Autoantibodies and peripheral arterial occlusive disease

Abstract

In patients with early manifestation of peripheral arterial occlusive disease (PAOD) and a less classical atherosclerotic risk profile, vasculitis is presumed to be the underlying disease. We performed a prospective study of the importance of determination of autoantibodies used for the diagnosis of vasculitis and collagen diseases in patients with symptomatic PAOD. 698 consecutive patients (mean age +/- SD: 68 +/- 10 years) were included who were referred from 1998 to 1999 for interventional treatment of PAOD. In 121 PAOD-patients (61 +/- 12 years) with a less pronounced atherosclerotic risk profile, or rarefied distal arteries without sclerosis of the media, or elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) independent from the stage IV of PAOD, the following autoantibodies were investigated: antinuclear antibodies (ANA), antibodies against extractable nuclear antigens (ENA): SCL 70, RNP, SS-A, SS-B, Jo-1, SM), double-stranded DNA antibodies (ds-DNA), antineutrophil cytoplasmatic antibodies (c- and p-ANCA), antiphospholipid antibodies [phosphatidylserine (APSA) and beta(2)-glycoprotein], smooth (SMA) and striated muscle (StrMA). ANA, SMA and StrMA were estimated by indirect immunofluorescence technique, ENA by Western-blot and the others by enzyme linked immunoassay. 38 PAOD-patients (35%) had increased autoantibody concentrations. The rate of different PAOD stages and localization did not differ between the group of patients with increased autoantibody concentrations and the group of patients without. But the group of patients with increased autoantibody concentrations had higher rates of elevated ESR [p-value of 0.0043, odds ratio of 7.1 (95% CI: 1.49-33.81)]. ANA were the most frequent autoantibodies detected in 17 (14%) of the 121 patients followed by APSA and autoantibodies directed against beta(2)-glycoprotein. During follow-up of 24 +/- 6 months no vasculitis or collagen diseases associated with the elevated autoantibody concentrations became clinically manifest in the 38 patients. Two patients died due to coronary heart disease. Four patients had a worsening of their PAOD but no amputation was performed. Out of the 83 patients without elevated concentrations of autoantibodies, eight patients died and three amputations were carried out. All in all, increased autoantibody concentrations in patients suffering from peripheral atherosclerosis are not a rare finding. A systematic determination of autoantibodies, especially in patients with a low atherosclerotic risk profile, does not increase the number of manifest or developing vasculitis of collagen disease.