Peripheral artery disease (PAD) is mostly related to
atherosclerosis. Autoimmunity and, in particular,
antibodies to
cardiolipin (aCL) and
phospholipid cofactors such as
beta2-glycoprotein I (beta2-gpI) might influence the development of
atheroma.
Beta2-glycoprotein I (beta2-gpI) has been found in
atheroma. It has previously been shown that
immunoglobulin A (
IgA) anti-beta2-gpI
antibodies are associated with a risk of
cerebral ischemia and
myocardial infarction. This case control study aimed to determine whether elevated levels of aCL/anti-beta2-gpI
antibodies are associated with a risk of symptomatic PAD (
sPAD). Cases comprised a nonselected population of patients with
sPAD (
intermittent claudication or critical
ischemia). Patient recruitment was based on arteriography changes. Controls were selected from patients admitted to orthopedic wards as a result of fractures or muscle-ligamentous disorders. Age, sex, race,
hypertension, smoking,
diabetes mellitus, and
hypercholesterolemia were evaluated as risk factors in both groups.
IgG/
IgM/
IgA aCL and anti-beta2-gpI were detected by
enzyme-linked immunoabsorbant assays (ELISA). To estimate the grade of association of
antibodies with
sPAD, odds ratios (OR) were calculated. Logistic regression was utilized for adjustment of confounding factors. Seventy-seven cases and 93 controls were studied. The mean age was 61.5 years for cases and 47.5 years for controls (p <0.001). Among the risk factors evaluated, the presence of
hypertension showed the strongest association with
sPAD (OR 12.1; 95%CI 5.8-30). The presence of
IgA anti-beta2-gpI was independently associated with
sPAD (OR 5.4; 95%CI 1.8-15.8; p = 0.01).
IgA aCL was strongly associated with the outcome (nonadjusted OR 11.5 after Agresti correction).
IgA aCL and
IgA anti-beta2-gpI
antibodies were not associated with any known risk factors for
sPAD or with arteriography changes. The occurrence of these
autoantibodies might represent one of the links between autoimmunity and
atherosclerosis in patients with
sPAD.