Association of high alpha2-Heremans–Schmid glycoprotein/fetuin concentration in serum and intima-media thickness in patients with atherosclerotic vascular disease and low bone mass

ObjectiveAlpha2-Heremans–Schmid glycoprotein (AHSG; fetuin), a member of the cystatin superfamily of cysteine protease inhibitors involved in vascular pathology and bone metabolism, has been reported to be reduced in patients with atherosclerosis and medial calcification related to end stage renal disease or dialysis. No data on fetuin in patients with peripheral artery disease associated with low bone mass and normal renal function are available in the literature. In the present study we evaluated serum fetuin concentrations, bone mass, and markers of bone turnover in patients with atherosclerosis of peripheral vessels and normal kidney function.Patients and methodsNinety consecutive patients with evidence of atherosclerotic plaques at the common carotid or femoral artery were studied. Severity grade of disease was documented by ultrasound measurement of intima-media thickness (IMT). Fasting serum levels of fetuin were measured by sandwich enzyme immunoassay.Main resultsThe mean patient serum concentration of fetuin was 57.68 ± 13.6 ng/ml, significantly higher than that of control subjects (41.6 ± 7.6 ng/ml; p < 0.001). The mean serum concentration of bone-specific alkaline phosphatase (BAP) were 8.4 ± 2.3 μg/l, significantly lower than controls (13.6 ± 1.6 μg/l; p < 0.001). Fetuin was correlated with IMT (r = 0.8530; p < 0.0001) and inversely correlated with BAP (r = −0.5503; p < 0.0001). Patients had a vertebral and femoral bone mass significantly lower than controls.ConclusionThis study documented for the first time that, in patients with atherosclerosis of peripheral vessels, serum fetuin levels were higher than in healthy subjects, and correlated with the severity of disease; further studies are required to analyse the role of AHSG as an independent predictor of atherosclerotic disease and low bone mass in patients with normal renal function.