Lipid profile and angiogenic markers in the detection of preeclampsia: The RECLAMA study.

IF 1.9 Q3 PERIPHERAL VASCULAR DISEASE
Daiana Ibarretxe, Sara Tameish, Ana González-Lleó, Èrica Cunillera, Natalia Andreychuk, Jara Ballestin, Alba Cabello, Lydia Cabau, Núria Amigó, Carme Grifoll
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引用次数: 0

Abstract

Introduction and objectives: Preeclampsia (PE) is a multisystem hypertensive disorder affecting 2-8% of pregnancies worldwide and represents a major cause of maternal and fetal morbidity and mortality. Its pathophysiology involves placental dysfunction leading to widespread maternal endothelial injury. Because endothelial damage is closely associated with abnormal lipid metabolism and angiogenic imbalance, the RECLAMA study aims to identify second-trimester biochemical and angiogenic markers associated with PE in a high-risk cohort and to compare them with those observed in a low-risk pregnant population.

Methods: In this pilot prospective case-control study, 98 pregnant women were recruited, including high-risk individuals (based on a high-risk result in first-trimester PE screening), women with chronic hypertension, and healthy controls. Clinical data and vascular parameters-carotid intima-media thickness (cIMT), pulse wave velocity (PWV), and augmentation index (AIx)-were collected at gestational week (GW) 14. Serum samples obtained at GW 24 were analyzed for a standard lipid profile, lipoprotein(a) [Lp(a)], and angiogenic factors (sFlt-1, PlGF, and the sFlt-1/PlGF ratio). Results were analyzed according to three patient groups: healthy controls (CG), at-risk patients who did not develop preeclampsia (NoPE), and patients who subsequently developed preeclampsia (PE).

Results: Women who subsequently developed PE had a significantly higher prevalence of pre-existing hypertension at baseline (38.46% vs 11.11% and 0% in the NoPE and control groups, respectively; p=0.0089). By the second trimester (GW 24), the PE group had elevated sFlt-1 levels and markedly reduced PlGF concentrations, resulting in a significantly higher sFlt-1/PlGF ratio compared with the NoPE and control groups (p<0.05). Standard lipid parameters show no significant differences, however a trend to higher triglycerides and lower HDL in PE women were observed. In addition, the PE cohort exhibited higher median levels of Lp(a) (37%) at GW 24. At baseline (GW 14), no significant differences were observed among groups in macrovascular markers, including cIMT, PWV, or AIx.

Conclusions: In this pilot study, the second-trimester sFlt-1/PlGF ratio was confirmed as a biomarker associated with preeclampsia. Standard lipid parameters show no significant differences, however a trend to proinflammatory atherogenic dyslipidaemia was observed. Moreover, Lp(a) showed a trend toward approximately 37% higher levels in patients who subsequently developed PE, warranting further investigation of this hypothesis-generating observation.

血脂和血管生成标志物在子痫前期检测中的应用:RECLAMA研究。
子痫前期(PE)是一种多系统高血压疾病,影响全世界2-8%的妊娠,是孕产妇和胎儿发病率和死亡率的主要原因。其病理生理涉及胎盘功能障碍导致广泛的母体内皮损伤。由于内皮损伤与脂质代谢异常和血管生成失衡密切相关,RECLAMA研究旨在确定高危人群妊娠中期与PE相关的生化和血管生成标志物,并将其与低危妊娠人群进行比较。方法:在这项前瞻性前瞻性病例对照研究中,招募了98名孕妇,包括高危个体(基于妊娠早期PE筛查的高危结果)、慢性高血压妇女和健康对照。临床数据和血管参数-颈动脉内膜-中膜厚度(cIMT),脉波速度(PWV)和增强指数(AIx)-在妊娠周(GW) 14收集。在GW 24获得的血清样本进行了标准血脂、脂蛋白(a) [Lp(a)]和血管生成因子(sFlt-1、PlGF和sFlt-1/PlGF比值)的分析。结果根据三组患者进行分析:健康对照组(CG)、未发生子痫前期的高危患者(NoPE)和随后发生子痫前期的患者(PE)。结果:随后发生PE的女性在基线时存在较高的高血压患病率(分别为38.46% vs 11.11%和0%,p=0.0089)。到妊娠中期(GW 24), PE组的sFlt-1水平升高,PlGF浓度显著降低,导致sFlt-1/PlGF比值显著高于NoPE组和对照组(结论:在本初步研究中,妊娠中期sFlt-1/PlGF比值被证实是与子痫前期相关的生物标志物。标准脂质参数显示无显著差异,但观察到促炎动脉粥样硬化性血脂异常的趋势。此外,Lp(a)在随后发展为PE的患者中显示出约37%的升高趋势,值得对这一假设产生的观察结果进行进一步研究。
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来源期刊
Clinica e Investigacion en Arteriosclerosis
Clinica e Investigacion en Arteriosclerosis PERIPHERAL VASCULAR DISEASE-
CiteScore
3.20
自引率
6.20%
发文量
44
审稿时长
40 days
期刊介绍: La publicación idónea para acceder tanto a los últimos originales de investigación como a formación médica continuada sobre la arteriosclerosis y su etiología, epidemiología, fisiopatología, diagnóstico y tratamiento. Además, es la publicación oficial de la Sociedad Española de Arteriosclerosis.
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