Circulating anti-beta2-glycoprotein antibodies have been associated with coronary artery disease and peripheral arterial disease. This auto-antibodies could activate endothelial cells leading to the expression of leukocyte adhesion molecules and increasing the release of pro-inflammatory cytokines.

On the other hand, endothelial dysfunction of atherosclerotic patients acts as a primary pathogenic event, as it occur before structural changes are evident on angiogram or ultrasound scan. Loss of endothelial normal function causes vasoconstriction, local coagulation alterations and an increase arterial wall proliferation. This situation s been attributed to a reduction in nitric oxide bioactivity, and to an increase oxygen-free radical formation in the context of the pro-inflammatory status found in atherosclerosis.

Hypothesis: Circulating Anti-beta2-glycoprotein I antibodies could be associated with endothelial dysfunction and nitric oxide metabolism disruption en patients with peripheral arterial disease.

Inclusion Criteria:

• Male gender
• Peripheral arterial disease diagnosis
• Intermittent claudication.
• Hemodynamic confirmation of the disease through non-invasive vascular studies.

Exclusion Criteria:

• Autoimmune disease
• Previous revascularization of the ischemic limb.
• Ischemic ulcers
• Previous history of organ transplants.
• Treatment with immunosuppressors

Cases: Male patients with intermittent claudication due to peripheral arterial disease after haemodynamic confirmation of the disease by Doppler and treadmill exercise testing. No previous history of autoimmune disease.

Controls: Healthy male subjects with normal results on vascular examination and no cardiovascular risk factors, who were not in receipt of any pharmacological treatment, matched by age within two years with PAD patients.