in 20-56% of lupus patients.…”

Section: Anti-phospholipid Antibodiesmentioning

confidence: 99%

Autoantibodies in Neuropsychiatric Lupus

et al. 2002

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The American College of Rheumatology presented a consensus document in 1999 proposing the classification of 19 different syndromes defined by neurological and psychiatric manifestations of systemic lupus erythematosus (SLE). The detection of autoantibodies in patient's serum or cerebrospinal fluid has not been used as diagnostic markers for the proposed neuropsychiatric lupus classifications as their disease associations remain highly contentious. Autoantibodies detected in the serum and/or cerebrospinal fluid, that have been reported to segregate with patients presenting with neuropsychiatric lupus include: (1) anti-neuronal antibodies, (2) brain-lymphocyte cross-reactive antibodies, (3) anti-ribosomal P antibodies, (4) anti-phospholipid antibodies and (5) anti-ganglioside antibodies. Tests for anti-neuronal, anti-brain-lymphocyte cross-reactive and anti-ganglioside antibodies remain highly specialized whereas tests for ribosomal P antibodies and for antiphospholipid antibodies are currently routinely available in most diagnostic laboratories. Anti-ribosomal antibodies segregate with SLE. Antiphospholipid P antibodies are markers for the antiphospholipid syndrome. This syndrome may be associated with another disease, commonly SLE. In this setting, neuropsychiatric manifestations in SLE may arise as a consequence of thrombotic episodes involving the cerebral vasculature. There is a pressing need for antibodies to ribosomal P and to phospholipids to be standardized for routine diagnostic application. We conclude that the search for specific antibody marker(s) that can be applied for the routine laboratory diagnosis for neuropsychiatric lupus remains elusive.

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“…Of these, stroke is the most common clinical manifestation, with an estimated frequency of 14% among APS patients 6. Indeed, stroke in a young patient should raise suspicion of APS—studies estimate that 20–25% of patients under the age of 50 presenting with cerebrovascular disease suffer from APS 7 8. Diagnostic criteria involve detection of antiphospholipid antibodies (lupus anticoagulant, anticardiolipin or anti-β2-glycoprotein 1 antibodies) and the presence of clinical features, namely vascular thrombosis or pregnancy morbidity (box 1).…”

Section: Discussionmentioning

confidence: 99%

Homonymous hemianopia in the primary antiphospholipid syndrome

Ho¹,

Ramessur

Gupta

et al. 2017

BMJ Case Reports

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A woman aged 26 years was referred by her GP to the eye casualty department with sudden-onset left homonymous hemianopia and right-sided headache. Full ophthalmic examination was normal with the exception of a left homonymous hemianopia confirmed with automated perimetry. Urgent CT imaging revealed a non-haemorrhagic cerebral infarct in the right parieto-occipital region. Subsequent blood tests confirmed a diagnosis of antiphospholipid syndrome with positivity in IgG anticardiolipin antibody, IgG anti-β2-GP1 antibody and the Lupus anticoagulant screen. MRI revealed extensive congenital abnormality at the Circle of Willis, affecting the right half of circulation. The unique dual pathologies may explain her predisposition to right-sided cerebral infarctions. This case highlights a rare but potentially fatal cause of visual disturbance in a young patient, and the importance of the multidisciplinary team approach in diagnosis and management.

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Antiphospholipid Syndrome

Cited by 26 publications

References 24 publications

Cerebral embolism from libman-sacks endocarditis

Cerebral embolism from libman-sacks endocarditis

Autoantibodies in Neuropsychiatric Lupus

Homonymous hemianopia in the primary antiphospholipid syndrome

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