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Rosemary A Fisher - One of the best experts on this subject based on the ideXlab platform.
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abnormal villous morphology mimicking a Hydatidiform Mole associated with paternal trisomy of chromosomes 3 7 8 and unipaternal disomy of chromosome 11
Diagnostic Pathology, 2016Co-Authors: N J Sebire, Michael J Seckl, Philippa C May, Baljeet Kaur, Rosemary A FisherAbstract:Pregnancies affected by non-molar chromosomal abnormality may sometimes demonstrate abnormal chorionic villous morphology that is similar to partial Hydatidiform Mole. Determination of the underlying aetiology may be difficult in such cases. This report describes a case referred to the regional trophoblastic disease unit as a possible Hydatidiform Mole that demonstrated both villous dysmorphology and abnormal p57KIP2 expression. Molecular genotyping revealed that while most chromosomes in the villous tissue were diploid and biparental, chromosomes 3, 7 and 8 were trisomic with an additional paternally derived chromosome. In contrast chromosome 11 showed uniparental disomy of paternal origin a situation more usually associated with complete Hydatidiform Moles. This unusual case highlights that exceptions may occur to the general rules of both histological morphology and immunoprofile, and that these can be resolved by detailed Molecular genetic investigations. The findings confirm that trisomic pregnancies may demonstrate morphological villous features similar to Hydatidiform Mole, and that loss of p57KIP2 expression occurs due to an absence of maternally transcribed genes on chromosome 11 and can therefore be independent of androgenetic complete Hydatidiform Mole.
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abnormal villous morphology mimicking a Hydatidiform Mole associated with paternal trisomy of chromosomes 3 7 8 and unipaternal disomy of chromosome 11
Diagnostic Pathology, 2016Co-Authors: N J Sebire, Michael J Seckl, Baljeet Kaur, Rosemary A FisherAbstract:Background Pregnancies affected by non-molar chromosomal abnormality may sometimes demonstrate abnormal chorionic villous morphology that is similar to partial Hydatidiform Mole. Determination of the underlying aetiology may be difficult in such cases.
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mutations in nlrp7 and khdc3l confer a complete Hydatidiform Mole phenotype on digynic triploid conceptions
Human Mutation, 2013Co-Authors: Masoumeh Fallahian, N J Sebire, Philip Savage, Michael J Seckl, Rosemary A FisherAbstract:Digynic triploidy is classically associated with a severely growth restricted fetus and a small nonmolar placenta. However, in genotyping Hydatidiform Moles as part of clinical practice, we identified two digynic triploid conceptions presenting with histopathological features of classical complete Hydatidiform Mole (CHM). Both cases occurred in women with a history of previous molar pregnancies and no normal pregnancies. Pathological review and genotyping of other molar pregnancies in these cases showed them to be typical CHM with negative p57(KIP2) immunostaining of the cytotrophoblast cells and villous stroma and to be diploid but biparental, confirming a diagnosis of familial recurrent Hydatidiform Mole (FRHM). Mutation screening of NLRP7 had identified a homozygous duplication, leading to a truncated protein, in case 1 whereas mutation screening of KHDC3L (C6orf221) in case 2 showed both the proband and her sister to be compound heterozygotes for mutations in KHDC3L. The observation of a single digynic, triploid conception presenting as a CHM in women with FRHM, where other pregnancies are diploid and biparental, supports the hypothesis that the role of both NLRP7 and KHDC3L in pregnancy is in setting and/or maintaining the maternal imprint. Clinically, a diagnosis of FRHM should be considered in women with genetically unusual conceptions that are phenotypically CHM.
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discrimination of complete Hydatidiform Mole from its mimics by immunohistochemistry of the paternally imprinted gene product p57kip2
The American Journal of Surgical Pathology, 2001Co-Authors: Diego H Castrillon, Stanislawa Weremowicz, Rosemary A Fisher, Christopher P Crum, David R GenestAbstract:The p57 KIP2 protein is a cell cycle inhibitor and tumor suppressor encoded by a strongly paternally imprinted gene. We explored the utility of p57 KIP2 as a diagnostic marker in Hydatidiform Mole, a disease likely the result of abnormal dosage and consequent misexpression of imprinted genes. Using
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discrimination of complete Hydatidiform Mole from its mimics by immunohistochemistry of the paternally imprinted gene product p57kip2
The American Journal of Surgical Pathology, 2001Co-Authors: Diego H Castrillon, Stanislawa Weremowicz, Rosemary A Fisher, Christopher P Crum, Deqin Sun, David R GenestAbstract:The p57KIP2 protein is a cell cycle inhibitor and tumor suppressor encoded by a strongly paternally imprinted gene. We explored the utility of p57KIP2 as a diagnostic marker in Hydatidiform Mole, a disease likely the result of abnormal dosage and consequent misexpression of imprinted genes. Using a monoclonal antibody on paraffin-embedded, formalin-fixed tissue sections, the authors evaluated p57KIP2 expression in normal placenta and in 149 gestations including 59 complete Hydatidiform Moles, 39 PHMs, and 51 spontaneous losses with hydropic changes. p57KIP2 was strongly expressed in cytotrophoblast and villous mesenchyme in normal placenta, all cases of partial Hydatidiform Moles (39 of 39) and all spontaneous losses with hydropic changes (51 of 51). In contrast, p57KIP2 expression in cytotrophoblast and villous mesenchyme was absent or markedly decreased in 58 of 59 complete Hydatidiform Moles. In all gestations p57KIP2 was strongly expressed in decidua and in intervillous trophoblast islands, which served as internal positive controls for p57KIP2 immunostaining. p57KIP2 immunohistochemistry can reliably identify most cases of complete Hydatidiform Mole irrespective of gestational age and is thus a useful diagnostic adjunct, complementary to ploidy analysis, in the diagnosis of Hydatidiform Mole.
N J Sebire - One of the best experts on this subject based on the ideXlab platform.
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heuristic neural network approach in histological sections detection of Hydatidiform Mole
Journal of medical imaging, 2019Co-Authors: Patison Palee, N J Sebire, Bernadette Sharp, Leonard Noriega, Craig PlattAbstract:A heuristic-based, multineural network (MNN) image analysis as a solution to the problematical diagnosis of Hydatidiform Mole (HM) is presented. HM presents as tumors in placental cell structures, many of which exhibit premalignant phenotypes (choriocarcinoma and other conditions). HM is commonly found in women under age 17 or over 35 and can be partial HM or complete HM. Appropriate treatment is determined by correct categorization into PHM or CHM, a difficult task even for expert pathologists. Image analysis combined with pattern recognition techniques has been applied to the problem, based on 15 or 17 image features. The use of limited data for training and validation set was optimized using a k -fold validation technique allowing performance measurement of different MNN configurations. The MNN technique performed better than human experts at the categorization for both the 15- and 17-feature data, promising greater diagnostic consistency, and further improvements with the availability of larger datasets.
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abnormal villous morphology mimicking a Hydatidiform Mole associated with paternal trisomy of chromosomes 3 7 8 and unipaternal disomy of chromosome 11
Diagnostic Pathology, 2016Co-Authors: N J Sebire, Michael J Seckl, Philippa C May, Baljeet Kaur, Rosemary A FisherAbstract:Pregnancies affected by non-molar chromosomal abnormality may sometimes demonstrate abnormal chorionic villous morphology that is similar to partial Hydatidiform Mole. Determination of the underlying aetiology may be difficult in such cases. This report describes a case referred to the regional trophoblastic disease unit as a possible Hydatidiform Mole that demonstrated both villous dysmorphology and abnormal p57KIP2 expression. Molecular genotyping revealed that while most chromosomes in the villous tissue were diploid and biparental, chromosomes 3, 7 and 8 were trisomic with an additional paternally derived chromosome. In contrast chromosome 11 showed uniparental disomy of paternal origin a situation more usually associated with complete Hydatidiform Moles. This unusual case highlights that exceptions may occur to the general rules of both histological morphology and immunoprofile, and that these can be resolved by detailed Molecular genetic investigations. The findings confirm that trisomic pregnancies may demonstrate morphological villous features similar to Hydatidiform Mole, and that loss of p57KIP2 expression occurs due to an absence of maternally transcribed genes on chromosome 11 and can therefore be independent of androgenetic complete Hydatidiform Mole.
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abnormal villous morphology mimicking a Hydatidiform Mole associated with paternal trisomy of chromosomes 3 7 8 and unipaternal disomy of chromosome 11
Diagnostic Pathology, 2016Co-Authors: N J Sebire, Michael J Seckl, Baljeet Kaur, Rosemary A FisherAbstract:Background Pregnancies affected by non-molar chromosomal abnormality may sometimes demonstrate abnormal chorionic villous morphology that is similar to partial Hydatidiform Mole. Determination of the underlying aetiology may be difficult in such cases.
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mutations in nlrp7 and khdc3l confer a complete Hydatidiform Mole phenotype on digynic triploid conceptions
Human Mutation, 2013Co-Authors: Masoumeh Fallahian, N J Sebire, Philip Savage, Michael J Seckl, Rosemary A FisherAbstract:Digynic triploidy is classically associated with a severely growth restricted fetus and a small nonmolar placenta. However, in genotyping Hydatidiform Moles as part of clinical practice, we identified two digynic triploid conceptions presenting with histopathological features of classical complete Hydatidiform Mole (CHM). Both cases occurred in women with a history of previous molar pregnancies and no normal pregnancies. Pathological review and genotyping of other molar pregnancies in these cases showed them to be typical CHM with negative p57(KIP2) immunostaining of the cytotrophoblast cells and villous stroma and to be diploid but biparental, confirming a diagnosis of familial recurrent Hydatidiform Mole (FRHM). Mutation screening of NLRP7 had identified a homozygous duplication, leading to a truncated protein, in case 1 whereas mutation screening of KHDC3L (C6orf221) in case 2 showed both the proband and her sister to be compound heterozygotes for mutations in KHDC3L. The observation of a single digynic, triploid conception presenting as a CHM in women with FRHM, where other pregnancies are diploid and biparental, supports the hypothesis that the role of both NLRP7 and KHDC3L in pregnancy is in setting and/or maintaining the maternal imprint. Clinically, a diagnosis of FRHM should be considered in women with genetically unusual conceptions that are phenotypically CHM.
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histopathological diagnosis of Hydatidiform Mole contemporary features and clinical implications
Fetal and Pediatric Pathology, 2010Co-Authors: N J SebireAbstract:Gestational trophoblastic neoplasia (GTN) encompasses several entities including complete (CHM) and partial (PHM) Hydatidiform Mole (HM), malignant choriocarcinoma, and placental-site trophoblastic tumor. HMs are genetically abnormal, nonviable conceptions, which are associated with significantly increased risk for development of complications due to persistence of abnormal trophoblast (persistent GTN; pGTN), which occurs following 15%% of CHM and 0.5%% of PHM. Diagnostic histological features of HM are present in the first trimester but these features differ from those traditionally described in the later second trimester. The characteristic morphological findings of early HM include aspects of villous dysmorphism and abnormal villous trophoblast hyperplasia, with other specific features allowing reliable distinction between CHM and PHM. Optimal management of molar disease depends on its early histological identification and subsequent surveillance by measurement of maternal human chorionic gonoadotropin...
David R Genest - One of the best experts on this subject based on the ideXlab platform.
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discrimination of complete Hydatidiform Mole from its mimics by immunohistochemistry of the paternally imprinted gene product p57kip2
The American Journal of Surgical Pathology, 2001Co-Authors: Diego H Castrillon, Stanislawa Weremowicz, Rosemary A Fisher, Christopher P Crum, David R GenestAbstract:The p57 KIP2 protein is a cell cycle inhibitor and tumor suppressor encoded by a strongly paternally imprinted gene. We explored the utility of p57 KIP2 as a diagnostic marker in Hydatidiform Mole, a disease likely the result of abnormal dosage and consequent misexpression of imprinted genes. Using
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partial Hydatidiform Mole clinicopathological features differential diagnosis ploidy and Molecular studies and gold standards for diagnosis
International Journal of Gynecological Pathology, 2001Co-Authors: David R GenestAbstract:Partial Hydatidiform Mole is optimally diagnosed histopathologically when four microscopic features coexist: 1) two populations of villi, 2) enlarged villi (> or = 3-4 mm) with central captivation, 3) irregular villi with geographic, scalloped borders with trophoblast inclusions, and 4) trophoblast hyperplasia (usually focal and involving syncytiotrophoblast). Pathologic mimics of partial Mole include Beckwith-Wiedemann syndrome, placental angiomatous malformation, twin gestation with complete Mole and existing fetus, early complete Hydatidiform Mole, and hydropic spontaneous abortion. Because partial Hydatidiform Mole results from diandric triploidy, flow cytometry (or another method to assess ploidy) can be utilized by pathologists for supporting diagnostic classification of problematic specimens, or for educational or quality assurance purposes. Confirmation of the histopathologic diagnosis by ploidy or Molecular studies is important for scientific reports of partial Hydatidiform Mole, especially when unusual or aggressive outcomes (such as choriocarcinoma) are reported.
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discrimination of complete Hydatidiform Mole from its mimics by immunohistochemistry of the paternally imprinted gene product p57kip2
The American Journal of Surgical Pathology, 2001Co-Authors: Diego H Castrillon, Stanislawa Weremowicz, Rosemary A Fisher, Christopher P Crum, Deqin Sun, David R GenestAbstract:The p57KIP2 protein is a cell cycle inhibitor and tumor suppressor encoded by a strongly paternally imprinted gene. We explored the utility of p57KIP2 as a diagnostic marker in Hydatidiform Mole, a disease likely the result of abnormal dosage and consequent misexpression of imprinted genes. Using a monoclonal antibody on paraffin-embedded, formalin-fixed tissue sections, the authors evaluated p57KIP2 expression in normal placenta and in 149 gestations including 59 complete Hydatidiform Moles, 39 PHMs, and 51 spontaneous losses with hydropic changes. p57KIP2 was strongly expressed in cytotrophoblast and villous mesenchyme in normal placenta, all cases of partial Hydatidiform Moles (39 of 39) and all spontaneous losses with hydropic changes (51 of 51). In contrast, p57KIP2 expression in cytotrophoblast and villous mesenchyme was absent or markedly decreased in 58 of 59 complete Hydatidiform Moles. In all gestations p57KIP2 was strongly expressed in decidua and in intervillous trophoblast islands, which served as internal positive controls for p57KIP2 immunostaining. p57KIP2 immunohistochemistry can reliably identify most cases of complete Hydatidiform Mole irrespective of gestational age and is thus a useful diagnostic adjunct, complementary to ploidy analysis, in the diagnosis of Hydatidiform Mole.
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complete Hydatidiform Mole comparison of clinicopathologic features current and past
Journal of Reproductive Medicine, 1998Co-Authors: R Mosher, Donald P Goldstein, M R Bernstein, Ross S Berkowitz, David R GenestAbstract:OBJECTIVE: To investigate whether changes have occurred in the pathologic and clinical features of complete molar gestation in recent years. STUDY DESIGN: Twenty-three contemporary complete Hydatidiform Moles (1994-1997) and 20 historical complete Moles (1969-1975) were compared regarding clinical features (gestational age at evacuation, maternal age, preevacuation diagnosis and persistence) and pathologic findings (volume of tissue, presence of gross cisterns, maximal villous size, percent of cavitated villi, percent of villi exhibiting circumferential trophoblast hyperplasia, and presence of necrosis and primitive stromal features). RESULTS: Contemporary complete Moles were evacuated at an earlier mean gestational age (8.5 vs. 17.0 weeks, P = .00008). Histologically, contemporary complete Moles had less circumferential trophoblastic hyperplasia (39% vs. 75% of villi, P = .03), a smaller mean maximal villous diameter (5.7 vs. 8.2 mm, P = .001), more primitive villous stroma (70% vs. 10% of cases, P = .0003) and less global necrosis (22% vs. 54% of cases, P = .02). CONCLUSION: These striking morphologic differences indicate that pathologic findings in complete molar gestations have changed significantly over the past several decades due to the current practice of very early uterine evacuation. Contemporary complete Moles are often characterized by subtle morphologic alterations that may result in their misclassification as partial Moles or nonmolar spontaneous abortions. It is important for pathologists to recognize the distinctive histopathologic features of early complete Hydatidiform Mole.
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natural history of twin pregnancy with complete Hydatidiform Mole and coexisting fetus
Obstetrics & Gynecology, 1994Co-Authors: Michael A Steller, David R Genest, M R Bernstein, Janice M Lage, Donald P Goldstein, Ross S BerkowitzAbstract:Objective:To investigate the clinical features and natural history of twin conceptions consisting of complete Hydatidiform Mole and a coexisting fetus.Methods:Since 1973, eight well-documented cases of twin pregnancy with complete Hydatidiform Mole and coexisting fetus have been treated at the New E
Michael J Seckl - One of the best experts on this subject based on the ideXlab platform.
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abnormal villous morphology mimicking a Hydatidiform Mole associated with paternal trisomy of chromosomes 3 7 8 and unipaternal disomy of chromosome 11
Diagnostic Pathology, 2016Co-Authors: N J Sebire, Michael J Seckl, Philippa C May, Baljeet Kaur, Rosemary A FisherAbstract:Pregnancies affected by non-molar chromosomal abnormality may sometimes demonstrate abnormal chorionic villous morphology that is similar to partial Hydatidiform Mole. Determination of the underlying aetiology may be difficult in such cases. This report describes a case referred to the regional trophoblastic disease unit as a possible Hydatidiform Mole that demonstrated both villous dysmorphology and abnormal p57KIP2 expression. Molecular genotyping revealed that while most chromosomes in the villous tissue were diploid and biparental, chromosomes 3, 7 and 8 were trisomic with an additional paternally derived chromosome. In contrast chromosome 11 showed uniparental disomy of paternal origin a situation more usually associated with complete Hydatidiform Moles. This unusual case highlights that exceptions may occur to the general rules of both histological morphology and immunoprofile, and that these can be resolved by detailed Molecular genetic investigations. The findings confirm that trisomic pregnancies may demonstrate morphological villous features similar to Hydatidiform Mole, and that loss of p57KIP2 expression occurs due to an absence of maternally transcribed genes on chromosome 11 and can therefore be independent of androgenetic complete Hydatidiform Mole.
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abnormal villous morphology mimicking a Hydatidiform Mole associated with paternal trisomy of chromosomes 3 7 8 and unipaternal disomy of chromosome 11
Diagnostic Pathology, 2016Co-Authors: N J Sebire, Michael J Seckl, Baljeet Kaur, Rosemary A FisherAbstract:Background Pregnancies affected by non-molar chromosomal abnormality may sometimes demonstrate abnormal chorionic villous morphology that is similar to partial Hydatidiform Mole. Determination of the underlying aetiology may be difficult in such cases.
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mutations in nlrp7 and khdc3l confer a complete Hydatidiform Mole phenotype on digynic triploid conceptions
Human Mutation, 2013Co-Authors: Masoumeh Fallahian, N J Sebire, Philip Savage, Michael J Seckl, Rosemary A FisherAbstract:Digynic triploidy is classically associated with a severely growth restricted fetus and a small nonmolar placenta. However, in genotyping Hydatidiform Moles as part of clinical practice, we identified two digynic triploid conceptions presenting with histopathological features of classical complete Hydatidiform Mole (CHM). Both cases occurred in women with a history of previous molar pregnancies and no normal pregnancies. Pathological review and genotyping of other molar pregnancies in these cases showed them to be typical CHM with negative p57(KIP2) immunostaining of the cytotrophoblast cells and villous stroma and to be diploid but biparental, confirming a diagnosis of familial recurrent Hydatidiform Mole (FRHM). Mutation screening of NLRP7 had identified a homozygous duplication, leading to a truncated protein, in case 1 whereas mutation screening of KHDC3L (C6orf221) in case 2 showed both the proband and her sister to be compound heterozygotes for mutations in KHDC3L. The observation of a single digynic, triploid conception presenting as a CHM in women with FRHM, where other pregnancies are diploid and biparental, supports the hypothesis that the role of both NLRP7 and KHDC3L in pregnancy is in setting and/or maintaining the maternal imprint. Clinically, a diagnosis of FRHM should be considered in women with genetically unusual conceptions that are phenotypically CHM.
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gestational trophoblastic disease current management of Hydatidiform Mole
BMJ, 2008Co-Authors: N J Sebire, Michael J SecklAbstract:#### Summary points Gestational trophoblastic disease consists of a pregnancy related group of disorders that were often fatal in the past. Much has been learnt in the past 50 years, however, and most women can now be cured. The United Kingdom has a highly centralised system for registering, monitoring, and treating women with this disease that requires close collaboration with non-specialist units and general practitioners. We review the important features for detection and successful management of the most common form of this disease, Hydatidiform Mole. The evidence is based on published studies—mostly retrospective case series—and expert opinion. Hydatidiform Mole affects 1-3 in every 1000 pregnancies. About 10% of Hydatidiform Moles transform into one of the malignant forms of gestational trophoblastic disease, known as gestational trophoblastic neoplasia (box 1). #### Box 1 Classification of gestational trophoblastic disease ##### Benign forms ##### Malignant forms Hydatidiform Moles are abnormal conceptions with excessive placental, and little or no fetal, development. The two major types—complete and partial—have distinctive histological and genetic features (boxes 2 and 3).1 2 3 4 5 6 7 Hydatidiform Moles affect women throughout the reproductive age range but are more common at the extremes of the range.8 Women under 16 have a six times higher risk of developing the disease than those aged 16-40, and women who conceive aged 50 or more have a one in …
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risk of recurrent Hydatidiform Mole and subsequent pregnancy outcome following complete or partial Hydatidiform molar pregnancy
British Journal of Obstetrics and Gynaecology, 2003Co-Authors: N J Sebire, Michael J Seckl, R A Fisher, Marianne Foskett, H Rees, E S NewlandsAbstract:Abstract Objective To determine pregnancy outcome, including the rate of repeat molar pregnancy, following histologically confirmed complete or partial Hydatidiform Mole. Design Retrospective review of a large supraregional database of registrations for gestational trophoblastic disease. Setting Supraregional Trophoblastic Disease Unit, London. Sample Women with pregnancies affected by complete or partial Hydatidiform Mole registered between 1992 and 1998. Methods All patients with a diagnosis of histologically confirmed complete or partial Hydatidiform Mole were identified and data on subsequent pregnancies compared between groups using comparison of proportion test. Main outcome measures Pregnancy outcome by partial or complete Mole subtype, with particular regard to risk of subsequent molar pregnancy. Results Of 2578 complete Moles, the subsequent pregnancy was affected by Hydatidiform Mole in 27 (1.9%) cases, including 22 (81%) complete Moles and 5 (19%) partial Moles. Of 2627 partial Moles, the subsequent pregnancy was also molar in 25 (1.7%) cases, including 17 (68%) partial Moles and 8 (32%) complete Moles. Overall recurrence risk for molar pregnancy was 1.8% (1 in 55), or a 20-fold increase compared with the background risk. Of 27 cases with repeat complete Moles, three had further complete Moles, suggesting the recurrence risk following two previous complete Moles is approximately 10%. There were no other significant differences in pregnancy outcome between cases with previous complete or partial Hydatidiform Mole and that expected in an unselected obstetric population. Conclusions Women having a pregnancy affected by a histologically confirmed complete or partial Hydatidiform Mole may be counselled that the risk of repeat Mole in a subsequent pregnancy is about 1 in 60 and if this were to occur, the majority of cases will be of the same type of Mole as the preceding pregnancy. However, >98% of women who become pregnant following a molar conception will not have a further Hydatidiform Mole and these pregnancies are at no increased risk of other obstetric complications.
Ross S Berkowitz - One of the best experts on this subject based on the ideXlab platform.
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treatment of Hydatidiform Mole using manual vacuum aspiration technical and tactical aspects
International Journal of Gynecological Cancer, 2021Co-Authors: Antonio Braga, Jorge Rezendefilho, Kevin M Elias, Lilian Padron, Neil S Horowitz, Ross S BerkowitzAbstract:Hydatidiform Mole (HM) represents the benign spectrum of gestational trophoblastic disease (GTD), an abnormal pregnancy characterized by aberrant fertilization of the oocyte.[1][1] The treatment of HM is uterine evacuation, usually done through electric vacuum aspiration (EVA). However, numerous
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changing trends in the clinical presentation and management of complete Hydatidiform Mole among brazilian women
International Journal of Gynecological Cancer, 2016Co-Authors: Antonio Braga, Valeria Moraes, Izildinha Maesta, Joffre Amim, Jorge Rezendefilho, Kevin M Elias, Ross S BerkowitzAbstract:Objective The aim of the study was to evaluate potential changes in the clinical, diagnostic, and therapeutic parameters of complete Hydatidiform Mole in the last 25 years in Brazil. Methods A retrospective cohort study was conducted involving the analysis of 2163 medical records of patients diagnosed with complete Hydatidiform Mole who received treatment at the Rio de Janeiro Reference Center for Gestational Trophoblastic Disease between January 1988 and December 2012. For the statistical analysis of the natural history of the patients with complete molar pregnancies, time series were evaluated using the Cox-Stuart test and adjusted by linear regression models. Results A downward linear temporal trend was observed for gestational age of complete Hydatidiform Mole at diagnosis, which is also reflected in the reduced occurrence of vaginal bleeding, hyperemesis and pre-eclampsia. We also observed an increase in the use of uterine vacuum aspiration to treat molar pregnancy. Although the duration of postmolar follow-up was found to decline, this was not accompanied by any alteration in the time to remission of the disease or its progression to gestational trophoblastic neoplasia. Conclusions Early diagnosis of complete Hydatidiform Mole has altered the natural history of molar pregnancy, especially with a reduction in classical clinical symptoms. However, early diagnosis has not resulted in a reduction in the development of gestational trophoblastic neoplasia, a dilemma that still challenges professionals working with gestational trophoblastic disease.
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complete Hydatidiform Mole in women aged 40 to 49 years
Journal of Reproductive Medicine, 2012Co-Authors: Kevin M Elias, Donald P Goldstein, Melina Shoni, Marilyn R Bernstein, Ross S BerkowitzAbstract:Objective To describe the clinical course of women aged 40 to 49 presenting with complete Hydatidiform Mole. Study design All cases of complete Mole diagnosed at the New England Trophoblastic Disease Center were reviewed. A total of 82 patients met the study criteria. Results Study patients had a mean age of 44.2 years, gravidity of 4.6 and parity of 2.6. The mean hCG on presentation was 230,484 mIU/mL. Most patients presented with abnormal vaginal bleeding (77%). Of the 82 patients, 83% underwent dilation and curettage without prophylactic chemotherapy; 53% of those patients developed gestational trophoblastic neoplasia (GTN). Patients who developed GTN were significantly more likely both before and after evacuation to have higher hCG levels than those who did not. There were no GTN cases among patients receiving either prophylactic chemotherapy or upfront hysterectomy. Aggressive upfront therapy was associated with shortened time to hCG normalization and fewer lines of surgical or chemotherapeutic therapy. Conclusion All women in their 40s with complete Mole are at high risk for GTN and might benefit from aggressive upfront therapy. Those patients with hCG levels >175,000 mIU/mL constitute an "ultra-high-risk" group for whom prophylactic chemotherapy or hysterectomy should be especially considered.
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complete Hydatidiform Mole in women older than age 50
Journal of Reproductive Medicine, 2010Co-Authors: Kevin M Elias, Donald P Goldstein, Ross S BerkowitzAbstract:OBJECTIVE: To describe the presentation, clinical course and outcomes of women aged 50 or older who present with a new diagnosis of complete Hydatidiform Mole. STUDY DESIGN: All cases of complete Hydatidiform Mole diagnosed at the New England Trophoblastic Disease Center from June 1970 to April 2009 were reviewed. Twenty-two patients met the study criteria. RESULTS: The mean age in the patient population was 52, gravidity 5.8, parity 3.7 and gestational age 10.4 weeks. The majority of patients (68.4%) reported regular menses immediately prior to the index pregnancy. The most common presenting symptoms were vaginal bleeding (81.0%), stigmata of pregnancy (47.6%) and nausea or vomiting (28.6%). We were unable to delineate characteristics that would distinguish those patients who developed gestational trophoblastic neoplasia (GTN) following dilation and curettage from those who did not. In contrast, 60% of the 15 patients initially treated with dilation and curettage developed GTN, while there were no cases of GTN among the 7 patients receiving primary hysterectomy. CONCLUSION: The risk of developing GTN in this age group appears to correspond to the choice of initial surgical therapy rather than hCG level or demographic factors. Hysterectomy should be considered as the initial treatment of choice.
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intraplacental choriocarcinoma arising in a second trimester placenta with partial Hydatidiform Mole
International Journal of Gynecological Pathology, 2008Co-Authors: Fabiola Medeiros, Ross S Berkowitz, Michael J Callahan, Julia A Elvin, David M Dorfman, Bradley J QuadeAbstract:We report a well-documented case of a 28-year-old woman, gravida 3, para 1, undergoing termination at 22 weeks for fetal congenital malformations with concurrent partial Hydatidiform Mole and choriocarcinoma. A fetal ultrasound showed spina bifida, and an elective termination was performed. One month later, the patient presented with vaginal bleeding, cough, and shortness of breath. A chest computed tomographic scan revealed multiple lung nodules. A pelvic ultrasound was consistent with retained products of conception, and endometrial sampling showed an atypical trophoblastic proliferation consistent with choriocarcinoma. The serum beta-human chorionic gonadotropin level was greater than 100,000 IU/mL. The placental pathology reviewed at our institution showed microscopic foci of choriocarcinoma arising in a partial Hydatidiform Mole. Flow cytometry performed on paraffin-embedded tissue showed a triploid peak, which confirmed the partial molar nature of this gestation. Immunohistochemistry showed nuclear p57 expression in the partial molar villous trophoblastic and stromal cells, but not in the severely atypical trophoblasts, further supporting the diagnosis of intraplacental choriocarcinoma distinct from the partial Mole. Although the Molecular pathogenesis remains to be elucidated, this report provides additional evidence that choriocarcinoma may arise directly from partial molar gestations. Moreover, it emphasizes the importance of thorough sampling of placentas with partial Hydatidiform Mole in search of minute foci of choriocarcinoma because they might represent a potential source of metastatic gestational trophoblastic disease.
