Placental Histological Lesions in Monochorionic Twins With Selective Fetal Growth Restriction Versus Growth‐Restricted Singletons: A Cohort Study
Jip A. Spekman, Sophie G. Groene, Anne T. R. Noll, Femke Slaghekke, Chiara C. M. M. Lap, Angélique van Dam, Liesbeth Lewi, Lotta Herling, E. J. T. Verweij, Monique C. Haak, Jeanine M. M. van Klink, Enrico Lopriore, Lotte E. van der MeerenABSTRACT
Objective
To determine the prevalence of placental histological lesions in the smaller twin's placental territory in monochorionic (MC) twins complicated by selective fetal growth restriction (sFGR), and compare it to FGR singletons.
Design
Cohort study with 1:1 comparison.
Setting
Leiden University Medical Center, The Netherlands.
Population
Forty‐four MC twin placentas with sFGR and 44 FGR singleton placentas, histologically evaluated between 2020 and 2025.
Methods
FGR was defined as birthweight < 10th percentile. sFGR was defined as birthweight discordance ≥ 20% between twins and birthweight < 10th percentile for the smaller twin. Placental parenchyma was examined using Amsterdam Consensus Statement criteria for maternal vascular malperfusion (MVM), fetal vascular malperfusion (FVM), and acute and chronic inflammation. Analyses of placental lesions were adjusted for gestational age at diagnosis of (s)FGR.
Main Outcome Measures
Prevalence of histological lesions.
Results
Median gestational age at birth was 37.1 weeks (IQR 32.0–38.1) for FGR singletons and 32.3 weeks (IQR 30.1–35.0) for sFGR twins ( p < 0.001). FVM was more common in smaller twins than sFGR singletons (45% versus 16%; OR 3.7 (95% CI: 1.0–13.2); p = 0.046), alongside a higher prevalence of abnormal cord insertions (84% versus 21%; p < 0.001). MVM prevalence was similar between smaller twins and FGR singletons (73% versus 75%; OR 0.8 (95% CI: 0.2–2.9); p = 0.779), as was chronic inflammation (27% versus 34%; OR 0.7 (95% CI: 0.2–2.3); p = 0.549).
Conclusions
The smaller twin's placental territory in sFGR showed lesions consistent with placental insufficiency, with prevalences of MVM and chronic inflammation comparable to FGR singletons and increased prevalence of FVM. These findings suggest that placental insufficiency may be involved in the pathophysiology of sFGR alongside unequal sharing.