2002
DOI: 10.1046/j.0007-0963.2001.04546.x
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Lupus anticoagulant and venous leg ulceration

Abstract: We suggest that lupus anticoagulant could be a hitherto unknown factor contributing to the development of venous leg ulcers.

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Cited by 16 publications
(15 citation statements)
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“…Previous studies have produced conflicting results: 2,15,20 one study reported low levels of PS activity in 25% of patients with LDS and CVU; 20 but another found a nonsignificant increase in PS activity in CVU cases. 18 Yasim et al also found recently significantly higher levels of PS activity in patients with VV vs controls, but all values were within normal range. 7 HHcy Often defined as an Hcy level Ն15 mol/L (95th percentile in the normal population); by definition, is present in 5% of the population.…”
Section: Resultsmentioning
confidence: 88%
“…Previous studies have produced conflicting results: 2,15,20 one study reported low levels of PS activity in 25% of patients with LDS and CVU; 20 but another found a nonsignificant increase in PS activity in CVU cases. 18 Yasim et al also found recently significantly higher levels of PS activity in patients with VV vs controls, but all values were within normal range. 7 HHcy Often defined as an Hcy level Ն15 mol/L (95th percentile in the normal population); by definition, is present in 5% of the population.…”
Section: Resultsmentioning
confidence: 88%
“…14 Similarly, consideration should be given to evaluating all patients with venous leg ulceration for aPLs, because there is a demonstrated association between the two. 15 More than 33% of patients with SLE may have aPLs, but not all of these patients will have clinical symptoms of the antiphospholipid syndrome. 16 However, LR is an ominous finding in patients with SLE and aPLs, as LR is a significant predictor for development of neuropsychiatric lupus erythematosus.…”
Section: Lr With Systemic Associations (Secondary) Congenitalmentioning
confidence: 99%
“…11,14 Laboratory results can indicate anaemia, elevated erythrocyte sedimentation rate, iron deficiency, zinc deficiency, decreased fibrinolytic activity, increased plasma and full blood viscosity, 15 or clotting disorders predisposing to thrombosis. [16][17][18] In the past, some of these observed phenomena, such as shunting of blood near ulcers, the fibrin cuff, iron accumulation, white cell accumulation, decreased fibrinolytic activity, binding of transforming growth factor-b and other growth factors by macromolecules such as fibrin or a-macroglobulin, 19 and various inflammatory responses to the vascular damage, were believed to be Ôthe final cause of venous ulcerationÕ. To date, it is still not clear whether they represent causative factors or epiphenomena.…”
Section: Venous Insufficiencymentioning
confidence: 99%