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Lipid profile and angiogenic markers in the detection of preeclampsia: The RECLAMA study
Daiana Ibarretxe1, Sara Tameish2, Ana González-Lleó1
1Unitat de Medicina Vascular i Metabolisme, Servei Medicina Interna, Hospital Universitari Sant Joan, 43204 Reus, Spain; Unitat de recerca en Lípids i arteriosclerosi (URLA), Universitat Rovira i Virgili, 43204 Reus, Spain; Institut d'Investigació Sanitaria Pere Virgili, 43204 Reus, Spain; Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas (CIBERDEM), Insituto de investigación Carlos III, 28029 Madrid, Spain.
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.
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