Is 'pre-eclampsia' simply a response to the side effects of a placental tachykinin?

Page, NM; Lowry, P. J.

doi:10.1677/joe.0.1670355

Cited by 23 publications

(16 citation statements)

References 70 publications

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“…This specific pregnancy disorder can be the result of multiple mechanisms of disease [9,10,13,16,20,21,25,32–36,42,43,46,47,53,56,57,59,64–66,70,78,80–82,84,87,88,91,102,105,111,112,116,120,123,129,134,136,144,154], is adaptive in nature [2,15,44,96,97,113,135] and has a long subclinical phase [19,22,63,67,68,98,100,122, 125,140,145]. Due to its syndromic nature, several attempts have been made to classify patients with PE into distinct subgroups in order to improve un derstanding of its pathophysiology [148–150,153], predict maternal/fetal complications [4,27,89,124,126] and to develop individualized preventive or therapeutic interventions [11,23,128,138].…”

Section: Introductionmentioning

confidence: 99%

Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia

Oggè

Chaiworapongsa²,

Romero

et al. 2011

Journal of Perinatal Medicine

238

145

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Objective Preeclampsia (PE) has been classified into early- and late-onset disease. These two phenotypic variants of PE have been proposed to have a different pathophysiology. However, the gestational age cut-off to define ‘early’ versus ‘late’ PE has varied among studies. The objective of this investigation was to determine the prevalence of lesions consistent with maternal underperfusion of the placenta in patients with PE as a function of gestational age. Study design A nested case-control study of 8,307 singleton pregnant women who deliver after 20 weeks of gestation was constructed based on a cohort. Cases were defined as those with PE (n=910); controls were pregnant women who did not have a hypertensive disorder in pregnancy (n=7,397). The frequency of maternal underperfusion of the placenta (according to the criteria of the Society for Pediatric Pathology) was compared between the two groups. Logistic regression was used for analysis. Estimated relative risks were calculated from adjusted odds ratios. Results 1) The prevalence of lesions consistent with maternal underperfusion was higher in patients with PE than in the control group [43.3% vs. 15.9%; unadjusted odds ratio 4.0 (95% CI 3.5–4.7); P<0.001]; 2) the estimated relative risk of maternal underperfusion lesions in PE was higher than in the control group; 3) the lower the gestational age at delivery, the higher the relative risk for these lesions; 4) early-onset PE, regardless of the gestational age used to define it (<32, 33, 34, 35 or 37 weeks) had a significantly higher frequency of placental lesions consistent with maternal underperfusion than late-onset PE (p<0.001 for all). Conclusions 1) The earlier the gestational age of preeclampsia at delivery, the higher the frequency of placental lesions consistent with maternal underperfusion; 2) our data suggests that demonstrable placental involvement as determined by pathologic examination differs in early- and late-onset preeclampsia; and 3) this phenomenon appears to be a continuum, and we could not identify a clear and unambiguous gestational age at which lesions consistent with underperfusion would not be present.

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Section: Introductionmentioning

confidence: 99%

Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia

Oggè

Chaiworapongsa²,

Romero

et al. 2011

Journal of Perinatal Medicine

238

145

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“…The expression of the gene TAC3 encoding NKB was found to be significantly higher in the preeclamptic placenta, suggesting that this might play a role in the mechanism leading to the increased circulating NKB levels in PE plasma [17]. Thus Page and Lowry [18] postulated that excessive placental secretion of NKB during the third trimester of pregnancy was associated with PE. Wareing et al [19] found no evidence that NKB could alter the vasoactive responsiveness of rat mesenteric arteries.…”

Section: Discussionmentioning

confidence: 99%

Third trimester plasma neurokinin B levels in women with and without preeclampsia

Geissbühler

Hillermann

Czarniecki

et al. 2008

The Journal of Maternal-Fetal & Neonatal Medicine

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“…Interestingly, their results also contained one to three women in each group of ten (weeks 11-13, 14-17, 22-26) who had levels of NKB substantially higher than the mean at 37-40 weeks although none of their women went on to develop pre-eclampsia. This perhaps indicated that they had identified pregnant women who were secreting 'corrective' levels of NKB into their maternal bloodstreams [11]. Sakamoto et al [25] showed similar increasing levels of NKB, but did find these to be significant, between weeks 24-35 and 36-40, when compared to non-pregnant women.…”

Section: Does Nkb Have Any Diagnostic Value?mentioning

confidence: 99%

“…The placenta was found to express unusually high levels of TAC 3 that encodes NKB [11], a gene previously believed not to be expressed in any peripheral tissue [12]. This expression was located to the outer syncytiotrophoblasts in an ideal position for secretion into the maternal blood [6].…”

Section: Introductionmentioning

confidence: 99%

“…In terms of a marker, placental NKB appeared to have several advantages over other candidate markers as it appeared not only unique to pre-eclampsia but also to pregnancy and was not associated with other known hypertensive disorders [5]. In addition, evidence from the infusion of high doses of NKB into female rats indicated that NKB might be involved in some of the haemodynamic events of pre-eclampsia [6,11]. Here, NKB was found to cause substantial pressor activity (believed initiated through the NKB preferred receptor NK3) and a 37% gain in uterine weight providing indirect evidence for an increase in blood supply to the uterus [6].…”

Section: Introductionmentioning

confidence: 99%

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Neurokinin B and pre-eclampsia: a decade of discovery

Page

2010

Reprod Biol Endocrinol

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At the start of the last decade, we provided evidence that levels of the peptide neurokinin B were highly elevated in pre-eclampsia. We hypothesized that elevated levels of neurokinin B may be an indicator of pre-eclampsia and that treatment with certain neurokinin receptor antagonists may be useful in alleviating the symptoms. At the time of the original hypothesis many questions remained outstanding. These included - Does neurokinin B have any diagnostic value in the detection and diagnosis of pre-eclampsia? - What is the cause of the elevated levels of neurokinin B during pre-eclampsia? - What is the physiological significance of neurokinin B in the placenta? This review discusses the answers to these questions taking into account the subsequent developments of the past ten years and analyzing the plethora of discoveries that have arisen from those initial observations.

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Is 'pre-eclampsia' simply a response to the side effects of a placental tachykinin?

Cited by 23 publications

References 70 publications

Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia

Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia

Third trimester plasma neurokinin B levels in women with and without preeclampsia

Neurokinin B and pre-eclampsia: a decade of discovery

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