Chronic villitis of unknown etiology and maternal arterial lesions in preeclamptic pregnancies

Labarrere, Carlos A.; Althabe, Omar

doi:10.1016/0028-2243(85)90077-2

Cited by 67 publications

(30 citation statements)

References 17 publications

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“…However, extensive involvement of the placenta by VUE has been associated with preterm and term fetal growth restriction 5,6,15,53,65,81–87 , spontaneous preterm delivery 15,85,88 , small for gestational age (SGA) associated with preeclampsia 15,82,89,90 , and fetal death 6,15,52,65,91 . The frequency of VUE in the “great obstetrical syndromes” 92–94 is displayed in Figure 6.…”

Section: Chronic Nonspecific Villitis (Villitis Of Unknown Etiologymentioning

confidence: 99%

Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance

Kim

Romero

Chaemsaithong

et al. 2015

American Journal of Obstetrics and Gynecology

420

308

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Chronic inflammatory lesions of the placenta are characterized by the infiltration of the organ by lymphocytes, plasma cells and/or macrophages, and may result from infections (viral, bacterial, parasitic) or be of immune origin (maternal anti-fetal rejection). The three major lesions are villitis (when the inflammatory process affects the villous tree), chronic chorioamnionitis (which affects the chorioamniotic membranes), and chronic deciduitis (which involves the decidua basalis). Maternal cellular invasion is a common feature of the lesions. Villitis of unknown etiology (VUE) is a destructive villous inflammatory lesion characterized by the infiltration of maternal T cells (CD8+ cytotoxic T cells) into chorionic villi. Migration of maternal T cells into the villi is driven by the production of T cell chemokines in the affected villi. Activation of macrophages in the villi has been implicated in the destruction of the villous architecture. VUE has been reported in association with preterm and term fetal growth restriction, preeclampsia, fetal death and preterm labor. Infants whose placentas have VUE are at risk for death and abnormal neurodevelopmental outcome at the age of 2. Chronic chorioamnionitis is the most common lesion in late spontaneous preterm birth and is characterized by the infiltration of maternal CD8+ T cells into the chorioamniotic membranes. These cytotoxic T cells can induce trophoblast apoptosis and damage the fetal membranes. The lesion is frequently accompanied by villitis of unknown etiology and evidence of maternal anti-fetal antibodies and deposition of complement in the umbilical vein. Chronic deciduitis consists of the presence of lymphocytes or plasma cells in the basal plate of the placenta. This lesion is more common in pregnancies resulting from egg donation and has been reported in a subset of patients with premature labor. Chronic placental inflammatory lesions are now considered to represent maternal anti-fetal rejection and this process can be associated with the development of a novel form of fetal systemic inflammatory response syndrome characterized by an elevation of the fetal plasma T cell chemokine (CXCL10). The evidence that maternal anti-fetal rejection may underlie the pathogenesis of many chronic inflammatory lesions of the placenta is reviewed. This article includes figures and histologic examples of all chronic inflammatory lesions of the placenta.

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Section: Chronic Nonspecific Villitis (Villitis Of Unknown Etiologymentioning

confidence: 99%

Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance

Kim

Romero

Chaemsaithong

et al. 2015

American Journal of Obstetrics and Gynecology

420

308

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“…Therefore, failure of transformation of the spiral arteries in the decidual segment represents a more severe disorder than lack of transformation of the myometrial segment only. Abnormal transformation of the decidual portion of the spiral arteries can be detected by examining the placental basal plate [33–35,37,39,41–45]. This has practical implications because the basal plate of the placenta is available for examination in all cases while a placental bed biopsy requires a specialized procedure generally performed during a cesarean delivery.…”

Section: Introductionmentioning

confidence: 99%

Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta

Labarrere

DiCarlo

Bammerlin

et al. 2017

American Journal of Obstetrics and Gynecology

131

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Background Failure of physiologic transformation of spiral arteries has been reported in preeclampsia, fetal growth restriction, fetal death, and spontaneous preterm labor with intact or ruptured membranes. Spiral arteries with failure of physiologic transformation are prone to develop atherosclerotic-like lesions of atherosis. There are striking parallels between preeclampsia and atherosclerotic disease, and between lesions of atherosis and atherosclerosis. Endothelial activation, identified by intercellular adhesion molecule-1 expression, is present in atherosclerotic-like lesions of heart transplantation and considered a manifestation of rejection. Similarly, endothelial activation/dysfunction has been implicated in the pathophysiology of atherosclerosis and preeclampsia. Intercellular adhesion molecule-1-overexpressing-activated endothelial cells are more resistant to trophoblast displacement than nonactivated endothelium and may contribute to shallow spiral artery trophoblastic invasion in obstetrical syndromes having failure of physiologic transformation. Objective To determine whether failure of spiral artery physiologic transformation was associated with activation of interstitial extravillous trophoblasts and/or spiral artery endothelium and presence of acute atherosis in the placental basal plate. Study Design A cross-sectional study of 123 placentas (19-42 weeks’ gestation) obtained from normal pregnancies (n = 22), preterm prelabor rupture of membranes (n = 26), preterm labor (n = 23), preeclampsia (n = 27), intrauterine fetal death (n = 15), and small for gestational age (n = 10) was performed. Failure of spiral artery physiologic transformation and presence of cell activation was determined using immunohistochemistry of placental basal plates containing a median of 4 (minimum: 1; maximum: 9) vessels per placenta. Endothelial/trophoblast cell activation was defined by the expression of intercellular adhesion molecule-1 (ICAM-1). Investigators examining microscopic sections were blinded to clinical diagnosis. Pairwise comparisons among placenta groups were performed with the Fisher’s exact and Wilcoxon rank sum tests using a Bonferroni-adjusted level of significance (.025). Results 87% (94/108) of placentas having spiral arteries with failure of physiologic transformation (actin-positive and cytokeratin-negative) in the basal plate, and 0% (0/15) of placentas having only spiral arteries with complete physiologic transformation (cytokeratin-positive and actin-negative), had arterial endothelial and/or interstitial extravillous trophoblasts reactive with the ICAM-1 activation marker (P < .001). A significant correlation (R2 = 0.84) was found between expression of spiral artery endothelial and interstitial extravillous trophoblast ICAM-1 (P < .001) in activated placentas. Lesions of atherosis were found in 31.9% (30/94) of placentas with complete and/or partial failure of physiologic transformation of spiral arteries that were ICAM-1-positive, in none of the 14 placentas with failure of physiolog...

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“…Originally described in preeclampsia, acute atherosis has also been found in other complications of pregnancy including spontaneous preterm labor (sPTL)/premature prelabor rupture of membrane (PPROM) [50], fetal death [50], gestational diabetes mellitus [5,15,24,50], gestational and chronic hypertension [15,24,27,28,50], systemic lupus erythematosus, and antiphospholipid antibody syndrome [14,24,31,34,37], intrauterine fetal growth restriction (IUGR) [13,16,19,20,22,32,50]. It is rarely observed in normal pregnancy [3,4,21,30,43,50]. The presence of acute atherosis has also been associated with a more severe form of preeclampsia [4,46,50].…”

Section: Introductionmentioning

confidence: 99%

Placental lesions associated with acute atherosis

Kim

Chaemsaithong

Romero

et al. 2014

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Acute atherosis is a lesion of the spiral arteries characterized by fibrinoid necrosis of the vessel wall, an accumulation of fat-containing macrophages, and a mononuclear perivascular infiltrate, which can be found in patients with preeclampsia, fetal death, small-for-gestational age (SGA), spontaneous preterm labor/premature prelabor rupture of membrane, and spontaneous mid-trimester abortion. This lesion is thought to decrease blood flow to the intervillous space which may lead to other vascular lesions of the placenta. The objective of this study was to test whether there is an association between acute atherosis and placental lesions that are consistent with maternal vascular underperfusion, amniotic fluid infection, fetal vascular thrombo-occlusive disease or chronic inflammation. Material and methods A retrospective cohort study of pregnant women who delivered between July 1998 and July 2014 at Hutzel Women’s Hospital/Detroit Medical Center was conducted examine 16,457 placentas. The frequency of placenta lesions (diagnosed using the criteria of the Perinatal Section of the Society for Pediatric Pathology) was compared between pregnancies with and without atherosis. Results Among 16,457 women who were enrolled, 10.2% (1,671/16,457) were excluded, leaving 14,786 women who contributed data for analysis. Among them, the prevalence of acute atherosis was 2.2% (326/14,786). Women with acute atherosis were more than six times as likely as those without to have placental lesions consistent with maternal underperfusion (adjusted odds ratio- aOR: 6.7; 95% CI 5.2–8.6). To a lesser degree, acute atherosis was also associated with greater risks of having either lesions consistent with fetal vascular thrombo-occlusive disease (aOR 1.7; 95% CI 1.2–2.3) or chronic chorioamnionitis (aOR 1.9; 95% CI 1.3–3), but not with other chronic inflammatory lesions, after adjusting for gestational age at delivery. In contrast, women with acute atherosis were 60% less likely to have lesions consistent with amniotic fluid infecition, adjusting for gestational age at delivery (aOR 0.4; 95% CI 0.3–0.5). Conclusions Acute atherosis is associated with increased risks of having placental lesions consistent with maternal vascular underperfusion, and to a lesser extent, chronic chorioamnionitis and those consistent with fetal vascular thrombo-occlusive disease.

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Chronic villitis of unknown etiology and maternal arterial lesions in preeclamptic pregnancies

Cited by 67 publications

References 17 publications

Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance

Chronic inflammation of the placenta: definition, classification, pathogenesis, and clinical significance

Failure of physiologic transformation of spiral arteries, endothelial and trophoblast cell activation, and acute atherosis in the basal plate of the placenta

Placental lesions associated with acute atherosis

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