A case of intrauterine growth restriction in association with placental mesenchymal dysplasia with abnormal placental lymphatic development.
ABSTRACT Placental mesenchymal dysplasia (PMD) is a rare human disorder associated with stillbirth, intrauterine growth restriction (IUGR) and Beckwith-Wiedemann syndrome. Although the morphology of this condition has been described in 86 cases, the underlying cellular origin is unclear. We investigate the placental cell type involved in a case of PMD associated with a live born female infant with IUGR. In PMD intermediate villi contain cisternae, lined by non-proliferative cells. Immunostaining reveals they are not of trophoblast or vascular endothelial origin. There is positive immunostaining for lymphatic endothelium; this abnormal lymphangiogenesis is in concordance with current hypotheses regarding the aetiology of PMD. Furthermore, such observations suggest that placental villous mesenchyme may differentiate into various cell types, even those not normally found in the human placenta.
SourceAvailable from: PubMed Central01/2015; 49(1):71-74. DOI:10.4132/jptm.2014.12.14
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ABSTRACT: Pre-eclampsia (PE) is characterized by failed remodeling of maternal vessels perfusing the placenta. Blood vessels and lymphatic system are involved in vessel remodeling and flow homeostasis in the uterus during pregnancy. This study aims to investigate the involvement of angiogenesis and lymphangiogenesis in PE. Placental and decidual tissues were obtained from pregnancies with PE (n = 90), including PE cases with decidual vasculopathy (DV) (n = 52) and without DV (n = 38), and healthy pregnancies (control, n = 20). The clinical characteristics of these groups were analyzed. The expression levels of VEGF1, CD34, PROX-1, VEGFR3, and CD31 in the placenta and decidua were detected through immunohistochemistry, reverse-transcription polymerase chain reaction, and Western blot. The lymphangiogenic markers PROX-1 and VEGFR3 were negatively expressed in the placenta but positively expressed in the decidua. The expression levels of the angiogenic markers VEGF1 and CD34 and the panendothelial marker CD31 were significantly lower in the placenta and decidua of the PE group than in those of the control group. The expression levels of VEGF1, CD34, and CD31 were significantly lower in the placenta and decidua with DV than in those without DV. Furthermore, the expression trends of PROX-1 and VEGFR3 was similar to those of VEGF1, CD34, and CD31 among the groups. Lymphangiogenesis occurred in the decidua but not in the placenta. Impaired angiogenesis and lymphangiogenesis were associated with PE, particularly in the presence of DV. Copyright © 2014 Elsevier Ltd. All rights reserved.Placenta 12/2014; 36(3). DOI:10.1016/j.placenta.2014.12.013 · 3.29 Impact Factor
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ABSTRACT: Placental mesenchymal dysplasia is an increasingly recognizable abnormality. Early cases have been confused with partial hydatidiform mole. Placental mesenchymal dysplasia is probably under-diagnosed because of being an unfamiliar clinical entity and also mistaken for gestational trophoblastic disease due to the similar sonographic findings of two entities. In this report, we describe the clinical, gross, and histopathological findings of placental mesenchymal dysplasia in two cases. The 33-week-preterm baby of a 26-year-old woman with cardiovascular disease and 342 gram placenta and the 19-week fetus with trisomy 21 of a 40 year-old woman were terminated. Macroscopically thick-walled vessels and microscopically hydropic villous with peripherally localized thick-walled vessels without trophoblastic cell proliferation were observed in both cases. These two cases represent a rare placental anomaly that is benign but it is challenging to distinguish placental mesenchymal dysplasia from an incomplete mole. Placental mesenchymal dysplasia should be included in the differential diagnosis of sonographic findings that show a normal appearing fetus and a placenta with cystic lesions. Placental mesenchymal dysplasia is associated with pregnancy-related hypertension. In conclusion, the most important point is “you can diagnose it if you consider it”. Key Words: Placental mesenchymal dysplasia, Molar pregnancy, Diagnostic errorsTurk Patoloji Dergisi 01/2015; DOI:10.5146/tjpath.2015.01301