Key result
Preeclampsia had lower unadjusted serum alamandine vs controls (151.0 vs 174.0 pg/mL; p=0.019), but the adjusted difference was not significant (B=24.76; 95% CI -3.45 to 52.97; p=0.085).
Why the study?
Preeclampsia involves endothelial dysfunction and renin-angiotensin system imbalance, and alamandine is a vasodilatory component of its protective pathways. This study evaluated maternal serum alamandine levels in preeclamptic versus normotensive pregnancies and their associations with clinical and laboratory parameters.
Case-Control (n=87)
Although unadjusted maternal serum alamandine levels were lower in preeclamptic women compared to normotensive controls, this difference lost statistical significance after multivariable adjustment, though independent associations with diastolic blood pressure and umbilical artery S/D ratio were observed.
Answers are grounded in this paper and cite their sources.
Adjusted alamandine levels did not differ significantly after adjustment; leaves open its biomarker or mechanistic role in preeclampsia.
Objectives: Preeclampsia is a gestational disorder characterized by endothelial dysfunction and renin-angiotensin system imbalance. Alamandine, a component of its protective pathways, has vasodilatory effects. This study aims to compare maternal serum alamandine levels between preeclamptic and normotensive pregnancies and evaluate their associations with clinical and laboratory parameters. Methods: This prospective observational case–control study included 40 women with preeclampsia and 47 normotensive women with singleton pregnancies in the third trimester between June and December 2025. Maternal serum alamandine levels were measured using the ELISA method. Participants’ demographic, clinical, laboratory, umbilical artery Doppler, and perinatal data were prospectively recorded. Alamandine levels were compared between groups; their associations with clinical and laboratory parameters were evaluated using correlation and regression analyses. Results: Maternal serum alamandine levels were significantly lower in women with preeclampsia compared to normotensive controls (151.0 ± 51.2 vs. 174.0 ± 39.5 pg/mL; p = 0.019). However, the between-group difference was no longer statistically significant after adjustment for maternal age, body mass index, umbilical artery S/D ratio, and aspirin use (B [control − preeclampsia] = 24.76 pg/mL; 95% CI: −3.45 to 52.97; p = 0.085). Serum alamandine concentrations showed weak inverse correlations with systolic and diastolic blood pressure. A weak inverse correlation was also observed with the spot urine protein-to-creatinine ratio; however, this association did not remain statistically significant after correction for multiple comparisons. In the multivariate analysis, diastolic blood pressure and the umbilical artery S/D ratio were independently associated with maternal serum alamandine levels. Conclusions: Maternal serum alamandine levels were lower in women with preeclampsia in the unadjusted analysis; however, this difference was not statistically significant after expanded multivariable adjustment. Alamandine concentrations showed associations with selected hemodynamic parameters, whereas the relationship with proteinuria remained uncertain. These findings suggest a potential role of circulating alamandine in the vascular alterations associated with preeclampsia; however, its predictive or prognostic value cannot be determined from the present study.
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Topçu et al. (2026) conducted a case-control in Preeclampsia (n=87). Preeclampsia vs. Normotensive pregnancy was evaluated on Maternal serum alamandine levels (pg/mL) (B 24.76, 95% CI -3.45 to 52.97, p=0.085). Preeclampsia had lower unadjusted serum alamandine vs controls (151.0 vs 174.0 pg/mL; p=0.019), but the adjusted difference was not significant (B=24.76; 95% CI -3.45 to 52.97; p=0.085).
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