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ObjectiveA link between bone metabolism and cardiovascular (CV) disease has been suggested mainly in the general population. In the current study we explored whether altered bone metabolism influence CV risk in patients with SLE.MethodsIn 138 consecutive patients with SLE, atherosclerosis was assessed by the presence of plaque and/or arterial wall thickening in carotid/femoral arteries by ultrasound. Bone mineral density (BMD) levels and hip/spinal cord fractures together with classical CV disease and osteoporosis risk factors including serum 25(OH) vitamin D3 and parathormone (PTH) levels were recorded in all patients. Serum osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-Β ligand were quantitated by commercial ELISA. Statistical analysis included both univariate and multivariate models.ResultsAbnormal PTH serum concentrations (>65 pg/mL)—but not 25(OH) vitamin D3 serum levels—were identified as a risk factor for both plaque formation and arterial wall thickening in patients with SLE (ORs (95% CIs): 8.2 (1.8 to 37.4) and 3.9 (1.3 to 11.8), respectively). This association remained significant following adjustment for vitamin D3 levels and classical CV risk factors. Moreover, an independent association between osteoporosis with plaque formation and arterial wall thickening was detected following adjustment for total steroid dose, premature menopause and disease duration (ORs (95% CIs): 5.3 (1.1 to 26.2) and 3.5 (1.1 to 11.4), respectively). An inverse correlation between femoral neck BMD values and intima–medial thickness scores was also observed (r: −0.42, p=0.008).ConclusionsThese findings further strengthen the concept of shared pathophysiological mechanisms between atherogenesis and altered bone metabolism in autoimmune populations, revealing heightened PTH levels as a potential marker for atherosclerosis among patients with SLE.

Background:Growing evidence supports a link between alterations in bone metabolism and cardiovascular (CV) disease in both general and autoimmune populations.Objectives:In the current study we aimed to explore whether vitamin D deficiency and/or increased parathormone (PTH) levels, as well as impairment of bone mass density, influence CV risk in patients with systemic lupus erythematosus (SLE).Methods:138 consecutive SLE patients were enrolled in the study. Clinical features, hematological, serological and immunological profile, as well as therapeutic regimens was recorded in all patients. Classical CV and osteoporosis risk factors were assessed in all participants. Intima-medial thickness scores (IMT) and carotid and/or femoral (C/F) plaque formation were evaluated by ultrasound. Assessment of bone mineral density (BMD) and asymptomatic osteoporotic fractures was also performed by dual X-ray absorptiometry and lateral thoracic and/or lumbar spine X-rays, respectively. Univariate and multivariate models were implemented for statistical analysis.Results:PTH -but not 25(OH)vitamin D3- serum levels were found to be increased in lupus patients with subclinical atherosclerosis (plaque formation and/or arterial wall thickening) compared to those without (51.1±27.7 vs 37.4±18.4 pg/ml, p= 0.003 and 54±32.7 vs 40±18.3 pg/ml, p= 0.02, respectively). Abnormal PTH serum concentrations (>65 pg/ml) in SLE patients was identified as a risk factor for both plaque formation and high IMT scores (>0.9mm) [OR 95% (CI): 8.2 (1.8-37.4) and OR 95% (CI): 3.9 (1.3-11.8), respectively]. High PTH levels were found to be associated with low 25(OH)vitaminD3 levels, advanced age and increased triglycerides in the lupus cohort. Moreover, SLE patients with plaque formation exhibited increased rates of osteoporosis (based on WHO classification) compared to those without [19.5% vs 5.3%, p= 0.017, OR 95% (CI): 4.4 (1.2-15.9)]. Finally, an inverse correlation between femoral neck BMD values and total IMT scores was observed (r:-0.42, p=0.008).Conclusion:Subclinical atherosclerosis in patients with lupus is associated with increased serum PTH levels and reduced bone mass density. These findings further support the presence of shared etiopathogenetic mechanisms between atherogenesis and altered bone metabolism.Disclosure of Interests:None declared

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