Basal plate remodeling in vascular-metabolic pregnancy disorders
Stefan Dugalić, Ljubiša Jovanović, Katarina Ivanović, Miloš Milinčić, Dara Pavlović, Aleksandra Lazarević, Miroslava GojnićAbstract
Objectives
To compare placental inflammatory lesions and basal plate vascularization between pregnancies complicated by maternal vascular–metabolic disorders and normoglycemic, normotensive pregnancies, and to determine whether basal plate vascularization differs among metabolic, hypertensive, thrombophilic, and combined disorder phenotypes.
Methods
This retrospective observational study included 680 singleton pregnancies with placental histopathology. Pregnancies were classified as complicated by maternal vascular–metabolic disorders or as belonging to a normoglycemic, normotensive comparison group without documented maternal vascular–metabolic disease. Placental inflammatory lesions (villitis and decidualitis) were recorded as present or absent. Basal plate vascularization was assessed using a three-level ordinal scoring system and compared between study groups and among vascular–metabolic disorder phenotypes.
Results
Maternal vascular–metabolic disorders were documented in 205 pregnancies, whereas 475 pregnancies constituted the comparison group. Villitis was more frequent in the vascular–metabolic disorder group than in the comparison group (13.2 % vs. 3.2 %, p<0.001), as was decidualitis (71.2 % vs. 16.8 %, p<0.001). Basal plate vascularization scores were higher in the vascular–metabolic disorder group (2.76 ± 0.45 vs. 2.59 ± 0.52, p<0.001). However, the absolute difference was modest, and the median score was 3.0 in both groups. Basal plate vascularization did not differ significantly among isolated metabolic, hypertensive, thrombophilic, and combined disorder phenotypes (p=0.216).
Conclusions
Maternal vascular–metabolic disorders were associated with a higher frequency of placental inflammatory lesions and slightly higher basal plate vascularization scores. However, the restricted scoring range, ceiling effect, unadjusted analyses, and retrospective observational design limit the clinical interpretation of these findings and preclude causal inference.