History of Fetal Growth Restriction Is More Strongly Associated With Severe Rather Than Milder Pregnancy-Induced Hypertension

Rasmussen, Svein; Irgens, Lorentz M.

doi:10.1161/hypertensionaha.107.096248

Cited by 32 publications

(24 citation statements)

References 37 publications

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“…The newborn's birth measurements from the Mild PE were 48.67±1.33 cm and for the group SP 46.42±2.36 vs. neonates from normotensive pregnancies (50.65±1.2cm; p<0.05). Also, these results, too, are same as from the associated literature in this area [5,7,14,15].…”

Section: Fetal Growth and Body Proportion During Pre-eclamptic Pregnasupporting

confidence: 86%

“…The US made every obstetrician's dream comes true, opening a window in the intra-uterine content,allowing fetus growth and development observation, as well as examining the placenta and determining the amount of amniotic fluid; and all of that is safe, direct, intentional and repeatable. Fetal growth measured with US with other risk factors could predict development of PE and poor neonatal outcomes [7,8].…”

Section: Fetal Growth and Body Proportion During Pre-eclamptic Pregnamentioning

confidence: 99%

“…This process can occur primarily because of maternal disease causing decreased oxygen-carrying capacity, a dysfunctional oxygen delivery system secondary to maternal vascular disease, or placental damage resulting from maternal disease [4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

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Fetal Growth and Body Proportion during Pre-Eclamptic Pregnancy

Jašović-Siveska¹

2015

OGIJ

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Purpose: To evaluate the effects of mild and severe PE on fetal growth and body proportion, measurement at serial ultrasound (US) examinations. Five to 7% of all pregnancies are complicated by preeclampsia (PE). Some forms of intrauterine growth restriction (IUGR) have been etiologically linked to PE, based on similar placental disease-abnormal implantation. Materials and Methods:Women (n=400) who had singleton pregnancies and underwent two or more second-and third-trimester obstetric US examinations were included in our study. The women were divided in three groups: 300 normotensive pregnancies (controls), 67 pregnancies with mild PE (MP) and 33 pregnancies with severe PE (SP). Inadequate fetal growth was defined as growth at or below 10 th percentile. We calculated US measurements between fetuses from normotensive and PE pregnancies (MP and SP). Results:In newborns of women with PE, mean birth weight and length were lower than in births without PE. Fetuses in PE pregnancies from 26 week of gestation (wg) with US scan had lower biometric parameters vs. then of normotensive pregnancies, especially values of abdominal circumference and femur length. In PE pregnancies, there could be faster aging of placenta and oligohydramnion. This is time before clinical onset of PE. Conclusion:Our results support the hypothesis that PE is a heterogeneous disorder which involving placental dysfunction and IUGR, often with asymmetric fetal body proportion and reduced fetal length. The results suggest that US measurements of fetal size are important predictors for PE and birth outcomes. IntroductionPreeclampsia is a multi-system disorder of unknown etiology. Women with preeclampsia usually develop raised blood pressure and proteinuria. Preeclampsia is also associated with abnormalities of coagulation system, disturbed liver function, renal failure and cerebral ischemia [1]. PE is characterized by vasospasm, increased peripheral vascular resistance, and thus reduced organ perfusion [1,2]. Also, it's well known that PE is associated with reduced fetal size. Fetal growth is dependent on genetic, placental and maternal factors. Intrauterine growth restriction (IUGR) refers to a condition in which a fetus is unable to achieve its genetically determined potential size. The most widely used definition of IUGR is a fetus whose estimated weight is below 10 th percentile for its gestational age [3][4][5].IUGR occurs when gas exchange and nutrient delivery to the fetus are not sufficient to allow it to thrive in utero. This process can occur primarily because of maternal disease causing decreased oxygen-carrying capacity, a dysfunctional oxygen delivery system secondary to maternal vascular disease, or placental damage resulting from maternal disease [4][5][6][7][8].Ultrasound (US) fetal biometry is the most widespread method used to establish gestational age, estimate fetal size and monitor its growth. US fetal biometry is gold standard for assessing fetal growth. The most commonly used measurements are the biparietal diameter, he...

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Section: Fetal Growth and Body Proportion During Pre-eclamptic Pregnasupporting

confidence: 86%

Section: Fetal Growth and Body Proportion During Pre-eclamptic Pregnamentioning

confidence: 99%

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Fetal Growth and Body Proportion during Pre-Eclamptic Pregnancy

Jašović-Siveska¹

2015

OGIJ

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“…It has been postulated that the mild late-onset form of preeclampsia is etiologically different from the severe early onset form (19,20). Whereas mild preeclampsia at term may represent a hypertensive response to minimally impaired (or perhaps even normal) perfusion of the placenta in highly sensitive or predisposed women, the severe disease could be the physiologic reaction of any mother due to profoundly reduced placental perfusion.…”

Section: Discussionmentioning

confidence: 99%

Gestational Hypertension, Preeclampsia, and Risk of Testicular Cancer

Pettersson

Richiardi²,

Cnattingius³

et al. 2008

Cancer Research

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Altered levels of pregnancy hormones have been suggested to initiate testicular cancer prenatally in the male fetus. The placenta is the main source of pregnancy hormones, and pregnancy hypertension and preeclampsia are associated with placental malfunction, including altered levels of hormones such as estrogen and human chorionic gonadotropin. We therefore evaluated fetal exposure to pregnancy hypertension and preeclampsia in relation to risk of testicular cancer in adolescent and adult life. We identified 293 cases of germ cell testicular cancer in the Swedish Cancer Register, and 861 controls in the Swedish Medical Birth Register. The standardized antenatal and delivery charts of the cases and controls were traced in the archives of the delivery units, and information about maternal and pregnancy characteristics such as gestational hypertension, proteinuria, anemia, and glucosuria were extracted. Odds ratios (OR) with 95% confidence intervals (CI) were calculated using conditional logistic regression. We found a strongly decreased risk of testicular cancer among subjects exposed to severe gestational hypertension (OR, 0.29; 95% CI, 0.12-0.74, compared with no hypertension), whereas the risk was increased among those exposed to mild gestational hypertension (OR, 1.62; 95% CI, 0.98-2.69) during the fetal period. The mechanism behind the association between pregnancy hypertension and testicular cancer is unclear, but our findings may reflect a potentially protective effect of the altered pregnancy hormones such as human chorionic gonadotropin that occur in severe gestational hypertension and preeclampsia. [Cancer Res 2008;68(21):8832-6]

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“…They also provide data that support but also some that argue against the concept that the pregnancy complication, preeclampsia, may be more than one disease. 1 In previous studies these authors demonstrated that women who have had a growth-restricted infant without preeclampsia are more likely to have preeclampsia in a subsequent pregnancy. 2 Those data and similar findings in the current study support pathological findings indicating the similarity of IUGR and preeclampsia.…”

mentioning

confidence: 98%

Preeclampsia More Than 1 Disease

Roberts

Catov

2008

Hypertension

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I n this issue of Hypertension, Rasmussen and Irgens provide strong support for the relationship of preeclampsia and intrauterine growth restriction (IUGR). They also provide data that support but also some that argue against the concept that the pregnancy complication, preeclampsia, may be more than one disease. 1 In previous studies these authors demonstrated that women who have had a growth-restricted infant without preeclampsia are more likely to have preeclampsia in a subsequent pregnancy. 2 Those data and similar findings in the current study support pathological findings indicating the similarity of IUGR and preeclampsia. 3 In preeclampsia, IUGR and interestingly also in about one third of cases of preterm birth, 4 the maternal myometrial and decidual vessels perfusing the placental site do not undergo the normal remodeling of pregnancy. In normal pregnancy trophoblastic invasion is associated with a greatly increased diameter and removal of vascular smooth muscle from the wall of these vessels. This results in large diameter, flaccid, unresponsive tubes that greatly increase placental perfusion. These changes are not present in pregnancies complicated by IUGR, preeclampsia, and some with preterm births. Implicit in the current study is the concept that preterm birth as well as IUGR is related to subsequent preeclampsia. Although preterm birth is not assessed directly, the effect of low birth weight (IUGR and preterm birth) was greater than the effect of IUGR alone. In a far smaller study our group was able to more directly support the relationship of preterm birth and preeclampsia, as women with early onset preeclampsia were more likely to have preterm birth in a subsequent nonpreeclamptic pregnancy. 5 The current study extends the prior observation of the relationship of IUGR and preeclampsia but also raises other interesting points. In this larger study the authors were able to determine a "dose response" for reduced growth, demonstrating that the smaller the baby the greater the odds ratio for a subsequent pregnancy with preeclampsia. Although this is what might be expected, what is not as straightforward was the fact that small babies increased the risk of early onset and severe preeclampsia more than they increased the risk for "mild" preeclampsia occurring at the end of pregnancy. This difference in the effect on different degrees of preeclampsia supports numerous observations suggesting that early onset preeclampsia may be a different disease than preeclampsia occurring at term. There are abundant epidemiological observations indicating differences in recurrence rates and relationship to later life cardiovascular disease. The authors of the current manuscript previously examined the database used in this study to test the relationship of preeclampsia to later-life cardiovascular mortality. A median of 14 years after a first pregnancy, women with preeclampsia before 37 weeks gestation had 8 times more cardiovascular deaths than women with normal pregnancy. For women with preeclampsia at term, the i...

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History of Fetal Growth Restriction Is More Strongly Associated With Severe Rather Than Milder Pregnancy-Induced Hypertension

Cited by 32 publications

References 37 publications

Fetal Growth and Body Proportion during Pre-Eclamptic Pregnancy

Fetal Growth and Body Proportion during Pre-Eclamptic Pregnancy

Gestational Hypertension, Preeclampsia, and Risk of Testicular Cancer

Preeclampsia More Than 1 Disease

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