Placental findings in pregnancies complicated with IUGR - histopathological and immunohistochemical analysis

Vol. 59 No. 3, 2018


Maria Violeta Novac, Mihaela Niculescu, Maria Magdalena Manolea, Anda Lorena Dijmarescu, Dominic Gabriel Iliescu, Marius Bogdan Novac, Luciana Teodora Rotaru, Manuela Florica Stoenescu, Maria Carmen Tabacu, Stefania Tudorache, Cristina Jana Busuioc, Ioana Andreea Gheonea

Objective: Placental lesions and placental ischemia are typical elements of intrauterine growth restriction (IUGR). The aim of this study is to analyze histological and immunohistochemical (IHC) changes in the placentas of IUGR fetuses. Materials and Methods: In this prospective study, 126 placentas from small for gestational age (SGA) pregnancies (newborns with birth weight <10th percentile) that formed the study group and 31 placentas from pregnancies without SGA representing control group, were included. Placentas were examined according to standard protocol. Histopathological and IHC examinations of placentas were performed for analysis. Results: A certain type of lesion of placental injury is increased in placentas from SGA pregnancies. These placental lesions were placental infarction (over 5%), increased syncytial knots, intervillous fibrinoid deposition, villous thrombohematoma. Other common placental lesions were probably related to fetal adaptation to placental ischemia or represent a placental change characteristic of pregnancy evolution. Conclusions: It seems that although IUGR/SGA fetuses are more commonly associated with histological placental abnormalities, it cannot be established whether these abnormalities certainly contribute to IUGR, as there are no specific placental lesions in SGA placentas. Pseudo-angiomatous aspect, associated with increased syncytial knots, was specific for vascular hypoxia. Especially the magnitude of modifications of the placental structure beyond the qualitative modifications, which also lead to functional changes, are involved in this pathology of pregnancy, the onset of lesions being triggered at the level of stem villi.

Corresponding author: Marius Bogdan Novac, Lecturer, MD, PhD; e-mail:; Cristina Jana Busuioc, Associate Professor, MD, PhD; e-mail:

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