Roman Mary J, Crow Mary K, Lockshin Michael D, Devereux Richard B, Paget Stephen A, Sammaritano Lisa, Levine Daniel M, Davis Adrienne, Salmon Jane E
Weill Medical College of Cornell University, and the Hospital for Special Surgery, New York, New York 10021, USA.
Arthritis Rheum. 2007 Oct;56(10):3412-9. doi: 10.1002/art.22924.
To determine the rate of atherosclerosis progression as well as the relationship of traditional risk factors, systemic lupus erythematosus (SLE)-related factors, and treatment to atherosis progression in SLE patients.
Outpatients in the Hospital for Special Surgery SLE Registry underwent serial carotid ultrasound and clinical assessment in a longitudinal study.
Among 158 patients, 77 (49%) had persistent absence of atherosclerosis (carotid plaque), 36 (23%) had unchanged atherosclerosis, and 45 (28%) had progressive atherosclerosis, defined as a higher plaque score (new plaque in 25 patients and more extensive plaque in 20 patients) after a mean +/- SD interval of 34 +/- 9 months. Multivariate determinants of atherosclerosis progression were age at diagnosis (odds ratio [OR] 2.75, 95% confidence interval [95% CI] 1.67-4.54 per 10 years, P < 0.001), duration of SLE (OR 3.16, 95% CI 1.64-6.07 per 10 years, P < 0.001), and baseline homocysteine concentration (OR 1.24, 95% CI 1.06-1.44 per mumoles/liter, P = 0.006). SLE patients with stable plaque and progressive plaque differed only in baseline homocysteine concentration. Atherosclerosis progression was increased across tertiles of homocysteine concentration (16.2%, 36.4%, and 56.1%; P = 0.001), and homocysteine tertile was independently related to progression of atherosclerosis (OR 3.14, 95% CI 1.65-5.95 per tertile, P < 0.001). Less aggressive immunosuppressive therapy and lower average prednisone dose were associated with progression of atherosclerosis in univariate, but not multivariate, analyses. Inflammatory markers and lipids were not related to atherosclerosis progression.
Atherosclerosis develops or progresses in a substantial minority of SLE patients during short-term followup (10% per year on average). Older age at diagnosis, longer duration of SLE, and higher homocysteine concentration are independently related to progression of atherosclerosis. These findings show that aggressive control of SLE and lowering of homocysteine concentrations are potential means to retard the development and progression of atherosclerosis in SLE.
确定动脉粥样硬化进展率，以及传统危险因素、系统性红斑狼疮（SLE）相关因素和治疗与SLE患者动脉粥样硬化进展的关系。
在一项纵向研究中，特殊外科医院SLE登记处的门诊患者接受了系列颈动脉超声检查和临床评估。
158例患者中，77例（49%）持续无动脉粥样硬化（颈动脉斑块），36例（23%）动脉粥样硬化无变化，45例（28%）有进展性动脉粥样硬化，定义为在平均±标准差34±9个月的间隔后斑块评分更高（25例出现新斑块，20例斑块范围扩大）。动脉粥样硬化进展的多变量决定因素为诊断时年龄（比值比[OR]2.75，每10年95%置信区间[95%CI]1.67 - 4.54，P < 0.001）、SLE病程（OR 3.16，每10年95%CI 1.64 - 6.07，P < 0.001）和基线同型半胱氨酸浓度（OR 1.24，每微摩尔/升95%CI 1.06 - 1.44，P = 0.006）。斑块稳定和进展的SLE患者仅在基线同型半胱氨酸浓度上存在差异。同型半胱氨酸浓度三分位数范围内动脉粥样硬化进展增加（分别为16.2%、36.4%和56.1%；P = 0.001），同型半胱氨酸三分位数与动脉粥样硬化进展独立相关（每三分位数OR 3.14，95%CI 1.65 - 5.95，P < 0.001）。在单变量分析而非多变量分析中，侵袭性较低的免疫抑制治疗和较低的平均泼尼松剂量与动脉粥样硬化进展相关。炎症标志物和血脂与动脉粥样硬化进展无关。
在短期随访期间，相当一部分SLE患者会发生或出现动脉粥样硬化进展（平均每年10%）。诊断时年龄较大、SLE病程较长和同型半胱氨酸浓度较高与动脉粥样硬化进展独立相关。这些发现表明，积极控制SLE和降低同型半胱氨酸浓度是延缓SLE患者动脉粥样硬化发生和进展的潜在手段。
