Elsevier

Placenta

Volume 25, Issue 7, August 2004, Pages 671-672
Placenta

Case report
Mesenchymal dysplasia of the placenta

https://doi.org/10.1016/j.placenta.2003.12.008Get rights and content

Abstract

Placental mesenchymal dysplasia is a rare human placental disorder in which the placenta is enlarged and contains cystic villi and dilated vasculature. It is important to recognize this disorder because it may mimic a partial hydatidiform mole. In contrast to a partial mole, mesenchymal dysplasia may coexist with a normal fetus. This case occurred at the Madigan Army Medical Center in Tacoma, Washington, in June 2002.

Introduction

Placental mesenchymal dysplasia (PMD) is a rare placental abnormality (one recent calculation of its incidence was 0.02%) that may grossly and microscopically resemble the much more common partial hydatidiform mole [1]. Placentas with this anomaly are typically larger than their normal counterparts and contain areas of cystic villi with dilated vasculature at the center, or with thinner vessels at the periphery [2], [3] (Figure 1). Grossly, these dilated villi may resemble a vascular abnormality or even fetal intestine (Figure 2). In contrast to partial moles, PMD is compatible with fetal life and is therefore an important diagnosis to consider when prenatal ultrasound reveals placental blebs.

Section snippets

Case report

A gravid 23-year-old multiparous woman was noted on prenatal ultrasound to have placental blebs. Her pregnancy and delivery were otherwise unremarkable and she delivered a 3250 g male infant at 39 weeks gestation. The child was subsequently diagnosed with vascular hamartoma of the face and abnormal eye movements (left eye ptosis) which was repaired. Gross examination of the placenta showed a 1258.0 g 23.0×18.0×3.5cm placenta with red-maroon cotyledons and numerous pale, translucent gray nodules

Discussion

Partial hydatidiform mole is a well-known form of gestational trophoblastic disease in which the ovum is fertilized by two sperm, resulting in a triploid conceptus. The product of conception in these cases may differentiate into fetal parts. Partial moles typically abort spontaneously in the first trimester. As in PMD, they may grossly display cystically dilated villi, but partial hydatidiform moles contain the characteristic syncytiotrophoblast proliferation and trophoblastic pseudoinclusions

Conclusion

PMD is an increasingly recognized placental abnormality that can be confused with partial hydatidiform mole. Unlike molar pregnancies, this condition can coexist with a viable fetus although there is an association with Beckwidth–Wiedemann syndrome. With the now frequent use of prenatal ultrasound, obstetrical physicians should consider PMD when a normal appearing fetus occurs with what appears to be a molar appearing placenta. Physicians and other researchers should follow these cases into

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    The occasional, co-occurrences of chorangioma or sites of chorangiomatosis may reflect a point(s) of overlap in their pathogeneses with PMD, as they likely represent proliferative developmental lesions of immature stem and intermediate villi,2,3,22,43–46 but, to date, PMD is distinguished by involvement of umbilical cord vessels and chorionic plate and very proximal stem villous vessels. Androgenetic-biparental mosaicism (ABM), in which a subset of cells in the placenta are diploid but harbor only paternal chromosomes, has been the most consistent molecular alteration observed in PMD.5,6,16,17,21,24,37–40 The androgenetic cells in ABM have pan-genomic paternal uniparental disomy (paternal alleles and imprinting at all loci), and detection of allelic imbalances consistent with ABM is considered confirmatory evidence for the diagnosis of PMD.4,7,11,13,17,24,28,41

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    The low ratio (methylated/unmethylated) in the father and the mother of the proband for Zac1 is similar to the observation made by Mackey et al. [8]. About 82 cases with PMD have been reported in the literature, none of them was reported in association with TNDM [4]. PMD may be suspected by prenatal ultrasonography and increased level of early second trimester maternal serum AFP, possibly because of the vascular anomalies seen with PMD which allow fetal serum AFP to leak into the maternal circulation [10].

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Disclaimer: The views expressed in this article are those of the authors and do not reflect the official policy of the United States Army, Department of Defense or the United States Government.

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