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Factor V Leiden mutation does not correlate with retinal vascular occlusion in white patients with Behçet’s disease
  1. Y Chen1,
  2. M R Stanford1,
  3. G R Wallace1,
  4. R W Vaughan1,
  5. E Kondeatis2,
  6. F Fortune3
  1. 1Department of Ophthalmology, King’s College, London SE1 7EH, UK
  2. 2Department of Tissue Typing, King’s College, London SE1 7EH, UK
  3. 3Department of Oral Medicine, University of Leeds, Leeds, UK
  1. Correspondence to: Dr Graham Wallace, Academic Unit of Ophthalmology, University of Birmingham, City Hospital, Dudley Road, Birmingham B18 7QU, UK; g.r.wallace{at}bham.ac.uk

https://doi.org/10.1136/bjo.87.8.1048

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    The factor V Leiden (FV Leiden) mutation causes resistance to activated protein C by substituting the Glu506 residue with arginine at the cleavage site for activated protein C. Heterozygous carriers of the FV Leiden mutation have an increased risk of venous thrombosis between threefold and sevenfold in population based and family studies.1,2 Behçet’s disease is a chronic inflammatory multisystem disorder that affects young adults. The principal cause of visual loss in this disease is recurrent retinal vein occlusion probably due to a combination of retinal vasculitis and thrombus formation. Thrombosis in Behçet’s disease carries a poor ocular and systemic prognosis, so the presence of an identifiable and significant risk factor could be an indicator for anticoagulant treatment.3 Two recent studies have implicated FV Leiden in the pathogenesis of thrombosis in Turkish patients with Behçet’s disease. In one study, 30% of patients with Behçet’s disease complicated by thrombosis were heterozygous or homozygous for factor V Leiden compared to 5.9% of factor V Leiden negative patients.4 In the second study, factor V Leiden was detected in 37.5% of patients with Behçet’s disease and a thrombotic history, compared to 9.4% of non-thrombotic patients.5 We have previously shown in a study of 106 Middle Eastern …

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