Sneddon's syndrome with antiphospholipid antibodies and arteriopathy.

Moral, A; Vidal, J; Moreau, I; D’Olhaberriague, Luis; Montalbán, J

doi:10.1161/01.str.22.10.1327

Cited by 16 publications

(7 citation statements)

References 11 publications

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“…The primary distinction between patients with primary phospholipid syndrome and Sneddon's syndrome is the involvement of large vessels in the former and exclusively medium-sized arteries in the latter [105,113,114]. Patients with antiphospholipid antibodies are more likely to experience cerebral ischemic or thrombotic events when also harboring primary hypertension or coronary disease, respectively [115].…”

Section: Anticardiolipins and Neurologic Syndromesmentioning

confidence: 99%

Antiphospholipid thrombosis syndromes

Bick

2003

Hematology/Oncology Clinics of North America

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Section: Anticardiolipins and Neurologic Syndromesmentioning

confidence: 99%

Antiphospholipid thrombosis syndromes

Bick

2003

Hematology/Oncology Clinics of North America

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“…In some cases, the gene responsible for the arteriopathy may play a role [ 41 , 65 ]. Besides, endothelial dysfunction may be secondary to acquired autoimmune or mediated by some unknown factors [ 66 , 67 ].…”

Section: Introductionmentioning

confidence: 99%

Sneddon’s syndrome: a comprehensive review of the literature

Xu²,

Liang³

2014

Orphanet J Rare Dis

116

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Sneddon’s syndrome (SS) is a rare non-inflammatory thrombotic vasculopathy characterized by the combination of cerebrovascular disease with livedo racemosa(LR). The Orpha number for SS is ORPHA820. It has been estimated that the incidence of SS is 4 per 1 million per annum in general population and generally occurs in women between the ages of 20 and 42 years. LR may precede the onset of stroke by years and the trunk and/or buttocks are involved in nearly all patients. The cerebrovascular manifestations are mostly secondary to ischemia (transient ischemic attacks and cerebral infarct). Other neurological symptoms range from headache, cerebral hemorrhage, seizures, cognitive and psychiatric disturbances. The involved internal organs include heart, kidney, and eyes. Histological findings of skin are characteristic and the involved vessels are small to medium-sized arteries at the border of dermis to subcutis with a distinct histopathological time course. The main diagnostic criteria are general LR with typical histopathological findings on skin biopsy and focal neurological deficits. The pathogenesis is related to hypercoagulable state and intrinsic small-vessel vasculopathy. The optimal management remains an unsolved problem and long-term anticoagulation have been recommended for cerebral ischemic events based on the presumed pathogenesis. There are controversial results in treatment of SS with immunomodulatory agents. The aim of this review is to comprehensively discuss this disease.

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“…The pathogenesis of the disease has until recently re mained obscure. In the past few years publications about the discovery of antiphospholipid antibodies (aPL) in some patients with Sneddon's syndrome have appeared [5][6][7][8][9][10]. The production of aPL, among which anticardioli pin antibodies (aCL) and lupus anticoagulant (LA) are investigated most frequently, is associated with a number of clinical manifestations known as the antiphospholipid syndrome (APS).…”

Section: Introductionmentioning

confidence: 99%

Sneddon's Syndrome and the Primary Antiphospholipid Syndrome

Калашникова¹,

Nasonov²,

Stoyanovich³

et al. 1994

Cerebrovasc Dis

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Forty-six patients (33 women, 13 men, mean age 40 years) with Sneddon''s syndrome characterized by an ischemic cerebrovascular disease combined with widespread livedo were studied. The clinical picture also included fetal loss (20 of 29 women who had become pregnant), peripheral venous thrombosis (12 patients), ischemic heart disease (18 patients), thrombocytopenia (8 of 40 patients), arterial hypertension (27 patients), headache (38 patients), and epileptic seizures (5 patients), and was similar to that of the antiphospholipid syndrome (APS). In 36 of 46 (78%) patients antiphospholipid antibodies (aPL) were found: anticardiolipin antibodies >5 GPL in 23 of 46 (50%) and lupus anticoagulant in 26 of 43 (61 %) patients. The presence of clinical and immunological manifestations of the APS in 78% of patients in the absence of typical systemic lupus erythematosus features allows one to consider these Sneddon''s syndrome cases as examples of primary APS. The pathogenesis of Sneddon''s syndrome in aPL-negative patients needs to be clarified.

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Sneddon's syndrome with antiphospholipid antibodies and arteriopathy.

Cited by 16 publications

References 11 publications

Antiphospholipid thrombosis syndromes

Antiphospholipid thrombosis syndromes

Sneddon’s syndrome: a comprehensive review of the literature

Sneddon's Syndrome and the Primary Antiphospholipid Syndrome

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