The sFlt-1/PlGF Ratio at 12, 24, and 32 Weeks Gestation in Twin Pregnancies as a Predictor of Placental Dysfunction

Abstract

Background: This study aims to assess the utility of the sFlt-1/PlGF ratio throughout pregnancy in predicting placental dysfunction and neonatal outcomes in twin pregnancies. Methods: Prospective study at a tertiary hospital. All pregnant women with a twin pregnancy who signed the informed consent were included. The sFlt-1/PlGF ratio was measured at 12, 24, and 32 weeks’ gestation. Results: Seventy patients were included, and 30% developed placental dysfunction. Differences were found in the mean sFlt-1/PlGF ratios at week 32 (13.6 vs. 31.8, p = 0.007). Optimal cutoffs at 12, 24, and 32 weeks to identify patients who develop placental dysfunction were 32.5, 8.5, and 30.5, respectively, with ORs of 4.25 (1.13–20.69 95% IC; p = 0.044), 13.5 (3.07–67.90 95% IC; p = 0.001), 14.29 (3.59–66.84 95% IC; p < 0.001). The sFlt-1/PlGF ratio at 32 weeks was associated with gestational age at birth. The sFlt-1/PlGF ratio in weeks 24 and 32 had a statistically significant negative correlation with the birth weight percentile in both twins. Conclusions: The potential of the sFlt-1/PlGF ratio as a predictive tool for placental dysfunction in twin pregnancies is underscored.

The sFlt-1/PlGF Ratio at 12, 24, and 32 Weeks Gestation in Twin Pregnancies as a Predictor of Late Preterm Birth and Perinatal Event Secondary to Prematurity

“…Although the sFlt-1/PlGF ratio has been mainly studied and applied to detect placental dysfunction, in our analyzed sample of patients with a twin pregnancy, only 44.74% of the women presenting preterm birth had an established diagnosis related to placental dysfunction, such as preeclampsia or fetal growth restriction [29][30][31][32][33][34]. This leads to a 55.26% remaining patients with a twin pregnancy without a diagnosis related to placental dysfunction, such as FGR or preeclampsia, in which the alteration of placental biomarkers such as the sFlt-1/PlGF ratio could be due to alternative physiopathological mechanisms, as reported in previous studies [35][36][37].…”