期刊
JOURNAL OF PERINATAL MEDICINE
卷 50, 期 3, 页码 319-326出版社
WALTER DE GRUYTER GMBH
DOI: 10.1515/jpm-2021-0427
关键词
aneuploidy; Doppler velocimetry; fetal growth restriction; fetal ultrasound; trisomy 13; trisomy 18; umbilical artery
资金
- Sociedad Profesional de Medicina Fetal `Fetalmed' Ltda., Chile
The study analyzed umbilical artery Doppler velocimetry in second- and third-trimester fetuses with trisomy 18 and 13, finding a high prevalence of abnormal Doppler velocimetry that increased with gestational age. This suggests placental insufficiency may play a significant role in the development of fetal growth restriction in these aneuploid fetuses.
Objectives To analyze umbilical artery (UA) Doppler velocimetry and its possible role in placenta-mediated fetal growth restriction (FGR) in second- and third-trimester fetuses with trisomy 18 and 13. Methods UA pulsatility index (PI) and half-peak systolic velocity deceleration time (hPSV-DT) were measured in fetuses with trisomy 18 and 13. Correlation with gestational age, birthweight, and perinatal outcome was analyzed. Results A total of 80 measurements were taken from 33 fetuses with trisomy 18 and 19 with trisomy 13. Overall, there was a high prevalence of abnormal UA Doppler velocimetry. In fetuses with trisomy 18, 54% (27/50) of the UA PI values and 58% (29/50) of the UA hPSV-DT values were abnormal. In fetuses with trisomy 13, 80% (24/30) of the UA PI values and 87% (26/30) of the UA hPSV-DT values were abnormal. The prevalence of abnormal UA Doppler velocimetry increased with gestational age in both types of aneuploidy. However, this trend was only significant for trisomy 13 (p<0.05). All fetuses with trisomy 18 and 86% of fetuses with trisomy 13 were classified at birth as FGR. There were no perinatal survivors in this series. Conclusions A high prevalence of abnormal UA Doppler velocimetry was found in second- and third-trimester fetuses with trisomy 18 and 13, which further increased with gestational age. These results may well correlate with alterations described previously in the placenta, suggesting placental insufficiency has an important role in the development of FGR in these autosomal aneuploid fetuses.
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