Abstract
The antiphospholipid syndrome is an autoimmune disease characterised by recurrent arterial or venous thrombosis, pregnancy morbidity and the persistence of positive antiphospholipid antibodies. Many other clinical manifestations may occur including heart valve disease, livedo reticularis, thrombocytopenia and neurological manifestations such as migraine and seizures. We review a number of other manfestations including stenotic lesions, coronary artery disease and accelerated atherosclerosis, skeletal disorders and the concept of seronegative antiphospholipid syndrome.
Highlights
The antiphospholipid (Hughes) syndrome (APS), first described in 1983, is an autoimmune disease characterised by recurrent arterial or venous thrombosis, pregnancy morbidity and the persistence of positive antiphospholipid antibodies [1]
We found a high prevalence of renal artery stenosis (RAS) in APS patients with uncontrolled hypertension compared to two control groups [5]
Histological examination in SLE patients with APS [8] and a case report of a resected superior mesenteric artery showed fibro-elastic thickening of the intima and thrombosis [9]. These findings suggest that thrombosis and intimal and smooth muscle hyperplasia may be responsible for the vasculopathy in APS
Summary
The antiphospholipid (Hughes) syndrome (APS), first described in 1983, is an autoimmune disease characterised by recurrent arterial or venous thrombosis, pregnancy morbidity and the persistence of positive antiphospholipid antibodies (aPL) [1]. Only thrombosis and pregnancy loss are included in the revised classification criteria for APS [2], other features are described [3] These include heart valve disease, livedo reticularis, thrombocytopenia and neurological manifestations such as migraine and seizures. High resolution ultrasound was used to determine carotid intima media thickness (cIMT), endothelium dependent flow mediated dilatation (FMD) and endothelium independent nitroglycerine mediated dilatation of the brachial artery This data showed significantly reduced FMD and increased cIMT in APS patients as compared to healthy individuals [39]. Observations by Ames et al of subclinical atherosclerosis using intima-medial thickness in patients with primary APS in their 4th decade are worth mentioning [41] This data indicates that endothelial dysfunction and pre-clinical atherosclerosis is prevalent in APS/aPL patients. Pathological livedo reticularis may be a clinical marker of the "seronegative APS" [46,50]
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