Are Early and Late Preeclampsia Distinct Subclasses of the Disease—What Does the Placenta Reveal?

Merwe, Johannes van der; Hall, David; Wright, Colleen A.; Schubert, Pawel; Grové, D.

doi:10.3109/10641950903572282

Cited by 94 publications

(60 citation statements)

References 22 publications

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“…This study meta-analyzes data from publications using this classification, and demonstrates a higher prevalence of both villous and vascular histopathological lesions in the placentae of PE pregnancies than in the placentae of normal pregnancies. The latter finding is in keeping with those of previous studies conducted prior to agreed Ruiz-Quiñonez (2014) 11 Devisme (2013) 7 Maloney (2012) 6 Pathak (2011) 10 Ogge (2011) 5 van Der Merwe (2010) 9 Vinnars (2010) 8 Kos (2005) 4 Devisme (2013) 7 Maloney (2012) 6 Ogge (2011) 5 Kos (2005) Ruiz-Quiñonez (2014) 11 Pathak (2011) 10 van Der Merwe (2010) 9 Vinnars (2010) classifications or when using different histopathological classifications for placental lesions.…”

Section: Association Of Placental Lesions With Pesupporting

confidence: 81%

“…Devisme (2013) 7 Maloney (2012) 6 Ogge (2011) 5 van Der Merwe (2010) 9 Vinnars (2010) 8 Devisme (2013) 7 Maloney (2012) 6 Ogge (2011) Figure 4 Forest plots of odds ratios (ORs) (random-effects model) for vascular lesions in pregnancies complicated by pre-eclampsia and normotensive pregnancies, for all studies (a) and for blinded (b) and unblinded (c) studies. Only first author given for each study.…”

Section: Pooled and Population Prevalence Of Histological Lesionsmentioning

confidence: 99%

“…This results in placental hypoxia and/or stress and the typical villous and vascular placental lesions associated with PE [1][2][3] . However, the literature on the prevalence, nature and severity of the placental histopathological lesions in PE is conflicting [4][5][6][7][8][9][10][11] . The lack of agreement between studies may result from differences in their design, with retrospective studies being prone to selection bias 8 and unblinded studies being susceptible to operator bias [4][5][6][7] .…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Placental histopathology associated with pre‐eclampsia: systematic review and meta‐analysis

Falco

Sivanathan

Laoreti

et al. 2017

Ultrasound in Obstet & Gyne

118

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Section: Association Of Placental Lesions With Pesupporting

confidence: 81%

Section: Pooled and Population Prevalence Of Histological Lesionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Placental histopathology associated with pre‐eclampsia: systematic review and meta‐analysis

Falco

Sivanathan

Laoreti

et al. 2017

Ultrasound in Obstet & Gyne

118

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“…[22][23][24][25][26] It has also been suggested that women with chronic hypertension or diabetes mellitus develop PE in the context of smaller increments of sFlt and sEng, because there is already preexisting maternal endothelial cell dysfunction. 27 Our finding of more significant alterations in angiogenic factors in early versus late-onset SPE are consistent with reports that more severe placental dysfunction distinguishes early onset from late-onset SPE in women without preexisting hypertension.…”

Section: Discussionmentioning

confidence: 99%

Angiogenic Factors in Superimposed Preeclampsia

et al. 2012

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Abstract-Imbalances in circulating angiogenic factors contribute to the pathogenesis of preeclampsia. To characterize levels of angiogenic factors in pregnant women with chronic hypertension, we prospectively followed 109 women and measured soluble fms-like tyrosine kinase 1 (sFlt1), soluble endoglin, and placental growth factor at 12, 20, 28, and 36 weeks' gestation and postpartum. Superimposed preeclampsia developed in 37 (34%) and was early onset (Ͻ34 weeks) in 9 and later onset (Ն34 weeks) in 28. Circulating levels of sFlt1 and the ratio of sFlt1 to placental growth factor were higher before clinical diagnosis at 20 weeks' gestation in women who subsequently developed early onset preeclampsia between 28 and 34 weeks compared with levels in women who never developed preeclampsia (Pϭ0.001) or who developed late-onset preeclampsia (Pϭ0.001). Circulating levels of sFlt1, soluble endoglin, and the ratio of sFlt1:placental growth factor were also significantly higher, and placental growth factor levels were significantly lower at the time of clinical diagnosis of superimposed preeclampsia in women with either early or late-onset superimposed preeclampsia compared with levels at similar gestational ages in those with uncomplicated chronic hypertension. We conclude that alterations in angiogenic factors are detectable before and at the time of clinical diagnosis of early onset superimposed preeclampsia, whereas alterations were observed only at the time of diagnosis in women with late-onset superimposed preeclampsia. Key Words: superimposed preeclampsia Ⅲ angiogenic factors Ⅲ chronic hypertension in pregnancy P reeclampsia (PE), a syndrome that manifests in the latter half of pregnancy and is characterized by maternal hypertension and proteinuria, develops in Ϸ3% to 5% of pregnant women. 1 PE may also develop in women with chronic (preexisting) hypertension and occurs 3 to 5 times more frequently compared with women who are normotensive at conception. [2][3][4] The diagnosis of superimposed PE (SPE) is often difficult, because women already have hypertension and some even have proteinuria. SPE is associated with even greater maternal and fetal morbidity and mortality than PE in women without preexisting hypertension. 2,5 The pathogenesis of PE, as well as SPE, is likely to involve placental vascular remodeling, leading to defective placentation, 6,7 placental ischemia, 8,9 and maternal endothelial cell dysfunction. 10 Emerging data suggest that placental ischemia is associated with increased production of placental proteins, which, on release into the maternal circulation, cause maternal systemic inflammation and endothelial cell dysfunction. 11,12 In particular, an imbalance in circulating proangiogenic and antiangiogenic factors released by the hypoxic placenta has gained currency as a critical link between placental dysfunction and several maternal manifestations of PE, particularly endothelial dysfunction and proteinuria. 13 Results from clinical trials suggest that the soluble forms of the vascular endothelial ...

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“…In general, it is thought that early-onset PE involves a placental defect, which is not as evident in late-onset PE. It appears that late-onset PE involved a different inflammatory component [34]. The impaired trophoblastic invasion of the placental bed and the following cascade in the early onset of PE might already determine the severity of the disease, and external factors like TRAP become less obvious.…”

Section: Discussionmentioning

confidence: 99%

Development of Late-Onset Preeclampsia in Association with Road Densities as a Proxy for Traffic-Related Air Pollution

Ries²,

Proietti³

et al. 2015

Fetal Diagn Ther

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Introduction: Previous epidemiological studies indicate an association between maternal exposure to air pollution and an increased risk of hypertensive disorders in pregnancy. We analyzed the association between the occurrence of mild/severe and early-/late-onset preeclampsia (PE) and traffic-related air pollution (TRAP). Materials and Methods: Based on retrospective data, 50 pregnant women with PE were selected and matched with a control group of healthy pregnant women according to their age, parity, and number of fetuses. The total length of major roads around the women's home within a radius of 100, 200, 300, and 500 m and the distances from the domicile to the nearest ‘first class' main road and freeway were used as a proxy indicator of TRAP. We compared a PE subgroup and control group in terms of their exposure to TRAP. Results: Late-onset PE cases showed a significantly higher occurrence with density of major roads within a radius of 100-300 m compared to early onset cases (p = 0.006; 0.02; 0.04). In addition, a significantly shorter distance to the nearest ‘first class' main road was observed in late-onset PE cases (p = 0.0078). Conclusions: Exposure to TRAP during pregnancy was associated with an increased risk for the development of late-onset PE.

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Are Early and Late Preeclampsia Distinct Subclasses of the Disease—What Does the Placenta Reveal?

Abstract: The early- and late-onset preeclampsia placentas showed clear histopathological differences, whereas late-onset preeclampsia and normal term placentas differed less. These findings support the contention that early- and late-onset preeclampsia are different subclasses of disease.

Cited by 94 publications

References 22 publications

Placental histopathology associated with pre‐eclampsia: systematic review and meta‐analysis

Placental histopathology associated with pre‐eclampsia: systematic review and meta‐analysis

Angiogenic Factors in Superimposed Preeclampsia

Development of Late-Onset Preeclampsia in Association with Road Densities as a Proxy for Traffic-Related Air Pollution

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