BACKGROUND: Preeclampsia (PE) is a complex pregnancy-specific disorder characterized by impaired placental function, angiogenic imbalance and increased maternal cardiovascular risk. Placental growth factor (PlGF) is an established angiogenic marker used in first-trimester PE screening, whereas lipoprotein(a) [Lp(a)] is a cardiovascular risk marker whose longitudinal behaviour during pregnancy remains insufficiently characterized. This study aimed to assess serial changes in PlGF and Lp(a) concentrations across pregnancy in women stratified by first-trimester PE risk.
METHODS: This prospective observational study included 53 pregnant women classified as low risk (n=29) or high risk (n=24) for preeclampsia according to first-trimester screening. PlGF and Lp(a) concentrations were measured in the first, second, and third trimesters. Serial changes in biomarker concentrations were assessed using Friedman tests and linear mixed-effects models to account for repeated measurements. Between-group differences were evaluated using trimester-specific Mann–Whitney U tests and mixed-effects models. Associations between Lp(a) and PlGF were assessed using Spearman’s rank correlation and longitudinal mixed-effects modelling.
RESULTS: Lp(a) concentrations changed significantly during pregnancy, showing a modest increase toward the third trimester. This pattern was supported by the Friedman test (p=0.002) and by mixed-effects modelling, in which third-trimester Lp(a) concentrations were significantly higher than those observed in the first and second trimesters. No significant differences in Lp(a) concentrations were observed between women at low and high first-trimester risk of preeclampsia in the longitudinal model (p=0.827). PlGF concentrations increased markedly across pregnancy, with significant differences between all trimesters (p<0.001). In trimester-specific analysis, PlGF was significantly lower in the high-risk group than in the low-risk group in the first trimester (31.9 vs. 42.7 pg/ml, p=0.023), whereas no significant between-group differences were observed in the second or third trimester. In the longitudinal mixed-effects model, the overall effect of preeclampsia risk group on PlGF did not reach statistical significance (p=0.060). The pattern of PlGF increase over pregnancy did not differ significantly between risk groups (p=0.319). No significant association was observed between Lp(a) and PlGF in trimester-specific correlation analyses or in longitudinal mixed-effects modelling.
CONCLUSIONS: PlGF and Lp(a) demonstrate different serial patterns during pregnancy in women stratified by first-trimester preeclampsia risk. PlGF shows a marked gestational increase and lower first-trimester concentrations in women classified as high risk, although longitudinal analysis did not confirm a significant overall difference between risk groups. In contrast, Lp(a) increases mainly in late pregnancy but is not associated with preeclampsia risk group or PlGF concentrations. Overall, Lp(a) did not show a PE risk-related pattern. similar to the first-trimester PlGF finding.