Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
Division of Internal Medicine, Hospital Universitario de Canarias, Tenerife, Spain.
Front Immunol. 2022 May 9;13:827355. doi: 10.3389/fimmu.2022.827355. eCollection 2022.
Elevated triglycerides or triglyceride-rich lipoproteins are an additional cause of cardiovascular (CV) disease. Given that patients with systemic lupus erythematosus (SLE) have a high prevalence of premature CV disease and show an altered lipid profile, our objective was to study whether three molecules that play a central role in the triglyceride metabolism: apolipoprotein C-III (ApoC3), angiopoietin-like protein 4 (ANGPLT4), and lipoprotein lipase (LPL) differ between SLE patients and controls, and how they are related to disease characteristics, including disease damage.
Cross-sectional study that included 347 women, 185 of them diagnosed with SLE and 162 age-matched controls. ANGPTL4, ApoC3 and LPL, and standard lipid profiles were analyzed in SLE patients and controls. A multivariable analysis was performed to assess whether ANGPTL4, ApoC3 and LPL molecules differ between patients and controls and to study their relationship with SLE disease damage.
After fully multivariable analysis that included classic CV risk factors, and the modifications that the disease itself produces over the lipid profile, it was found that ApoC3 was significantly lower (beta coef. -1.2 [95%CI -1.6- -0.8) mg/dl, <0.001), and ANGPTL4 (beta coef. 63 [95%CI 35-90] ng/ml, <0.001) and LPL (beta coef. 79 [95%CI 30-128] ng/ml, p=0.002) significantly higher in patients with SLE compared to controls. Disease damage score was significantly and independently associated with higher serum levels of LPL (beta coef. 23 [95%CI 10-35] ng/ml, p=0.001). Mediation analysis suggested that the relationship between disease damage and LPL was direct and not mediated by ApoC3 or ANGPLT4.
The ApoC3, ANGPLT4 and LPL axis is disrupted in patients with SLE. Disease damage explains this disturbance.
升高的甘油三酯或富含甘油三酯的脂蛋白是心血管疾病的另一个病因。鉴于系统性红斑狼疮（SLE）患者存在过早发生心血管疾病的高患病率，并且表现出脂质谱异常，我们的目标是研究在甘油三酯代谢中起核心作用的三种分子：载脂蛋白 C-III（ApoC3）、血管生成素样蛋白 4（ANGPLT4）和脂蛋白脂肪酶（LPL）在 SLE 患者和对照组之间是否存在差异，以及它们与疾病特征（包括疾病损害）的关系如何。
这是一项横断面研究，共纳入 347 名女性，其中 185 名为 SLE 患者，162 名为年龄匹配的对照组。分析 SLE 患者和对照组的 ANGPTL4、ApoC3 和 LPL 以及标准脂质谱。进行多变量分析以评估 ANGPTL4、ApoC3 和 LPL 分子在患者和对照组之间是否存在差异，并研究它们与 SLE 疾病损害的关系。
在充分考虑经典心血管危险因素以及疾病本身对脂质谱产生的改变进行多变量分析后，发现 ApoC3 显著降低（β系数-1.2[95%CI-1.6 至-0.8]mg/dl，<0.001），而 ANGPTL4（β系数 63[95%CI35 至 90]ng/ml，<0.001）和 LPL（β系数 79[95%CI30 至 128]ng/ml，p=0.002）在 SLE 患者中明显高于对照组。疾病损害评分与血清 LPL 水平升高显著相关（β系数 23[95%CI10 至 35]ng/ml，p=0.001）。中介分析表明，疾病损害与 LPL 之间的关系是直接的，而不是通过 ApoC3 或 ANGPLT4 介导的。
SLE 患者的 ApoC3、ANGPLT4 和 LPL 轴发生紊乱。疾病损害解释了这种紊乱。
