BACKGROUND: Hypercoagulable states, which include the presence of anticardiolipin antibodies (ACAs), have been associated with skin ulceration. Resistance to activated protein C (APC), resulting from the factor V Leiden mutation, is a common risk factor for venous thrombosis. Its prevalence among patients with venous leg ulcers is not known. OBJECTIVE: Our purpose was to determine the prevalence of factor V Leiden and ACA in patients with venous leg ulceration. METHODS: Twenty-nine consecutive patients with venous leg ulcers were studied. Resistance to APC was first determined by functional assay based on the partial thromboplastin time. Patients with an abnormally low APC ratio were then subjected to molecular analysis for confirmation of factor V Leiden. Measurements of ACA were performed by enzyme-linked immunosorbent assay. RESULTS: APC resistance was detected in 11 of 26 patients. However, only 2 of these 11 patients (7.7% overall) were found to be heterozygous for the factor V Leiden mutation. ACA was present in neither patient with the Leiden mutation but was found in 6 of 21 patients tested (29% overall). CONCLUSION: The factor V Leiden mutation, unlike ACA, may not be more prevalent in patients with venous leg ulcers than in the general population. Our results emphasize the importance of molecular analysis for factor V Leiden in patients with APC resistance.
BACKGROUND: Hypercoagulable states, which include the presence of anticardiolipin antibodies (ACAs), have been associated with skin ulceration. Resistance to activated protein C (APC), resulting from the factor V Leiden mutation, is a common risk factor for venous thrombosis. Its prevalence among patients with venous leg ulcers is not known. OBJECTIVE: Our purpose was to determine the prevalence of factor V Leiden and ACA in patients with venous leg ulceration. METHODS: Twenty-nine consecutive patients with venous leg ulcers were studied. Resistance to APC was first determined by functional assay based on the partial thromboplastin time. Patients with an abnormally low APC ratio were then subjected to molecular analysis for confirmation of factor V Leiden. Measurements of ACA were performed by enzyme-linked immunosorbent assay. RESULTS: APC resistance was detected in 11 of 26 patients. However, only 2 of these 11 patients (7.7% overall) were found to be heterozygous for the factor V Leiden mutation. ACA was present in neither patient with the Leiden mutation but was found in 6 of 21 patients tested (29% overall). CONCLUSION: The factor V Leiden mutation, unlike ACA, may not be more prevalent in patients with venous leg ulcers than in the general population. Our results emphasize the importance of molecular analysis for factor V Leiden in patients with APC resistance.