Evaluation of High-Sensitivity C-Reactive Protein and Serum Lipid Profile in Southeastern Nigerian Women with Pre-Eclampsia

TLDR

The study aimed to quantify how inflammation and triglycerides mediate the relationship between prepregnancy BMI and preeclampsia risk. Using a nested case‑control design with 55 preeclamptic and 165 control women, the authors measured CRP and triglycerides at ≤20 weeks and applied conditional logistic regression to compare total and direct effects of BMI, calculating the mediation proportion. Results showed that higher BMI increased preeclampsia risk (1.7‑fold for 4‑unit and 2.9‑fold for 8‑unit increases), but when controlling for CRP and triglycerides the risk attenuated to 1.4‑ and 2.0‑fold, indicating inflammation was a stronger mediator and that roughly one‑third of BMI’s effect is mediated by inflammation and triglycerides.

Abstract

The objective of this study was to quantify the mediating role of inflammation and triglycerides in the association between prepregnancy body mass index (weight (kg)/height (m)2) and preeclampsia. The authors conducted a nested case-control study of 55 preeclamptic women and 165 pregnant controls from the Pregnancy Exposures and Preeclampsia Prevention Study (Pittsburgh, Pennsylvania, 1997-2001). Serum samples collected at < or = 20 weeks' gestation were analyzed for levels of C-reactive protein and triglycerides. The adjusted odds ratio (AOR) from a multivariable conditional logistic regression model assessing the total effect of body mass index on preeclampsia risk was compared with the AOR from the same model after results were controlled for C-reactive protein, triglycerides, and confounding factors (direct-effects model). The percentage of the total effect that was mediated through inflammation and triglycerides was calculated as 100 - [ln(direct-effects AOR)/ln(total-effects AOR)]. In the total-effects model, 4- and 8-unit increases in body mass index were associated with 1.7-fold (95% confidence interval (CI): 1.3, 2.3) and 2.9-fold (95% CI: 1.6, 5.2) increases in preeclampsia risk, whereas in the direct-effects model, these AORs were 1.4 (95% CI: 1.0, 1.9) and 2.0 (95% CI: 1.0, 3.8), respectively. Inflammation was a more important mediator than triglycerides. These findings suggest that approximately one third of the total effect of body mass index on preeclampsia risk is mediated through inflammation and triglyceride levels.