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Mesenchymal Dysplasia (mesenchymal + dysplasia)
Kinds of Mesenchymal Dysplasia Selected AbstractsMesenchymal dysplasia of the placentaPATHOLOGY INTERNATIONAL, Issue 9 2000Makiko Ohyama A severe case of placental mesenchymal dysplasia occurred in association with intrauterine fetal death (IUFD). The gravida-1, para-1 mother was a 26-year-old Japanese. The first pregnancy was unremarkable and a healthy female infant was delivered. The present pregnancy had been uneventful until 34 weeks of gestation when IUFD was detected. The 1516-g (mean ± SD, 2050 ± 387 g) stillborn infant had no external abnormalities and the karyotype was 46,XX. The placenta was markedly enlarged (1050 g; mean ± SD, 452 ± 202 g), and approximately 80% was occupied by extraordinary enlarged villous structures with a myxoid appearance. Histologically, the dysplastic villi had myxoid stroma and a decreased number of, occasionally obliterated, fetal vessels. There was no abnormal trophoblastic proliferation. Large-sized fetal vessels in the chorionic plate frequently contained organized thrombi. This is the first case of placental mesenchymal dysplasia, which possibly lead to the IUFD. [source] Suspected involvement of the X chromosome in placental mesenchymal dysplasiaCONGENITAL ANOMALIES, Issue 4 2002Masayoshi Arizawa ABSTRACT, So far, 46 cases of placental mesenchymal dysplasia have been reported worldwide. We encountered 15 cases of placental mesenchymal dysplasia (PMD) including 7 cases delivered in our hospital. The incidence of PMD in our hospital was therefore, 7/30, 758 (0.02%). The PMD had a peculiar appearance. In the gross findings, large placenta with intestine-like dilatation of the vessels on the fetal side was reported. Microscopically, cistern-like dilatation of the stem villi, fetal artery thrombosis, and villous hemorrhage were reported. However, we believe most of these findings are secondary rather than the primary of mesenchymal dysplasia. Therefore, we investigated 15 other cases of mesenchymal dysplasia, and found including vascular abnormality of the stem, intermediate and terminal villi in all case of PMD. The abnormality was observed in the vessels of the periphery of the stem villi and their vessel walls were thin and appeared weak. The intermediate villous vessels were unusual, tangled. The terminal villous abnormalities showed chorangiosis and stromal hyperplasia. These findings are mesenchymal dysplasia origin. Moreover, PMD showed female-predominant. 14/15 was female among our cases, We discuss the relationship between mesenchymal dysplasia and the X chromosome in this paper. [source] Mesenchymal dysplasia of the placentaPATHOLOGY INTERNATIONAL, Issue 9 2000Makiko Ohyama A severe case of placental mesenchymal dysplasia occurred in association with intrauterine fetal death (IUFD). The gravida-1, para-1 mother was a 26-year-old Japanese. The first pregnancy was unremarkable and a healthy female infant was delivered. The present pregnancy had been uneventful until 34 weeks of gestation when IUFD was detected. The 1516-g (mean ± SD, 2050 ± 387 g) stillborn infant had no external abnormalities and the karyotype was 46,XX. The placenta was markedly enlarged (1050 g; mean ± SD, 452 ± 202 g), and approximately 80% was occupied by extraordinary enlarged villous structures with a myxoid appearance. Histologically, the dysplastic villi had myxoid stroma and a decreased number of, occasionally obliterated, fetal vessels. There was no abnormal trophoblastic proliferation. Large-sized fetal vessels in the chorionic plate frequently contained organized thrombi. This is the first case of placental mesenchymal dysplasia, which possibly lead to the IUFD. [source] Placental mesenchymal dysplasia,can it be predicted prenatally?PRENATAL DIAGNOSIS, Issue 7 2009A case report No abstract is available for this article. [source] Placental mesenchymal dysplasia associated with fetal aneuploidyPRENATAL DIAGNOSIS, Issue 3 2005Marta C. Cohen Abstract Objectives To describe three cases of placental mesenchymal dysplasia (PMD) associated with abnormal karyotype and review the cases reported in the literature. Methods The cases were retrieved from the files of three different institutions. A search of the English language literature was performed using Medline database. Results Placental abnormalities suggestive of molar changes were seen on the prenatal ultrasound scans. Histologically, the cases had large, hydropic stem villi with myxomatous stroma, cistern formation and ,chorangiomatoid' changes. The placental and fetal karyotypes identified were trisomy 13 (47,XX,t(1:13)(q32;q32)+ 13); Klinefelter syndrome (47,XXY) and triploidy (69,XXX). Including these 3 cases, of 66 reported cases, 51 (78%) were female and 14 (22%) male (ratio 3.6:1); the karyotype was normal in 32/36 (89%) and abnormal in 4/36 (11%); Beckwith,Wiedemann syndrome was confirmed or suspected in 15/66 (23%). Excluding termination of pregnancies, intrauterine death occurred in 18/54 (33%) cases. Conclusion Molar ultrasonographic appearances associated with increased maternal serum alpha-fetoprotein but normal, or slightly elevated, levels of ß human Chorionic Gonadotrophin should raise the clinical suspicion of PMD. The diagnosis of this condition should not be disregarded when an abnormal fetus and/or an abnormal karyotype are demonstrated. Copyright © 2005 John Wiley & Sons, Ltd. [source] |