Our aim is to investigate a possible association of circulating anti-beta2-glycoprotein I antibodies (ABGPI) with the endothelial dysfunction, nitric oxide bioactivity dysregulation, and the inflammatory status that surrounds peripheral arterial disease. We carried out an observational translational study, including 50 male patients with intermittent claudication and a healthy control group of 10 male subjects, age and sex matched with the cases. Flow-mediated arterial dilatation (FMAD) was assessed as a surrogate of endothelial dysfunction, and C-reactive protein (hsCRP) was determined as a marker of inflammation. Nitrite plasma levels were measured by colorimetric analysis. Circulating ABGPI titer was detected with indirect immunofluorescence. Titers <1？:？10 represented the reference range and the lower detection limit of the test. Circulating ABGPI titer ≥1？:？10 was detected in 21 (42%) patients and in none of the control subjects ( ). Patients with ABGPI titer ≥1？:？10 had a lower FMAD ( ). The CRP levels were higher in patients with ABGPI titer ≥1？:？10 ( ). The nitrite plasma levels were higher in patients with ABGPI titer ≥1？:？10 ( ). These data suggest that these circulating ABGPI may collaborate in the development of atherosclerosis; however, further prospective studies are required to establish a causal relationship. 1. Introduction The endothelium is responsible for maintaining the balance between the different factors involved in the vascular wall function. In atherosclerosis, this balance is broken, and the endothelium is no longer able to regulate vascular homeostasis. This situation causes endothelial dysfunction characterised by vasospasm, vasoconstriction, local coagulation alterations, abnormal fibrinolysis, and an increase in arterial wall cell proliferation. Endothelial dysfunction acts as a primary pathogenic event, as it occurs before structural change are evident on angiogram or ultrasound scan, and it is not correlated with the disease’s severity . The loss of endothelial regulation has been attributed to a reduction in nitric oxide bioactivity and to an increased oxygen-free radical formation in the context of the proinflammatory status found in atherosclerosis [2, 3]. On the other hand, there is currently a wide variety of data pointing to a possible autoimmune origin of atherosclerosis [4–11]. This hypothesis is biologically plausible, as chronic vascular inflammation observed in atherosclerosis is based on the dysregulation of the immune system activity. In this context, circulating anti-beta2-glycoprotein I antibodies
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