Department of Rheumatology, Peripheral General Hospital Athens Georgios Gennimatas, Athens, Greece.
Department of Pathophysiology, National and Kapodistrian University of Athens School of Medicine, Athens, Greece.
Lupus Sci Med. 2020 Sep;7(1). doi: 10.1136/lupus-2020-000393.
A 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.
In 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 D 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.
Abnormal PTH serum concentrations (>65 pg/mL)-but not 25(OH) vitamin D 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 D 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).
These 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.
主要在一般人群中提出了骨代谢与心血管（CV）疾病之间的联系。在本研究中，我们探讨了改变的骨代谢是否会影响 SLE 患者的 CV 风险。
在 138 例连续的 SLE 患者中，通过超声评估颈动脉/股动脉中斑块和/或动脉壁增厚的存在来评估动脉粥样硬化。记录所有患者的骨矿物质密度（BMD）水平、髋部/脊柱骨折以及包括血清 25（OH）维生素 D 和甲状旁腺激素（PTH）水平在内的经典 CV 疾病和骨质疏松症危险因素。通过商业 ELISA 定量血清护骨素（OPG）和核因子 kappa-B 配体受体激活剂。统计分析包括单变量和多变量模型。
异常的 PTH 血清浓度（>65pg/mL）-而不是 25（OH）维生素 D 血清水平-被确定为 SLE 患者斑块形成和动脉壁增厚的危险因素（比值比（95%置信区间）：8.2（1.8 至 37.4）和 3.9（1.3 至 11.8））。调整维生素 D 水平和经典 CV 危险因素后，这种相关性仍然显著。此外，在调整总类固醇剂量、早绝经和疾病持续时间后，骨质疏松症与斑块形成和动脉壁增厚之间存在独立的相关性（比值比（95%置信区间）：5.3（1.1 至 26.2）和 3.5（1.1 至 11.4）））。还观察到股骨颈 BMD 值与内膜中层厚度评分之间存在负相关（r：-0.42，p=0.008）。
这些发现进一步加强了自身免疫人群中动脉粥样硬化和改变的骨代谢之间存在共同病理生理机制的概念，揭示了升高的 PTH 水平可能是 SLE 患者动脉粥样硬化的潜在标志物。
