Classification of placental lesions

Redline, Raymond W.

doi:10.1016/j.ajog.2015.05.056

Cited by 357 publications

(264 citation statements)

References 62 publications

(49 reference statements)

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“…4 F, uterine tenderness, fetal tachycardia (fetal heart rate >160 beats per min), and/or (placental) histologic criteria compatible with inflammation. [17][18][19] Women with preexisting medical conditions such as thyroid insufficiency, chronic hypertension, or diabetes mellitus were excluded from the case and the control groups. Other exclusion criteria included premature rupture of membranes and/or fetal anomaly.…”

Section: Methodsmentioning

confidence: 99%

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Gormley

Ona

Kapidzic

et al. 2017

American Journal of Obstetrics and Gynecology

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BACKGROUND:The maternal signs of preeclampsia, which include the new onset of high blood pressure, can occur because of faulty placentation. We theorized that transcriptomic analyses of trophoblast subpopulations in situ would lend new insights into the role of these cells in preeclampsia pathogenesis. OBJECTIVE: Our goal was to enrich syncytiotrophoblasts, invasive cytotrophoblasts, or endovascular cytotrophoblasts from the placentas of severe preeclampsia cases. Total RNA was subjected to global transcriptional profiling to identify RNAs that were misexpressed compared with controls. STUDY DESIGN: This was a cross-sectional analysis of placentas from women who had been diagnosed with severe preeclampsia. Gestational age-matched controls were placentas from women who had a preterm birth with no signs of infection. Laser microdissection enabled enrichment of syncytiotrophoblasts, invasive cytotrophoblasts, or endovascular cytotrophoblasts. After RNA isolation, a microarray approach was used for global transcriptional profiling. Immunolocalization identified changes in messenger RNA expression that carried over to the protein level. Differential expression of noneprotein-coding RNAs was confirmed by in situ hybridization. A 2-way analysis of variance of non-coding RNA expression identified particular classes that distinguished trophoblasts in cases vs controls. Cajal body foci were visualized by coilin immunolocalization. RESULTS: Comparison of the trophoblast subtype data within each group (severe preeclampsia or noninfected preterm birth) identified many highly differentially expressed genes. They included molecules that are known to be expressed by each subpopulation, which is evidence that the method worked. Genes that were expressed differentially between the 2 groups, in a cell-typeespecific manner, encoded a combination of molecules that previous studies associated with severe preeclampsia and those that were not known to be dysregulated in this pregnancy

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Section: Methodsmentioning

confidence: 99%

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Gormley

Ona

Kapidzic

et al. 2017

American Journal of Obstetrics and Gynecology

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“…The process begins in the subchorionic fibrin and at the membranous choriodecidual interface, extends to the fibrous chorion and amnion, and finally necrosis of the amniotic epithelium occurs. 20 Then, acute funisitis develops with involvement, in first instance, of the umbilical vein (phlebitis), which exhibits a higher expression of interleukin (IL)-8 mRNA and a pattern of gene expression suggestive of a greater predisposition to a proinflammatory response in comparison to arteries. Thereafter, polymorphonuclear (PMN) cells infiltrate arteries (arteritis), and the concentration of umbilical cord IL-6 increases, which is a marker of severity and is associated with a poorer infant prognosis.…”

mentioning

confidence: 99%

Chorioamnionitis and neonatal morbidity: current perspectives

Henríquez¹,

Rodrigo²

2017

RRN

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Abstract:The term chorioamnionitis (CA) is commonly used to refer to different clinical or pathological conditions characterized by an infectious and/or inflammatory process that affects primarily the chorioamniotic membranes, but also the amniotic fluid, vessels of the chorionic plate, and, eventually, the umbilical cord (funisitis) and the fetus. Its incidence is higher at lower gestational ages, and the main mechanism is believed to be the ascending bacterial infection from the maternal genital tract. It can be diagnosed by clinical criteria, amniotic fluid examination for inflammatory mediators, and/or isolation of microorganisms, or by histopathological examination of the placenta. CA is an important cause of stillbirth and is related to an increased incidence of premature rupture of membranes, preterm delivery, and adverse maternal and neonatal outcomes such as early-onset neonatal sepsis and necrotizing enterocolitis. An independent causal association to other neonatal morbidities is more controversial. The heterogeneity in the diagnostic criteria and in the operative definitions for morbidity makes comparison of studies difficult, and results are inconsistent. In addition, the intensity and duration of the process are usually not considered. For all these reasons, evidence-based recommendations for the management of mother and infant under these circumstances are difficult to establish, and clinical practice varies widely.

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“…This study formed part of an institutional audit into the need for placental pathology. Using Redman's classification, placental pathology was characterized according to histological lesions, signifying either inflammatory or vascular pathology, or indeed confirming a normal placenta [11,12] The criteria for each category are summarised in Table 1.1.…”

Section: Methodsmentioning

confidence: 99%

“…Pathological lesions were categorized according to Redman's classification as signifying either vascular pathology relating to maternal malperfusion or intrauterine inflammation, each with important clinical applications [11,12].…”

Section: Introductionmentioning

confidence: 99%

Placental inflammation and its relationship to cervicovaginal fetal fibronectin in preterm birth

Krogt¹,

Ridout

Seed

et al. 2017

European Journal of Obstetrics & Gynecology and Reproductiv

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words Main text word count: 1864 words Condensation: 25words:There is a significant association between a positive fetal fibronectin and inflammatory placental pathology. Infective morbidity may be increased in women with a raised quantitative fFN who deliver preterm. Short title: Placental inflammation and fFN in women who deliver preterm Abstract ObjectiveLate miscarriage and preterm birth are frequently thought to be associated with inflammation and infection, although in most cases the underlying cause of early delivery remains unknown. The placenta is the organ that links mother and fetus during pregnancy, and postnatal examination may provide useful information about pathophysiology.The relationship between placental pathological lesions and predictive markers of early delivery has not been explored. We sought to characterize preterm deliveries according to placental pathology and relate these to the performance of reliable predictive markers, fetal fibronectin and cervical length. Study DesignThis is a retrospective subanalysis from a larger prospective cohort study on sonographic cervical length, quantitative fetal fibronectin and risk of spontaneous preterm birth. Our cohort was comprised of high-risk asymptomatic women attending the Prematurity Surveillance Clinic at St Thomas' Hospital between 2002 and 2015, who went on to have a late miscarriage or preterm delivery (16 to 36 +6 weeks') and who had available placental histology.The placental pathology of these preterm deliveries was characterized according to the lesions identified, and categorized (according to the Redman classification) into inflammatory (e.g. chorioamnionitis) or non-inflammatory (histologically normal or vascular lesions indicating e.g. malperfusion).We sought to relate placental findings to the performance of reliable predictive markers, in women who delivered early. Standard clinical cut offs for cervical length (< 25mm) and fetal fibronectin (>50 ng/mL) were used to identify the proportion of preterm births that were accurately predicted by the tests or who showed a false negative result, in relation to their placental histology findings. Binomial logistic regression was carried out to evaluate the relationship between placental inflammation, quantitative fFN and cervical length as continuous variables. Results105 women who had a late miscarriage or preterm delivery (16-36 +6 weeks') and available placenta pathology were identified. 66% (42/64) of those with inflammatory placental pathology had a positive fetal fibronectin swab result compared to 15% (6/41) of those with noninflammatory placental pathology (chi-squared 25.9, 95% CI 31.5 to 65.6, p<0.0001).A logistic regression model subanalysis of women in whom both CL and quantitative fFN results were available (n=66) revealed a highly statistically significant relationship with inflammatory placental lesions (p=0.003 and p=0.001 respectively). Placental inflammation was found to be associated with both increasing levels of fFN and a shortening cervix. ConclusionThere...

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Classification of placental lesions

Cited by 357 publications

References 62 publications

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Chorioamnionitis and neonatal morbidity: current perspectives

Placental inflammation and its relationship to cervicovaginal fetal fibronectin in preterm birth

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