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Published on: October 12, 2017
Increased low-density lipoprotein susceptibility to oxidation in pregnancies and fetal growth restriction
Isabel Sánchez-Vera1, Bartolomé Bonet, Marta Viana
1School of Medicine, Universidad San Pablo-CEU, Madrid, Spain.
Insights
Fetal growth restriction (FGR) increases low-density lipoprotein (LDL) susceptibility to oxidation, potentially damaging the placenta and affecting fetal weight. This oxidative stress is linked to reduced placental hormone secretion in FGR pregnancies.
Area of Science:
- Obstetrics and Gynecology
- Cardiovascular Research
- Perinatal Medicine
Background:
- Pregnancies with fetal growth restriction (FGR) exhibit placental alterations like atherosis and infarction.
- Low-density lipoprotein (LDL) oxidation is implicated in atherosclerosis pathogenesis.
- The role of LDL oxidation in FGR-related placental changes requires investigation.
Purpose of the Study:
- To assess LDL susceptibility to oxidation in pregnancies complicated by FGR.
- To examine the relationship between LDL oxidation, fetal growth, and placental hormone secretion in FGR.
Main Methods:
- A prospective cohort study involving 55 women with FGR and 50 controls.
- Blood samples collected at 15, 24, and 32 weeks of gestation.
- LDL oxidation assessed via lag phase measurement; cholesterol, triglycerides, vitamin E, estradiol, progesterone, and placental lactogen quantified.
Main Results:
- Women with FGR showed increased LDL susceptibility to oxidation in the second and third trimesters compared to controls.
- Third-trimester FGR pregnancies had lower estradiol, progesterone, and placental lactogen levels.
- A positive correlation was observed between LDL oxidation lag phase and birth weight/estradiol levels in the third trimester.
Conclusions:
- Fetal growth restriction is associated with heightened LDL susceptibility to oxidation.
- Increased LDL oxidation may contribute to placental dysfunction, altered endocrine function, and reduced fetal weight in FGR.
Objective:
Atherosis and placental infarction have been observed in pregnancies complicated by fetal growth restriction (FGR). Low-density lipoprotein (LDL) oxidation plays a central role in the pathogenesis of atherosclerosis; therefore, it could be involved in the placental alterations observed in FGR. The aims of the present study were to estimate LDL susceptibility to oxidation in pregnancies complicated by FGR and to evaluate their relationship with fetal growth and placental hormone secretion.
Methods:
A cohort prospective study was carried out in 50 women with uncomplicated pregnancies and 55 women with FGR. Blood was drawn at 15, 24, and 32 weeks of gestation. Low-density lipoprotein oxidation was initiated by the addition of CuCl2 and formation of conjugated dienes was monitored. Cholesterol, triglycerides, vitamin E, estradiol, progesterone, and placental lactogen were determined.
Results:
Women with FGR showed a lag phase (minutes from addition of CuCl2) similar to the control group in the first trimester of pregnancy (85.3 +/- 3.3 versus 81.3 +/- 5.6). But in the second and third trimester, they showed a lower lag phase than the control group: 69.6 +/- 3.6 versus 84.4 +/- 3.5 (P < .05) and 69.9 +/- 3.4 versus 95.6 +/- 3.4 (P < .001). During the third trimester, pregnancies complicated with FGR showed lower levels of estradiol, progesterone, and human placental lactogen than those in the control group. In the third trimester, a positive correlation was found between the lag phase and the birth weight (P = .001) and with the plasma levels of estradiol (P = .002).
Conclusion:
Fetal growth restriction is associated with an increased LDL susceptibility to oxidation, a process that could damage the placenta, leading to alterations in placental endocrine function and fetal weight. Pregnancies complicated by fetal growth restriction show an increased LDL susceptibility to oxidation, a process that may lead to placental dysfunction and growth delay.
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