1994
DOI: 10.1515/jpme.1994.22.1.71
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Predictors of perinatal outcome in intrauterine growth retardation: a long term study

Abstract: S1F is the best predictor of severe IUGR and significant for all the perinatal outcomes selected; S2F is the best predictor of mild IUGR and significant for SGA; UA RI is the best parameter for recognizing mild IUGR and evolution to severe IUGR.

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Cited by 6 publications
(2 citation statements)
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“…In our study we have determined that activity state percentages less than 25% and UA RI values more than > 0.70 are significantly related to neonatal respiratory distress syndrome; moreover IUGR fetuses with an activity state < 25% and UA RI > 0.70 are at higher risk for RDS than other IUGR fetuses while fetuses with an activity state > 25% and an UA RI < 0.70are not at high risk for RDS but can be considered at risk for other perinatal outcomes äs previously described (5).…”
Section: Discussionmentioning
confidence: 62%
“…In our study we have determined that activity state percentages less than 25% and UA RI values more than > 0.70 are significantly related to neonatal respiratory distress syndrome; moreover IUGR fetuses with an activity state < 25% and UA RI > 0.70 are at higher risk for RDS than other IUGR fetuses while fetuses with an activity state > 25% and an UA RI < 0.70are not at high risk for RDS but can be considered at risk for other perinatal outcomes äs previously described (5).…”
Section: Discussionmentioning
confidence: 62%
“…[1] SGA is one of the "Great Obstetrical Syndromes" [2,3] and it is often associated with other pregnancy complications such as preeclampsia (PE), preterm prelabor rupture of the membranes (pPROM), and preterm labor and delivery as well as increased risk of future health and developmental problems. [4][5][6][7][8][9][10][11][12] The known maternal risk factors for SGA include race, maternal age (≥35 years), low maternal body mass index (BMI), chronic hypertension, smoking, maternal occupation, substance abuse and maternal birth weight. [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] In addition, mechanisms of disease involved in SGA include: 1) abnormal physiologic transformation of the spiral arteries; [33][34][35][36] 2) chronic uteroplacental ischemia; [37][38][39][40][41][42][43][44][45][46][47] 3) endothelial cell dysfunction; [48-51] 4) increased trophoblast apoptosis/necrosis;[52] 5) intravascular inflammation [T helper 1 (Th1)-biased immune response]; [53]…”
Section: Introductionmentioning
confidence: 99%