Perinatal outcome of placental massive perivillous fibrin deposition: a case–control study

Devisme, Louise; Chauvière, Claire; Franquet-Ansart, Hélène; Chudzinski, Anastasia; Stichelbout, Morgane; Houfflin‐Debarge, V.; Subtil, D.

doi:10.1002/pd.5013

Cited by 23 publications

(24 citation statements)

References 26 publications

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“…Diffuse hyperechogenic lesions increasing with advancing gestation 134,143,144 Burton. Placental-derived fetal growth restriction.…”

Section: Ultrasoundmentioning

confidence: 99%

“…138 On ultrasound, these lesions appear as diffuse hyperechogenic lesions increasing in size with advancing gestation. 134,143,144 Placental vascular lesions associated with FGR have been known to present with abnormally high levels of maternal serum alpha-fetoprotein and human chorionic gonadotrophin at 15-18 weeks of gestation. 125,[145][146][147] There is also an association between the vasculopathies of the spiral arterioles leading to preeclampsia and FGR, a placental jellylike ultrasound appearance and high maternal serum alpha-fetoprotein levels at 18-28 weeks.…”

Section: Expert Reviewsmentioning

confidence: 99%

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Pathophysiology of placental-derived fetal growth restriction

Burton

Jauniaux

2018

American Journal of Obstetrics and Gynecology

670

475

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Placental-related fetal growth restriction arises primarily due to deficient remodeling of the uterine spiral arteries supplying the placenta during early pregnancy. The resultant malperfusion induces cell stress within the placental tissues, leading to selective suppression of protein synthesis and reduced cell proliferation. These effects are compounded in more severe cases by increased infarction and fibrin deposition. Consequently, there is a reduction in villous volume and surface area for maternal-fetal exchange. Extensive dysregulation of imprinted and nonimprinted gene expression occurs, affecting placental transport, endocrine, metabolic, and immune functions. Secondary changes involving dedifferentiation of smooth muscle cells surrounding the fetal arteries within placental stem villi correlate with absent or reversed end-diastolic umbilical artery blood flow, and with a reduction in birthweight. Many of the morphological changes, principally the intraplacental vascular lesions, can be imaged using ultrasound or magnetic resonance imaging scanning, enabling their development and progression to be followed in vivo. The changes are more severe in cases of growth restriction associated with preeclampsia compared to those with growth restriction alone, consistent with the greater degree of maternal vasculopathy reported in the former and more extensive macroscopic placental damage including infarcts, extensive fibrin deposition and microscopic villous developmental defects, atherosis of the spiral arteries, and noninfectious villitis. The higher level of stress may activate proinflammatory and apoptotic pathways within the syncytiotrophoblast, releasing factors that cause the maternal endothelial cell activation that distinguishes between the 2 conditions. Congenital anomalies of the umbilical cord and placental shape are the only placental-related conditions that are not associated with maldevelopment of the uteroplacental circulation, and their impact on fetal growth is limited.

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“…Diffuse hyperechogenic lesions increasing with advancing gestation 134,143,144 Burton. Placental-derived fetal growth restriction.…”

Section: Ultrasoundmentioning

confidence: 99%

Section: Expert Reviewsmentioning

confidence: 99%

Pathophysiology of placental-derived fetal growth restriction

Burton

Jauniaux

2018

American Journal of Obstetrics and Gynecology

670

475

View full text Add to dashboard Cite

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“…Yet, changes in placental histology are frequently reported in such pregnancy complications. The changes include placental lesions, which comprise chronic inflammatory lesions, massive fibrin deposition and maternal vascular malperfusion (Pathak et al 2011;Kim et al 2015;Devisme et al 2017;Wright et al 2017). Villitis of unknown aetiology (VUE) is one of the key placental inflammatory lesions (Kim et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Abnormal placental CD8⁺ T‐cell infiltration is a feature of fetal growth restriction and pre‐eclampsia

Lager

Sovio

Eddershaw

et al. 2020

The Journal of Physiology

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Placental pathological abnormalities are more frequently observed in complicated pregnancies than in healthy pregnancies. r Infiltration of CD8 + T-cells into the placental villous tissue occurred in both fetal growth restriction and pre-eclampsia, whereas CD79α + B-cell infiltration was only apparent with reduced fetal growth. r Vascularization, fibrin depositions, macrophage and neutrophil infiltration in the placenta did not differ between healthy and complicated pregnancies.

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“…Massive perivillous fibrin deposition is usually observed in patients with antiphospholipid syndrome, 20,21 in which antiphopholipid antibodies downregulate trophoblast expression of endogenous annexin V, which results in blood coagulation on the surface of trophoblasts. 22 As in the current case, MPVFD was observed in patients with SLE with double-positivity for lupus anticoagulant and anticardiolipin antibody.…”

Section: Discussionmentioning

confidence: 99%

Peculiar blood flow profiles among placental chorionic villous vessels of an abnormally thick placenta in a case of systemic lupus erythematosus characterized using microvascular imaging

Inoue

Horinouchi

Yoshizato

et al. 2020

J of Obstet and Gynaecol

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We present a patient with systemic lupus erythematosus receiving long-term steroid therapy, who had myometrial thinning, markedly thickened placenta, and fetal growth restriction (FGR). Blood flow profiles of the myometrium, decidua and placental villous vessels (VV) were described using superb microvascular imaging (SMI) at 35 weeks' gestation. Images showed no decidual blood flow underneath the placenta sitting on a thin myometrium and sparse VV distribution and non-visualization of peripheral VV flow. Emergency cesarean hysterectomy was performed at 36 weeks. Histological findings showed missing decidua on the thin myometrium, which indicated placenta accreta spectrum, and massive perivillous fibrin deposition and increased numbers of syncytial knots in the placenta. We speculated that the thick placenta and peculiar VV flow profiles resulted from congestion of the intervillous space and intervillous underperfusion/low intraplacental oxygenation, respectively, resulting in FGR. Superb microvascular imaging is useful for diagnosing placenta accreta spectrum and understanding the pathophysiology of thick placenta and FGR.

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Perinatal outcome of placental massive perivillous fibrin deposition: a case–control study

Cited by 23 publications

References 26 publications

Pathophysiology of placental-derived fetal growth restriction

Pathophysiology of placental-derived fetal growth restriction

Abnormal placental CD8⁺ T‐cell infiltration is a feature of fetal growth restriction and pre‐eclampsia

Peculiar blood flow profiles among placental chorionic villous vessels of an abnormally thick placenta in a case of systemic lupus erythematosus characterized using microvascular imaging

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Perinatal outcome of placental massive perivillous fibrin deposition: a case–control study

Cited by 23 publications

References 26 publications

Pathophysiology of placental-derived fetal growth restriction

Pathophysiology of placental-derived fetal growth restriction

Abnormal placental CD8+ T‐cell infiltration is a feature of fetal growth restriction and pre‐eclampsia

Peculiar blood flow profiles among placental chorionic villous vessels of an abnormally thick placenta in a case of systemic lupus erythematosus characterized using microvascular imaging

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Abnormal placental CD8⁺ T‐cell infiltration is a feature of fetal growth restriction and pre‐eclampsia