Placental disease and abnormal umbilical artery Doppler waveforms in trisomy 21 pregnancy: A case-control study

Corry, Edward; Mone, Fionnuala; Segurado, Ricardo; Downey, Paul; McParland, Peter; McAuliffe, Fionnuala M.; Mooney, Eoghan E.

doi:10.1016/j.placenta.2016.09.001

Cited by 14 publications

(9 citation statements)

References 23 publications

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“…Chromosomal abnormalities with or without heart malformations may feature diverse villous abnormalities 20 and indeed some authors report that the increased incidence of placental lesions of poor uteroplacental perfusion which may worsen the prognosis in heart malformations. 18,38–40 This was not the case in our material, neither was placental dysmaturity, 20 however, as patterns of chronic hypoxic placental injury were more common in group 3. Lesions of shallow placental implantation, fetal vascular malperfusion (except for postmortem placental regressive changes), and placental hypoxic lesions were the least common or showed no significant differences.…”

Section: Discussioncontrasting

confidence: 51%

Patterns of Placental Injury in Congenital Anomalies in Second Half of Pregnancy

Stanek

2019

Pediatr Dev Pathol

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Background Placental pathology in fetal congenital anomalies in second half of pregnancy is largely unknown. Methods Twenty-six clinical and 45 independent placental phenotypes from pregnancies ≥20 weeks of gestation with congenital anomalies divided into 4 groups were retrospectively compared with analysis of variance or χ 2 with 3 degrees of freedom and with Bonferroni correction for multiple comparisons: group 1 : 112 cases with heart malformations (with or without chromosomal anomalies), group 2 : 41 cases with abnormal karyotypes and anomalies other than heart malformations, group 3 : 87 cases with intrathoracic or intraabdominal mass-forming anomalies (mostly congenital diaphragmatic hernias and adenomatoid airway malformation), and group 4 : 291 miscellaneous cases with mostly skeletal, renal, and central nervous system anomalies not fulfilling the criteria of inclusion into groups 1 to 3. Results Eight of 26 clinical (30.8%) and 16 of 45 (35.5%) placental phenotypes varied statistically significantly among the 4 groups ( P < .05), of those, 7 (26.9%) and 4 (8.9%), respectively, remained statistically significant after Bonferroni correction ( P Bonferroni ≤ .002). Those placental phenotypes were placental weight, chorionic disc chorionic microcysts, fetal vascular ectasia, and luminal vascular abnormalities of chorionic villi. Conclusions Fetal anomalies in second half of pregnancy feature abnormal clinical phenotypes much more frequently than abnormal placental phenotypes. Chromosomal abnormalities with or without heart malformations tend to feature villous edema, and erythroblastosis of fetal blood, likely due to fetal heart failure. Mass-forming fetal anomalies feature placental histological lesions of shallow placental implantation, diffuse chronic hypoxic patterns of placental injury, and lesions of fetal vascular malperfusion, likely stasis-induced.

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Section: Discussioncontrasting

confidence: 51%

Patterns of Placental Injury in Congenital Anomalies in Second Half of Pregnancy

Stanek

2019

Pediatr Dev Pathol

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“…Trisomy 21 fetuses have a progressively higher incidence of abnormal umbilical artery impedance indices throughout pregnancy. This alteration, that likely begins around the mid second trimester and increases with gestational age, has been strongly correlated with placental findings such as disturbance of syncytiotrophoblast formation, as in preeclampsia and FGR, and a large irregular hypovascular villi and abnormalities of the trophoblastic layer. In the third trimester, the placenta of trisomic (13, 18, 21, and) fetuses exhibit a significant reduction in small muscular artery count and a small muscular artery to villous ratio.…”

Section: Chromosomal Abnormalitiesmentioning

confidence: 75%

Genetic syndromes associated with isolated fetal growth restriction

2020

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Early onset fetal growth restriction (FGR) may be due to impaired placentation, environmental or toxic exposure, congenital infections or genetic abnormalities. Remarkable research, mainly based on retrospective series, has been published on the diverse genetic causes. Those have become more and more relevant with the improvement in the accuracy of the analysis techniques and the rising of breakthrough genomewide methods such as the whole genome sequencing. However, no publication has presented an integrated view of management of those fetuses with an early and severe affection. In this review, we explored to which extent genetic syndromes can cause FGR fetuses without structural defects. The most common chromosomal abnormalities (Triploidies and Trisomy 18), submicroscopic chromosomal anomalies (22q11.2 microduplication syndrome) and single gene disorders (often associated with mild ultrasound findings) related to early and severe FGR had been analysed. Finally, we addressed the impact of epigenetic marks on fetal growth, a matter of growing importance. At the end of this review, we should be able to provide an adequate counseling to parents in terms of diagnosis, prognosis and management of those pregnancies.

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“…Los hallazgos en fetos con SD se correlacionan con los estudios histopatológicos de placentas de SD que demuestran una larga serie de alteraciones ultraestructurales, tanto en calidad como cantidad, de las vellosidades coriales, y cordón umbilical con hipotorsión [15][16][17][18][19][20][21] . Un interesante resumen publicado por Corry, et al 22 en 2016, que aplica los nuevos consensos en histopatología, demuestra que las placentas de los fetos con SD tienen mala perfusión vascular fetal en un 48% y defectos de maduración vellositaria en un 39%.…”

Section: Discussionunclassified

Doppler de arteria umbilical en fetos con síndrome de Down

Bustos-Vidal¹,

Herrera-Alcaíno²

2024

RECHOG

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La aneuploidía más común entre los recién nacidos vivos es el síndrome de Down (SD). En estos niños el crecimiento está disminuido, con una frecuencia del 25% de restricción del crecimiento intrauterino, pero no se ha establecido el papel de la insuficiencia placentaria. El objetivo es estudiar la resistencia placentaria a través del Doppler de arteria umbilical con índice de pulsatilidad (IP) y el tiempo medio de desaceleración (t/2), y el posible efecto de la insuficiencia placentaria en fetos con SD. Método: Se realizó Doppler en la arteria umbilical en 78 fetos con SD, se midieron el IP y el t/2, y se compararon los resultados con los pesos de nacimiento. Resultados: Se estudiaron 78 fetos con SD con 214 mediciones Doppler. El t/2 y el IP estaban alterados en el 71,5% y el 65% de las mediciones, respectivamente. La incidencia de t/2 alterado aumenta con la edad gestacional desde un 28,6% a las 15-20 semanas hasta un 89,3% sobre las 36 semanas (p < 0,01); cifras similares se observan para el IP. La clasificación de los pesos fue: 64% adecuados, 12% grandes y 24% pequeños para la edad gestacional. La última medición de t/2 antes del parto era normal en el 17% y estaba alterada en el 83%. En el caso del IP, los valores fueron normales en el 27% y anormales en el 73%. El peso de nacimiento, la edad gestacional y el porcentaje de niños adecuados para la edad gestacional eran significativamente mayores en el grupo con Doppler normal que en el grupo con Doppler alterado. El z-score del t/2 estaba marcadamente alterado (−2.23), pero el del peso de nacimiento solo estaba algo disminuido (−0,39). La mortalidad perinatal fue del 10%, significativamente mayor cuando el flujo diastólico era ausente o reverso. Conclusiones: El estudio demuestra que los fetos con SD tienen una alta incidencia de alteración del Doppler umbilical para el IP y el t/2, lo cual sugiere una insuficiencia placentaria grave. Este deterioro parece iniciarse hacia el final del segundo trimestre y aumenta con la edad gestacional. Sin embargo, en estos fetos, la insuficiencia placentaria produce una ligera caída en el crecimiento fetal. Como hipótesis general pensamos que en los fetos con SD hay datos claros de insuficiencia placentaria, pero habría algún factor que les protegería de una restricción grave del crecimiento.

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Placental disease and abnormal umbilical artery Doppler waveforms in trisomy 21 pregnancy: A case-control study

Cited by 14 publications

References 23 publications

Patterns of Placental Injury in Congenital Anomalies in Second Half of Pregnancy

Patterns of Placental Injury in Congenital Anomalies in Second Half of Pregnancy

Genetic syndromes associated with isolated fetal growth restriction

Doppler de arteria umbilical en fetos con síndrome de Down

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