2002
DOI: 10.1111/j.1471-0528.2002.01045.x
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Does endothelial cell activation occur with intrauterine growth restriction?

Abstract: It is possible that in fetal growth restriction without pre-eclampsia endothelial cell activation does not occur. This might be either because there is no release of 'factor X' or because of maternal resistance to its effects. To test this hypothesis, we took blood samples from 26 women with pre-eclampsia (without fetal growth restriction), 13 women with fetal growth restriction (without pre-eclampsia) and 24 normal pregnant controls, and measured the circulating levels of three markers of endothelial cell act… Show more

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Cited by 70 publications
(29 citation statements)
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“…Although the pathogenesis of PIH is poorly understood, the role of the placenta in mediating PIH is well accepted, as the condition is resolved upon delivery of the placenta following childbirth. While the association between angiogenic factors and PIH has been recently discovered (9)(10)(11), numerous reports highlight the proposed contribution of leukocyte activation and several proinflammatory cytokines to the development of PIH, including TNFα (TNF), IL-6, IL-1 receptor antagonist, and IL-8 (12)(13)(14)(15)(16)(17)(18). Further studies implicate a generalized phenomenon of maternal immune cell activation via NFκB, a critical regulator of inflammation (19,20).…”
Section: Introductionmentioning
confidence: 99%
“…Although the pathogenesis of PIH is poorly understood, the role of the placenta in mediating PIH is well accepted, as the condition is resolved upon delivery of the placenta following childbirth. While the association between angiogenic factors and PIH has been recently discovered (9)(10)(11), numerous reports highlight the proposed contribution of leukocyte activation and several proinflammatory cytokines to the development of PIH, including TNFα (TNF), IL-6, IL-1 receptor antagonist, and IL-8 (12)(13)(14)(15)(16)(17)(18). Further studies implicate a generalized phenomenon of maternal immune cell activation via NFκB, a critical regulator of inflammation (19,20).…”
Section: Introductionmentioning
confidence: 99%
“…Preeclampsia (PE) and small for gestational age (SGA) neonates share several mechanisms of disease, such as chronic uteroplacental ischemia [1][2][3][4][5][6][7][8] and endothelial cell dysfunction [9][10][11][12][13][14][15]. However, it is unclear why pregnant women with similar insults develop PE, while others deliver an SGA neonate but do not develop PE.…”
Section: Introductionmentioning
confidence: 99%
“…SGA is considered a syndrome because smallness at birth can be caused by many factors, including defective placentation [8,51], infection [52,53], chromosomal anomalies [54,55], genetic disorders [56][57][58], and environmental factors [59] such as smoking [60,61], alcohol exposure [62], and cocaine use [63]. Moreover, in a subset of patients without preeclampsia with SGA fetuses, there is also evidence of leukocyte activation [64] as well as endothelial cell dysfunction [65][66][67].…”
Section: Introductionmentioning
confidence: 99%