Massive perivillous fibrinoid causing recurrent placental failure

Abstract

Objective To establish the incidence, recurrence rate and consequences of massive perivillous fibrinoid.Design Retrospective analysis of the histology of all placentas with a diagnosis of massive perivillous fibrinoid between 1991 and 1998, together with the maternal case records. Setting The histopathology department of the Rotunda Hospital, Dublin, Ireland.Population A relatively homogeneous group of pregnant women in the northern part of Dublin City, which is the catchment area for the Rotunda Hospital, delivered between 1991 and 1998. Methods Retrospective review of archival placental pathology and maternal charts.Main outcome measures The incidence of massive perivillous fibrinoid, perinatal outcome and recurrence rate. Results The incidence of massive perivillous fibrinoid was 0.028%, with a recurrence rate of approximately 18%. All the infants suffered intrauterine growth restriction; there was a 31% fetal loss rate and a 33% preterm delivery rate. Conclusions Massive perivillous fibrinoid is associated with intrauterine death, intrauterine growth restriction and preterm delivery. It has a significant recurrence rate and both the clinical findings of intrauterine growth restriction and the postmortem findings imply a syndrome of chronic placental insufficiency.

Evidence of an imbalance of angiogenic/antiangiogenic factors in massive perivillous fibrin deposition (maternal floor infarction): a placental lesion associated with recurrent miscarriage and fetal death

“…4 Naeye et al described an association between MPFD and stillbirth as well as fetal growth restriction. 4 Subsequently, additional case reports and case series have reported this pathologic finding in pregnancies with spontaneous abortion, 1, 5 spontaneous preterm delivery, 2, 5 and early-onset fetal growth restriction. 2 In a case-series reported by Andres et al, among 60 pregnancies with MPFD, the prevalence of fetal death was 40% and among the live-born infants, 40% delivered preterm and 58% had birthweights below 10 th percentile for gestational age.…”

“…2 Similarly, in many cases included in the current study, patients had prior poor pregnancy outcomes, although placental pathology was not available for review. The strong association between MPFD and serious adverse pregnancy outcomes such as fetal death, 2, 4-7, 10, 11, 13-16 fetal growth restriction 1, 2, 4, 6-12 or recurrent miscarriage 4, 5, 10 strengthens the value of placental pathologic examination in such cases. If MPFD is diagnosed, subsequent pregnancies are also at risk for these complications.…”

“…1 This condition was first described by Benirschke and Driscoll in 1967 and its frequency is 0.09-0.5%. 1-4 MPFD is associated with recurrent serious adverse pregnancy outcomes including spontaneous abortion, 1, 5 fetal growth restriction, 1, 2, 4, 6-12 and fetal death. 2, 4-7, 10, 11, 13-16 The proposed etiologies include autoimmunity (such as anti-phospholipid 6, 10, 11 or anti-urokinase antibodies) 6 and cytotoxicity due to proliferation of “X-cells” which are extravillous trophoblasts that can produce major basic protein similar to that of eosinophil granules.…”

Perivellosa disease massive fibrin deposition, association with Down syndrome: case report and literature review

“…1 It is a disease with high morbidity, mortality and obstetric likelihood of recurrence; In relation to the infant also increases neonatal morbidity and mortality in later stages have been documented neurodevelopmental disorders. The etiology is unknown so far, most theories agree on an immunological component responsible for the pathogenesis.…”

Increasing of Syncytial Knot and Fibrinoid Deposit in High-Cd Accumulated Human Placentas

“…Additionally, an aggregation of syncytiotrophoblast (STB) cells which is called syncytial knot (STK) is considered as Cd-induced morphological changes Akbulut et al, 2009) which is resulted from hypoxia (Heazell et al, 2007). Moreover, other histological findings such as fibrinoid deposit (Fd) (Kaufmann et al, 1996;Bane & Gillian, 2003), and polymorphonuclear (PMN) cell infiltration in chorionic plate (histological chorioamnionitis; HCA) (Murtha et al, 2002;Redline et al, 2003) and in basal plate (decidual inflammation) were considered as histopathologies in placenta as well. Furthermore, Cd has pro-inflammatory properties, which induce chemokine IL-8 recruiting neutrophil and macrophage (Olszowski et al, 2012).…”