Background Whether scleroderma patients have an increased atherosclerotic risk or not is still a matter of dabate. Existing evidence suggests that impaired vitamin D metabolism, common in autoimmune diseases, might contribute to the development of atherosclerosis.

Objective To evaluate the relationship between vitamin D status and subclinical atherosclerosis in scleroderma patients.

Methods 20 scleroderma patients were evaluated. Radio frequency-based echo-tracking (Aloka alpha-10 Prosound, 15Mhz transducer) was performed to evaluate subclinical atherosclerosis. Several parameters were measured: intima-media-tchikness (IMT), βeta (stiffness parameter), Ep (pressure-strain elasticity modulus), AC (arterial compliance), AI (augmentation index), PWV (pulse wave velocity) in common carotid artery. 25(OH)D level was measured in the sera by an ELISA kit [DIASource^® 25-Hydroxyvitamin D Total ELISA assay (Nivelles, Belgium)]. 25(OH)D levels were considered normal for values ≥30 ng/ml, insufficient for values between 20–30 ng/ml and deficient for values under 20 ng/ml.

Results The medium level of vitamin D was 20.71ng/ml, 37.5% of the patients being classified as insufficiency and 37.5% as deficiency. Patients with IMT ≥0.9mm had significantly lower levels of 25OH)D than those with normal IMT (13.78ng/ml vs. 25.67ng/ml, p = 0.034). Strong negative correlations were observed between vitamin D status and arterial rigidity parameters: β index (p < 0.001, r = -0.894), elastic modulus (p = 0.001, r = -0.760) and pulse wave velocity (p = 0.001, r = -0.728). Differences between groups were statistically significant when using ANOVA tests for beta index [F(2,13) = 13.069, p = 0.001] and elastic modulus [F(2,13) = 4.45, p = 0.034]. Post hoc Games Howell tests conformed the differences. βeta index was higher in patients with vitamin D insufficiency (7.10 ± 1.52, p = 0.004) or deficiency (11.3 ± 0.56, p = 0.05) compared to those with normal 25(OH) D levels (4.15 ± 0.07) and significantly higher in patients with deficiency compared with those with insufficiency (p < 0.001). Elastic modulus was higher in patients with insufficient (86.16 ± 27.48, p = 0.036) or deficient vitamin D levels (139.25 ± 54.09, p = 0.011) compared to those with normal status (53.25 ± 1.06) and higher in patients with deficiency compared with those with insufficiency (p = 0.04). Arterial compliance is higher in patients with normal vitamin D status than those with insufficient levels, in patients with insufficient levels compared with those with deficient levels but the difference are not significant (p = 0.77, p = 0.54).

Coincidence or not, the patient with the lowest 25 (OH)D in the group had significant carotid artery stenosis and developed stroke.

Conclusions We identified a strong negative correlation between 25(OH)D levels and arterial rigidity parameters, suggesting that low vitamin D status can be an additional risk factor factor for atherosclerosis in scleroderma patients.