Chimeric Singleton Placenta Comprising Placental Mesenchymal Dysplasia and Complete Hydatidiform Mole with Live Birth and Postpartum Diagnosis of Gestational Trophoblastic Neoplasia.

INTRODUCTION: Placental mesenchymal dysplasia (PMD) is a benign lesion that is often misdiagnosed as complete (CHM) or partial hydatidiform mole. PMD usually results in live birth but can be associated with several fetal defects. Herein, we report PMD with CHM in a singleton placenta with live birth. CASE PRESENTATION: A 34-year-old gravida 2, para 1, living 1 (G2P1L1) woman was referred on suspicion of a molar pregnancy in the first trimester. Maternal serum human chorionic gonadotrophin levels were increased during early pregnancy, with multicystic lesions and placentomegaly observed on ultrasonography. Levels decreased to normal with no fetal structural abnormalities observed. A healthy male infant was delivered at 34 gestational weeks. Placental p57KIP2 immunostaining and short tandem repeat analysis revealed three distinct histologies and genetic features: normal infant and placenta, PMD, and CHM. Gestational trophoblastic neoplasia was diagnosed and up to fourth-line chemotherapy administered. CONCLUSION: Distinguishing PMD from hydatidiform moles is critical for avoiding unnecessary termination of pregnancy. CHM coexisting with a live fetus rarely occurs. This case is unique in that a healthy male infant was born from a singleton placenta with PMD and CHM.

Giant Mesenchymal Hepatic Hamartomas With Adrenal Involvement Precipitating Respiratory Failure: A Myxomatous Mystery in a Three-Month-Old.

The combination of placental mesenchymal dysplasia and hepatic mesenchymal hamartomas is an extremely rare finding. We present the case of a three-month-old female born at 35 weeks gestation with a history of placental mesenchymal dysplasia who presented with non-bilious, non-bloody emesis, and episodes of respiratory distress due to multiple enlarging abdominal cystic lesions. The patient's presentation was unique due to both liver and adrenal solid and cystic lesions. After extensive imaging and multiple biopsies, expert interpretation of biopsy tissue revealed hepatic mesenchymal hamartoma within the liver and the adrenal gland. To our knowledge, this is one of the few documented cases of unresectable hepatic mesenchymal hamartomas with adrenal involvement successfully undergoing a whole liver transplant.

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.

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

BACKGROUND: 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. CASE PRESENTATION: 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. CONCLUSIONS: 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.

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.

Infantile hepatic hemangioma and hepatic mesenchymal hamartoma in an infant associated with placental mesenchymal dysplasia: a case report.

BACKGROUND: Although infantile hepatic hemangioma and hepatic mesenchymal hamartoma are relatively common in benign pediatric liver tumors, coexistence of the two tumors is rare. Placental mesenchymal dysplasia is also a rare disorder. We report the case of a baby girl born after a pregnancy complicated by placental mesenchymal dysplasia, who developed both infantile hepatic hemangioma and hepatic mesenchymal hamartoma. CASE PRESENTATION: The patient was born at 32 weeks and 5 days of gestation for impending placental abruption, weighing 1450 g. Liver tumors, composed of both hypervascular solid and large cystic lesions, were detected after birth and markedly increased to create abdominal distention within 9 months. Diagnostic imaging suspected the coexistence of infantile hepatic hemangioma and cystic hepatic mesenchymal hamartoma. Following propranolol therapy for infantile hepatic hemangioma and needle puncture of a large cyst, the cystic lesions and adjacent hypervascular lesions were partially resected via laparotomy. Pathological findings confirmed the coexistence of hepatic mesenchymal hamartoma and infantile hepatic hemangioma, which had no association with androgenetic/biparental mosaicism. The postoperative course was uneventful, and the tumor had not regrown after 3 years. CONCLUSIONS: Although the coexistence of infantile hepatic hemangioma and hepatic mesenchymal hamartoma associated with placental mesenchymal dysplasia is extremely rare, the pathological and pathogenetic similarities between these disorders suggest that they could have derived from similar embryologic origins rather than being a mere coincidence. Further follow-up is required, with careful attention to the potential for malignant hepatic mesenchymal hamartoma transformation.

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

BACKGROUND: Placental mesenchymal dysplasia (PMD) is a morphological abnormality resembling partial hydatidiform moles. It is often associated with androgenetic/biparental mosaicism (ABM) and complicated by Beckwith-Wiedemann syndrome (BWS), an imprinting disorder. These phenomena suggest an association between PMD and aberrant genomic imprinting, particularly of CDKN1C and IGF2. The existence of another type of PMD containing the biparental genome has been reported. However, the frequency and etiology of biparental PMD are not yet fully understood. RESULTS: We examined 44 placental specimens from 26 patients with PMD: 19 of these were macroscopically normal and 25 exhibited macroscopic PMD. Genotyping by DNA microarray or short tandem repeat analysis revealed that approximately 35% of the macroscopic PMD specimens could be classified as biparental, while the remainder were ABM. We performed a DNA methylation analysis using bisulfite pyrosequencing of 15 placenta-specific imprinted differentially methylated regions (DMRs) and 36 ubiquitous imprinted DMRs. As expected, most DMRs in the macroscopic PMD specimens with ABM exhibited the paternal epigenotype. Importantly, the biparental macroscopic PMD specimens exhibited frequent aberrant hypomethylation at seven of the placenta-specific DMRs. Allelic expression analysis using single-nucleotide polymorphisms revealed that five imprinted genes associated with these aberrantly hypomethylated DMRs were biallelically expressed. Frequent aberrant hypomethylation was observed at five ubiquitous DMRs, including GRB10 but not ICR2 or ICR1, which regulate the expression of CDKN1C and IGF2, respectively. Whole-exome sequencing performed on four biparental macroscopic PMD specimens did not reveal any pathological genetic abnormalities. Clinical and molecular analyses of babies born from pregnancies with PMD revealed four cases with BWS, each exhibiting different molecular characteristics, and those between BWS and PMD specimens were not always the same. CONCLUSION: These data clarify the prevalence of biparental PMD and ABM-PMD and strongly implicate hypomethylation of DMRs in the pathogenesis of biparental PMD, particularly placenta-specific DMRs and the ubiquitous GRB10, but not ICR2 or ICR1. Aberrant hypomethylation of DMRs was partial, indicating that it occurs after fertilization. PMD is an imprinting disorder, and it may be a missing link between imprinting disorders and placental disorders incompatible with life, such as complete hydatidiform moles and partial hydatidiform moles.

A Challenging Diagnosis: Placental Mesenchymal Dysplasia-Literature Review and Case Report.

We describe a 22-year-old woman (2-gravid) case who was referred to our clinic at 18 weeks of gestation for a placenta with vesicular lesions discovered on prenatal examination routine. An ultrasound exam at 31 weeks of gestation showed numerous vesicular lesions, which gradually augmented as the pregnancy advanced. A live normal-appearing fetus was confirmed by intrauterine growth restriction (IUGR). The maternal serum ß-human chorionic gonadotropin level remained in normal ranges. At some point, a multidisciplinary medical consensus considered the termination of the pregnancy, but the patient refused to comply. At 33 weeks of gestation, preterm premature rupture of membranes (pPROM) occurred, and she spontaneously delivered a 1600 g healthy female baby with a good long-term outcome. Placental mesenchymal dysplasia (PMD) was retrospectively diagnosed after confronting the data from ultrasound, chorionic villus sampling (CVS), amniocentesis, pathological examination, and immunohistochemical stain. The lack of sufficient reports of PMD determines doctors to be cautious and reserved, approaching these cases more radically than necessary. We reviewed this disease and searched for all cases of PMD associated with healthy, live newborns.

Prenatal Diagnosis of Placental Mesenchymal Dysplasia with 46, X, Isochromosome Xq/45, X Mosaicism.

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. We present a unique placental mesenchymal dysplasia patient with amniotic fluid karyotyping as 46, X, iso(X) (q10). Detailed molecular testing of the amniotic fluid, fetal cord blood, non-dysplastic placenta and dysplastic placenta was conducted after termination of pregnancy, from which we proved biparental/androgenetic (46, X, i(X) (q10)/45, X) mosaicism in different gestational tissues. A high portion of androgenetic cells in dysplastic placenta (74.2%) and near 100% of biparental cells in the fetus's blood and amniotic fluid were revealed. Delicate mosaic analyses were performed, and possible pathogenesis and embryogenesis of this case were drawn up.

Localized Placental Mesenchymal Dysplasia in Monochorionic Diamniotic Twin Placenta with Beckwith-Wiedemann Syndrome.

IntroductionPlacental mesenchymal dysplasia (PMD) is often associated with Beckwith-Wiedemann syndrome. Case report: A 27-year-old woman with preeclampsia prematurely delivered twin girls. One side of the placenta was larger with numerous grape-like vesicles, histologically with large, cystic, stem villi with cisterns without syncytiotrophoblastic hyperplasia. This side showed mosaicism for chromosome 11 by FISH and hypomethylation at ICR2 by MLPA. The smaller side of the placenta was normal macroscopically, microscopically, and karyotypically. There was symmetric growth restriction, macroglossia and hypoglycemia of the girl corresponding to the abnormal placental side, and lesser symmetric growth restriction and mild hypoglycemia in the other girl. Conclusion: Localized placental mesenchymal dysplasia can occur in monochorionic diamniotic twin placenta with Beckwith-Wiedemann syndrome. Fetal affects may be asymmetric. PMD can be associated with mosaicism monosomy of chromosome 11.

Displasia mesenquimal placentaria asociada con restricción del crecimiento intrauterino de inicio temprano: reporte de un caso / Placental mesenchymal dysplasia associated with early onset intrauterine growth restriction: a case report

Resumen ANTECEDENTES: La displasia mesenquimal placentaria es una anomalía de la vasculatura y del tejido conectivo placentario que altera la estructura y la función de las vellosidades, se asocia con un desenlace perinatal adverso. CASO CLÍNICO: Paciente de 21 años, primigesta, con 15.2 semanas de embarazo establecidas por fetometría, con placenta corporal anterior, de morfología anormal, con múltiples imágenes hipoecogénicas que semejan racimos de uvas, sin flujo vascular en el Doppler color. La valoración ecográfica de las 33 semanas reportó fetometría para 27.2 semanas, anhidramnios y placentomagelia, con alteración en los parámetros de la flujometría Doppler. En la prueba sin estrés se diagnosticó restricción del crecimiento intrauterino estadio IV. La imagen del feto fue heterogénea en el flanco derecho de 4.7 x 4.1 cm. El embarazo finalizó por cesárea con una recién nacida con Apgar 8-9, de 930 gramos, placenta agrandada con vellosidades hidrópicas. El estudio histopatológico reportó: displasia mesenquimal placentaria. La resección del tumor abdominal fue electiva, por vía laparoscópica, al cuarto mes de vida, con diagnóstico histopatológico de hamartoma mesenquimal hepático. CONCLUSIÓN: La displasia mesenquimal placentaria es una anomalía placentaria benigna, relacionada con restricción del crecimiento intrauterino de inicio temprano que puede evolucionar, incluso, a la muerte del feto por hipoxia crónica debido a las anomalías en la vasculatura microscópica que afectan el desarrollo de las vellosidades terminales e interfiere en el intercambio de gases, nutrientes y electrolitos en el espacio intervelloso.

Abstract BACKGROUND: Placental mesenchymal dysplasia is an anomaly of the vasculature and placental connective tissue which alters the structure and function of the villi, being associated with an adverse perinatal outcome. CLINICAL CASE: Patient 21 years old, primigestation, with 15.2 weeks of pregnancy established by fetometry, with anterior body placenta, abnormal morphology, with multiple hypoechogenic images resembling clusters of grapes, without vascular flow in color Doppler. Ultrasound evaluation at 33 weeks, reporting fetometry for 27.2 weeks, anhydramnios and placentomagelia, with alteration in Doppler parameters, as well as in a non-stress test diagnosing fetal growth restriction stage IV. Fetus with heterogeneous image on the right flank of 4.7 x 4.1 cm. Abdominal pregnancy interruption was decided, obtaining a live female newborn, Apgar 8/9, weight 930 grams, enlarged placenta with hydropic villi. The histopathology study reports placental mesenchymal dysplasia. Abdominal tumor resection was performed electively by laparoscopy at 4 months of age with a histopathological diagnosis of hepatic mesenchymal hamartoma. CONCLUSION: Placental mesenchymal dysplasia is a benign placental anomaly, related to early-onset intrauterine growth restriction that can even progress to fetal death by chronic hypoxia due to abnormalities in the microscopic vasculature that affect the development of the terminal villi and interfere with the exchange of gases, nutrients and electrolytes in the intervillous space.

When a vesicular placenta meets a live fetus: case report of twin pregnancy with a partial hydatidiform mole.

BACKGROUND: Hydatidiform moles exhibit a distinctive gross appearance of multiple vesicles in the placenta. The advances in cytogenetic technologies have helped uncover novel entities of hydatidiform moles and enabled elaborate diagnoses. However, management of a vesicular placenta with a coexistent live fetus poses a bigger challenge beyond hydatidiform moles. CASE PRESENTATION: A 33-year-old woman was referred to our department for suspected hydatidiform mole coexistent with a live fetus at 24 weeks' gestation. The patient had conceived through double embryo transplantation, and first-trimester ultrasonography displayed a single sac. Mid-trimester imaging findings of normal placenta parenchyma admixed with multiple vesicles and a single amniotic cavity with a fetus led to suspicion of a singleton partial molar pregnancy. After confirmation of a normal diploid by amniocentesis and close surveillance, the patient delivered a healthy neonate. Preliminary microscopic examination of the placenta failed to clarify the diagnosis until fluorescence in situ hybridization showed a majority of XXY sex chromosomes. The patient developed suspected choriocarcinoma and achieved remission for 5 months after chemotherapy, but relapsed with suspected intermediate trophoblastic tumor. CONCLUSION: We report a rare case of twin pregnancy comprising a partial mole and a normal fetus that resembled a singleton partial molar pregnancy. Individualized care is important in conditions where a vesicular placenta coexists with a fetus. We strongly recommend ancillary examinations in addition to traditional morphologic assessment in such cases.

Placental spectrum features between mesenchymal dysplasia and partial hydatidiform mole coexisting with a live fetus.

We report a case of a singleton hydrops pregnancy with placental gross and microscopic features between partial hydatidiform mole (PHM) and placental mesenchymal dysplasia (PMD) in a diploid live fetus. Pregnancy was complicated by early onset of growth restriction and pre-eclampsia. A female newborn was born at 29 weeks with no congenital malformations. Histology of the placenta revealed mixed phenotype of PMD and PHM, and genetic test results were normal.

Sudden fetal death with placental mesenchymal dysplasia complicated by placenta previa.

Placental mesenchymal dysplasia (PMD) is a rare placental abnormality that is closely related to severe pregnancy complications. A 27-year-old woman with fetal growth restriction and placenta previa was referred to a university hospital at 22 gestational weeks (GW). She was suspected of having a twin pregnancy with a complete or partial hydatidiform mole and coexisting normal live fetus, because two separate placentas, an enlarged one with multiple cystic lesions and a normal one, were shown on ultrasound examinations. At 27 GW, she experienced a sudden intrauterine fetal death (IUFD) after bleeding due to placenta previa, despite confirmation of fetal well-being at 2 h before bleeding. After delivery, histopathological examination confirmed the diagnosis of PMD. This is the first documented case of a woman with PMD and placenta previa who had a sudden IUFD after bleeding. Patients with both PMD and placenta previa should be considered at extremely high risk for IUFD.

Differentiating complete hydatidiform mole and coexistent fetus and placental mesenchymal dysplasia: A series of 9 cases and review of the literature.

To identify the differentiating features in clinical presentation, management, and maternal/fetal outcome in complete hydatidiform mole and coexistent fetus compared with placental mesenchymal dysplasia. Between 1997 and 2015, five women with complete hydatidiform mole and coexistent fetus and four women with placental mesenchymal dysplasia were managed at the University of California San Francisco. Clinical features were analyzed and compared with previously published data. Of the five cases of complete hydatidiform mole and coexistent fetus, two had live births. ß-hCG levels were > 200,000 IU/L in all cases. On imaging, a clear plane between the cystic component and the placenta favored a diagnosis of complete hydatidiform mole and coexistent fetus. None of the patients went on to develop gestational trophoblastic neoplasia (GTN), with a range of follow-up from 2 to 38 months. Combining this data with previously published work, the live birth rate in these cases was 38.8%, the rate of persistent GTN was 36.2%, and the rate of persistent GTN in patients with reported live births was 27%. Of the four cases of placental mesenchymal dysplasia, all four had live births. One patient developed HELLP syndrome and intrauterine growth restriction; the remaining three were asymptomatic. Maternal symptoms, fetal anomalies, ß-hCG level, and placental growth pattern on imaging may help differentiate between complete hydatidiform mole and coexistent fetus and placental mesenchymal dysplasia. There was not an increased risk of gestational trophoblastic neoplasia in patients with complete hydatidiform mole and coexistent fetus who opted to continue with pregnancy.

Variants in Maternal Effect Genes and Relaxed Imprinting Control in a Special Placental Mesenchymal Dysplasia Case with Mild Trophoblast Hyperplasia.

Placental mesenchymal dysplasia (PMD) and partial hydatidiform mole (PHM) placentas share similar characteristics, such as placental overgrowth and grape-like placental tissues. Distinguishing PMD from PHM is critical because the former can result in normal birth, while the latter diagnosis will lead to artificial abortion. Aneuploidy and altered dosage of imprinted gene expression are implicated in the pathogenesis of PHM and also some of the PMD cases. Diandric triploidy is the main cause of PHM, whereas mosaic diploid androgenetic cells in the placental tissue have been associated with the formation of PMD. Here, we report a very special PMD case also presenting with trophoblast hyperplasia phenotype, which is a hallmark of PHM. This PMD placenta has a normal biparental diploid karyotype and is functionally sufficient to support normal fetal growth. We took advantage of this unique case to further dissected the potential common etiology between these two diseases. We show that the differentially methylated region (DMR) at NESP55, a secondary DMR residing in the GNAS locus, is significantly hypermethylated in the PMD placenta. Furthermore, we found heterozygous mutations in NLRP2 and homozygous variants in NLRP7 in the mother's genome. NLRP2 and NLRP7 are known maternal effect genes, and their mutation in pregnant females affects fetal development. The variants/mutations in both genes have been associated with imprinting defects in mole formation and potentially contributed to the mild abnormal imprinting observed in this case. Finally, we identified heterozygous mutations in the X-linked ATRX gene, a known maternal-zygotic imprinting regulator in the patient. Overall, our study demonstrates that PMD and PHM may share overlapping etiologies with the defective/relaxed dosage control of imprinted genes, representing two extreme ends of a spectrum.

Clinical manifestations of placental mesenchymal dysplasia in Japan: A multicenter case series.

AIM: This study aimed to evaluate the clinical features and pregnancy outcomes of placental mesenchymal dysplasia (PMD) in Japan. METHODS: We requested detailed clinical information and placental tissue of PMD cases in 2000-2018 from Japanese facilities with departments of obstetrics and gynecology and analyzed the pregnancy course and neonatal outcomes. RESULTS: We collected 49 cases of PMD. Of 18 patients with measured maternal serum alpha-fetoprotein (MSAFP) levels, 15 (83.3%) had elevated levels. Maternal serum human chorionic gonadotropin (MShCG) levels were transiently elevated in five (17.8%) of 28 patients. Forty-seven patients continued their pregnancies. All pregnancies were singleton and 40 (85.1%) were associated with adverse events including fetal growth restriction (FGR), threatened premature delivery, fetal demise, and hypertensive disorder of pregnancy in 34 (72.3%), 14 (29.8%), eight (17.0%), and six (12.8%) patients, respectively. Of 47 infants, there were eight stillbirths. There were 40 (85.1%) female infants, and eight (17.0%) had Beckwith-Wiedemann syndrome. Of 39 live births, 23 (59.0%) were associated with premature induction of labor or cesarean section for obstetric indications related to FGR. Eighteen (46.2%) neonates had complications. PMD-affected placentas were pathologically heterogeneous in both grossly PMD-affected and non-affected areas. CONCLUSIONS: Our study included the largest number of PMD cases with detailed clinical information. PMD is a high-risk condition for both the mother and the child. Elevated MSAFP levels with normal MShCG levels indicate PMD. Conventional perinatal management of FGR in Japan might be effective in reducing the fetal mortality rate.

Placental mesenchymal dysplasia - morphology and differential diagnosis.

Placental mesenchymal dysplasia is a rare placental lesion characterized by placentomegaly, vascular abnormalities and formation of cystic structures in the placental parenchyma. It can be associated with various genetic abnormalities, fetal growth restriction or intrauterine fetal demise. Placental mesenchymal dysplasia needs to be distinguished from its main differential diagnosis, partial hydatidiform mole. The aim of this article is to provide readers with a basic overview of the morphology and differential diagnosis of this pathological entity.

Hepatic mesenchymal hamartoma and undifferentiated embryonal sarcoma of the liver: a pathologic review.

This review highlights two rare entities that are predominantly seen in children: hepatic mesenchymal hamartoma (HMH) and undifferentiated embryonal sarcoma of the liver (UESL). HMH is a benign lesion predominantly seen in the first 2 years of life, while UESL is malignant and usually identified in patients between 6 and 10 years of age. UESL may arise in the background of HMH, and the association has been supported by similar chromosomal aberrations (19q13.4). The diagnosis of both lesions is primarily based on histologic evaluation, as the clinical and radiological features are not always typical. The clinicopathologic characteristics, pathogenesis, differential diagnoses and treatment for both lesions are discussed.

Placental mesenchymal dysplasia in a normal female infant: a rare case report with follow-up.

Placental mesenchymal dysplasia (PMD) is a rare disorder of unknown etiology, which is often misdiagnosed as partial hydatidiform mole because of their similarity in ultrasonographic, gross, and histologic presentations. However, the treatment and prognosis of these two conditions are different. Patients with PMD often have intrauterine growth restriction, intrauterine fetal death, and Beckwith-Wiedemann syndrome, but there may also be a normal fetus. PMD with a normal female infant is extremely rare, and only a few cases have been reported. We report a case of PMD in a normal female infant and its follow-up results.