Altered placental development in pregnancies resulting in sudden infant death syndrome (SIDS)

作者：Widdows Kate; O'Malley Aiveen; O'Neill Bill; Kingdom John; Gillan John; Ansari Tahera^*

来源：Early Human Development, 2012, 88(10): 805-811.

DOI：10.1016/j.earlhumdev.2012.05.006

• Sudden infant death syndrome
• Placenta
• Villous trophoblast
• Stereology

Background: Sudden infant death syndrome (SIDS) is postulated to be a developmental disorder originating during fetal life in utero. Knowledge regarding the intrauterine environment in which SIDS infants develop is, however, inadequate and how the placenta develops prior to a SIDS event has not been studied.
Aim: To investigate the morphological development of the placenta obtained from full-term infants who subsequently succumbed to SIDS.
Study design: To estimate the percentage and total volumes of the chorionic villi and villous trophoblast membrane using stereological techniques.
Subjects: Placentas were obtained retrospectively from normal birthweight (SIDS-NBW n = 18) and small-for-gestational age (SIDS-SGA, n = 14) infants who had succumbed to SIDS, and compared to either control (n = 8) or SGA placentas (n = 7), respectively.
Results: SIDS-NBW placentas displayed evidence of augmented villous growth shown by significantly greater volumes of placental chorionic villi (gas-exchanging (GE) villi) in comparison to controls: this was not observed for SIDS-SGA placentas. However, both SIDS-NBW and SIDS-SGA placentas displayed significantly greater volumes of the cytotrophoblast (CT) (SIDS-NBW only), syncytiotrophoblast (SIDS-SGA only) and syncytial knots (SCT-K) and those displaying apoptotic syncytial nuclei (AP SCT-K). In contrast, SGA placentas displayed significantly reduced volumes of chorionic villi, GE villi and the villous trophoblast indicating a SIDS-specific effect associated with augmented placental growth.
Conclusions: Our findings provide initial evidence that placental abnormality, although not necessarily causative, may precede a subset of SIDS cases supporting the hypothesis that the origins of SIDS begin during fetal life in utero.

• 出版日期2012-10