Placental Mesenchymal Dysplasia Research Articles

Zebras in a snowstorm: ultrasound guidance for differentiating placental mesenchymal dysplasia from hydatidiform mole

Zebras in a snowstorm: ultrasound guidance for differentiating placental mesenchymal dysplasia from hydatidiform mole

Placental mesenchymal dysplasia: A case report and review of literature.

Placental mesenchymal dysplasia is a rare disorder of the placenta with only a few reported cases. A case of interstitial dysplasia of the placenta was reported. The diagnosis and differential diagnosis were made by gross observation, microscopic findings, and immunohistochemistry.

Placental mesenchymal dysplasia associated with severe fetal growth restriction: A case report

Placental mesenchymal dysplasia associated with severe fetal growth restriction: A case report

Displasia mesenquimal placentaria. A propósito de un caso

Placental mesenchymal dysplasia is a rare condition that, due to placental characteristics, can be confused with a molar disease. Among the most frequent findings is an enlarged placenta and the presence of “grape-shaped vesicles”. The suspected diagnosis is made through ultrasound, but the definitive diagnosis will be given by the anatomo-pathological study. We present the case of a 30-year-old patient, IIG IP, who came at 30 weeks plus 4 days of gestation, who underwent an obstetric echosonogram showing a total occlusive central placenta with a large hydropic appearance, a transverse fetus with intrauterine growth restriction and later anhydramnios; for which obstetric resolution was decided by segmental cesarean section, obtaining a female newborn with a birth weight of 1,100 g and placenta with multiple vesicles, for which an anatomopathological study was carried out, that reported placental mesenchymal dysplasia.

Displasia mesenquimal placentaria

Placental mesenchymal dysplasia is a rare entity, confused with ultrasound and macroscopy with partial mole due to vesicular lesions and the presence of a fetus. Microscopy reveals hydropic trunk villi with great mesenchymal hyperplasia and prominent vascular lesions but without hyperplasia of the trophoblastic epithelium. The fetus, usually female, may be normal or present malformations, tumors or chromosomopathies. We present the study of four cases of placental mesenchymal dysplasia; three first-pregnancies, aged 39 and 20, and a second-pregnancy, aged 26. The oldest in the third trimester presented with preeclampsia and a female stillbirth with pulmonary and splenic anomalies, the other two presented vaginal bleeding and pelvic pain and one case was a finding in prenatal control at 8 weeks of gestation. In three cases, fetus and embryo were observed, two of them had a necropsy.

EP16.25: Placental mesenchymal dysplasia with normal fetus: a rare case report

EP16.25: Placental mesenchymal dysplasia with normal fetus: a rare case report

EP18.44: Diagnosis and management of pregnancy with placental mesenchymal dysplasia

EP18.44: Diagnosis and management of pregnancy with placental mesenchymal dysplasia

EP15.31: Placental mesenchymal dysplasia: a case of IUGR associated with veinous placental thrombosis

EP15.31: Placental mesenchymal dysplasia: a case of IUGR associated with veinous placental thrombosis

EP15.29: Case of placental mesenchymal dysplasia with fetal growth restriction, postnatal follow‐up and histopathological correlation

EP15.29: Case of placental mesenchymal dysplasia with fetal growth restriction, postnatal follow‐up and histopathological correlation

Placental Mesenchymal Dysplasia - Prenatal Diagnosis and Clinical Outcome

Placental mesenchymal dysplasia is an uncommon vascular anomaly of the placenta with characteristics of placentomegaly and multicystic appearance and with or without association with fetal chromosomal anomaly. In the beginning, it could be confused with a partial hydatidiform mole.

A Rare Case of Biparental Placental Mesenchymal Dysplasia: A Case Report and Literature Review [ID: 1336615

INTRODUCTION: Placental mesenchymal dysplasia (PMD) is a rare placental anomaly associated with high perinatal mortality; it is predominantly seen in female fetuses and very few cases have been reported. The evaluation of first- and second-trimester products of conception is of the utmost importance when assessing molar pathologies such as complete hydatidiform moles, partial hydatidiform moles, and nonmolar samples. METHODS: We report a monochorionic 46XX,69XXY pregnancy with placental mesenchymal dysplasia (PMD) with possible androgenetic biparental mosaicism etiology (Instituto Nacional de Perinatología Isidro Espinosa de los Reyes approval number P-270-18). RESULTS: The patient is a 28-year-old gravida 2, para 1, female with no notable past medical history. She had a previous pregnancy resulting in an uncomplicated abdominal delivery at 39 weeks of gestation 5 years prior. The patient was transferred to our health center at 24.2 weeks of gestation with a molar component because of USG data consistent with a probable hepatic tumor, perimembranous ventricular septal defect, and probable PMD. Ultrasound at 24.3 weeks of gestation demonstrated a single intrauterine pregnancy with one-third of the placenta appearing normal, the second third showing irregular cystic masses, and the remaining third with larger cysts. Placental mesenchymal dysplasia was diagnosed retrospectively based on data from the gross, histologic, and genetic components. CONCLUSION: To our knowledge, this is the first reported case of PMD with a 46XX,69XXY karyotype. A radical and cautious approach to PMD cases is needed because of the lack of sufficient data and reports.

Placental Mesenchymal Dysplasia Co-existing with High Grade Villitis of Unknown Aetiology (VUE): A Very Rare Case Report and Literature Review

The present case study reports about Placental mesenchymal dysplasia co-existing with high grade villitis of unknown aetiology (VUE). Placental Mesenchymal Dysplasia (PMD) is a rare placental lesion characterized by unusual abnormality of the stem villi of the placenta that could be mistaken for hydatidiform mole due to the presence of both cysts and normal-appearing parenchyma. A 30-year-old G2 P1 (full-term normal delivery) seen in fetal medicine clinic at 20 weeks within view of high risk on combined screening (low PAPP-A and high HCG). An ultrasound scan showed an appropriately grown baby with an abnormal placenta consisting of multiple lacunae more than 50% of the placental mass with increased thickness. A second opinion at tertiary care hospital confirmed the presence of prominent lakes on the placenta. Growth scans also showed IUGR with increasingly abnormal Doppler scans as the pregnancy progressed. At 35 weeks, EFW was < 3rd centile with static growth and patient had Induction of labour at 35 +4 weeks with vaginal delivery of a live male neonate weighing 2325g admitted to the neonatal intensive care unit (NICU) admission due to prematurity. The baby was discharged from NICU at day 5, achieving developmental milestones at the age of 23 weeks post-delivery. On microscopic histological examination, the chorionic plate showed no significant abnormality. The villous architecture was highly abnormal, and some villi were markedly enlarged with myxoid stroma and central degeneration. There were very occasional foci of apparent trophoblastic proliferation with villous architecture abnormalities seen in the form of clusters of large, immature intermediate villi. These features were in keeping with mesenchymal dysplasia. A highly unusual finding in this context was a florid infiltrate of CD3 positive T cells consistent with high-grade villitis of unknown aetiology concluding very rare co-existence of both conditions.

Placental mesenchymal dysplasia- A case report

Placental mesenchymal dysplasia is an underdiagnosed and a rare vascular anomaly of the placenta. It is characterized by the presence of grape-like vesicles, which, on ultrasonography gives the appearance of a partial mole. Histologically it can be differentiated by partial mole by the absence of trophoblastic proliferation. It is essential to make a correct diagnosis as the management and outcome of both these entities are vastly different. We present this case of placental mesenchymal dysplasia, not just because of its rarity but to highlight its radiological, gross and histopathological features to keep it in mind as a differential diagnosis and in making the correct diagnosis.

Complete hydatidiform mole with a coexisting foetus of term pregnancy: a case report and review of the literature

A case of a complete mole with a full term live foetus misdiagnosed as placental mesenchymal dysplasia prenatally is being reported here. The infant was delivered at term, and the placenta was accompanied with molar changes. Both the mother and baby were healthy with no complications at one-year follow-up. This report systematically summarises identification methods to reduce the rate of misdiagnosis for better pregnancy outcomes. Keywords: Complete hydatidiform mole; Twin pregnancy; Placental mesenchymal dysplasia; Gestational trophoblastic neoplasia.

Placental mesenchymal dysplasia complicated with sudden fetal demise and amniotic fluid embolism: a case report

Placenta mesenchymal dysplasia (PMD) is a rare placental anomaly associated with various fetal and maternal complications. Whether close ultrasound surveillance can prevent intrauterine fetal demise (IUFD) in patients with PMD is still under investigation. Amniotic fluid embolism (AFE) is a rare, lethal, and unpredictable maternal complication that has never been described in association with PMD. Here, we report a case of PMD, in which the fetus eventually demised in utero despite weekly color Doppler monitoring, and the mother subsequently encountered AFE during delivery. A 43-year-old woman who had received three frozen embryo transfer, was found to have a singleton pregnancy with an enlarged multi-cystic placenta at 8 weeks' gestation. Fetal growth restriction (FGR) was noted since the 21stweek. The fetus eventually demised in-utero at 25 weeks despite weekly color Doppler surveillance. Cesarean section was performed under general anesthesia due to placenta previa totalis and antepartum hemorrhage. During surgery, the patient experienced a sudden blood pressure drop and desaturation followed by profound coagulopathy. AFE was suspected. After administration of inotropic agents and massive blood transfusion, the patient eventually survived AFE. PMD was confirmed after pathological examination of the placenta. While FGR can be monitored by color Doppler, our case echoed previous reports that IUFD may be unpreventable even under intensive surveillance in PMD cases. Although AFE is usually considered unpredictable, PMD can result in cumulative risk factors contributing to AFE. Whether a specific link exists between the pathophysiology of PMD and AFE requires further investigation.

Prenatal differential diagnosis of placental mesenchymal dysplasia and molar disease with coexistent live twin fetuses

Background: Numerous hypoechoic cysts in the placenta on prenatal ultrasonography with a live fetus may indicate twin pregnancy with a complete hydatidiform mole with a coexistent fetus, partial mole, confined placental mosaicism, or placental mesenchymal dysplasia (PMD). Ultrasonographic appearances of these are similar; however, the differential diagnosis should be made because maternal and fetal prognoses differ. Cases: We present two cases of twin pregnancies with numerous placental cystic lesions. The first case was a partial hydatidiform mole in monochorionic diamniotic twins with a diploid karyotype that underwent a spontaneous abortion at 20 gestational weeks. The second case was PMD in dichorionic diamniotic twins; live twin neonates were delivered at 34 gestational weeks. Emergency cesarean section delivery was performed due to severe preeclampsia and fetal growth restriction in twin A at 34 weeks of gestation. Conclusions: Numerous hypoechoic cysts in the placenta on prenatal ultrasonography with a normal live fetus warrants chromosomal analysis and serial ultrasonographic examination to differentiate between PMD and molar pregnancy with a coexisting normal fetus to avoid unnecessary termination.

Placental Mesenchymal Dysplasia and Beckwith-Wiedemann Syndrome.

Placental mesenchymal dysplasia (PMD) is characterized by placentomegaly, aneurysmally dilated chorionic plate vessels, thrombosis of the dilated vessels, and large grapelike vesicles, and is often mistaken for partial or complete hydatidiform mole with a coexisting normal fetus. Androgenetic/biparental mosaicism (ABM) has been found in many PMD cases. Beckwith-Wiedemann syndrome (BWS) is an imprinting disorder with complex and diverse phenotypes and an increased risk of developing embryonal tumors. There are five major causative alterations: loss of methylation of imprinting control region 2 (KCNQ1OT1:TSS-DMR) (ICR2-LOM), gain of methylation at ICR1 (H19/IGF2:IG-DMR) (ICR1-GOM), paternal uniparental disomy of 11 (pUPD11), loss-of-function variants of the CDKN1C gene, and paternal duplication of 11p15. Additional minor alterations include genetic variants within ICR1, paternal uniparental diploidy/biparental diploidy mosaicism (PUDM, also called ABM), and genetic variants of KCNQ1. ABM (PUDM) is found in both conditions, and approximately 20% of fetuses from PMD cases are BWS and vice versa, suggesting a molecular link. PMD and BWS share some molecular characteristics in some cases, but not in others. These findings raise questions concerning the timing of the occurrence of the molecularly abnormal cells during the postfertilization period and the effects of these abnormalities on cell fates after implantation.

Twin pregnancy with complete hydatidiform mole and co-existing fetus: A report of 15 cases with a clinicopathological analysis and DNA genotyping.

Complete hydatidiform mole (CHM) with co-existing fetus (CHMCF) is very uncommon. In this study, we investigated the clinicopathological features and DNA genotype in 15 CHMCF. Seven patients (46.7%) developed post-molar gestational trophoblastic disease (GTD), 5 of which had lung metastasis. CHMCF was histologically characterized by a mixed pattern of CHM and the non-molar placenta, mimicking partial hydatidiform mole and placental mesenchymal dysplasia. p57 immunostaining showed a divergent staining pattern, positive in the normal placenta and negative in the CHM component. DNA genotyping of the CHM villi demonstrated exclusively paternal alleles consisting of homozygous/monospermic (n=9) and heterozygous/dispermic patterns (n=5) at multiple informative loci. We conclude that CHMCF confers a high risk for post-molar GTD. DNA genotyping contributes significantly to the precision diagnosis of CHMCF.

Aberrant hypomethylation at imprinted differentially methylated regions is involved in biparental placental mesenchymal dysplasia

Aberrant hypomethylation at imprinted differentially methylated regions is involved in biparental placental mesenchymal dysplasia

Dealing with symptoms in the general population: lessons learned from the Danish Symptom Cohort

<b>Background:</b> Placental mesenchymal dysplasia (PMD) is a distinct syndrome of unknown aetiology that is associated with significant fetal morbidity and mortality. Intrauterine growth restriction is common, yet, paradoxically, many of the associated fetuses/newborns have been diagnosed with Beckwith-Wiedemann syndrome (BWS). <b>Methods:</b> We report two cases of PMD with high levels of androgenetic (complete paternal uniparental isodisomy) cells in the placenta and document, in one case, a likely androgenetic contribution to the fetus as well. <b>Results:</b> The same haploid paternal complement found in the androgenetic cells was present in coexisting biparental cells, suggesting origin from a single fertilisation event. <b>Conclusions:</b> Preferential allocation of the normal cells into the trophoblast explains the absence of trophoblast overgrowth, a key feature of this syndrome. Interestingly, the distribution of androgenetic cells appears to differ from that reported for artificially created androgenetic mouse chimeras. Androgenetic mosaicism for the first time provides an aetiology for PMD, and may be a novel mechanism for BWS and unexplained intrauterine growth restriction.