Association of sFlt-1 and C-reactive protein with outcomes in severe preeclampsia A cohort study

To determine the association between soluble FMS-like tyrosine kinase-1 (sFlt-1) and high-sensitivity C-reactive protein (hs-CRP) with maternal and perinatal outcomes in patients with preeclampsia (PE) with severe features. A cohort study was conducted on 100 patients, 60 with PE with severe features, and 40 healthy women in the third trimester of pregnancy. Admission serum levels of sFlt-1 and hs-CRP and clinical and epidemiological parameters were evaluated to quantify the predictive ability of adverse maternal and perinatal outcomes using hierarchical multiple regression and receiver operating characteristic curves. Compared to controls, patients with PE and severe features had significantly higher levels of sFlt-1 but not hs-CRP. sFlt-1 and hs-CRP proved to be reasonable parameters for the prediction of composite adverse maternal outcomes. However, we found no correlation between these 2 biomarkers. PE integrated estimate of risk scores were correlated only with sFlt-1 levels. Regarding fetal outcomes, unlike hs-CRP, sFlt-1 was strongly associated with birth weight and Apgar score < 7 at 5 minutes. Following multivariate analysis, maternal age, previous hypertension, sFlt-1, and hs-CRP levels remained independently associated with composite adverse maternal outcomes. sFlt-1 levels were elevated in patients with PE and severe features. Both sFlt-1 and hs-CRP may predict composite adverse maternal outcomes but do not correlate with each other and differ in perinatal morbidity patterns. These data support the hypothesis that the varied outcomes in PE may result from different pathogenic pathways.

Automated summary

This study aimed to examine the association between sFlt-1 and hs-CRP with maternal and perinatal outcomes in patients with severe features of preeclampsia. Results showed that sFlt-1 and hs-CRP may serve as reasonable predictors of adverse maternal outcomes, but they do not correlate with each other and differ in perinatal morbidity patterns. These findings support the hypothesis that different pathogenic pathways may lead to varied outcomes in preeclampsia.