European Journal of Obstetrics & Gynecology and Reproductive Biology
Clinicopathologic characteristics and subsequent pregnancy outcome in 139 complete hydatidiform moles
Introduction
Gestational trophoblastic disease (GTD) includes a spectrum of conditions, all arising from placental tissue. The villous forms of GTD include partial and complete hydatidiform moles as well as invasive moles [1], [2]. The non-villous forms consist of the placental site nodule, exaggerated placental site, placental site trophoblastic tumor (PSTT), choriocarcinoma and the epitheloid trophoblastic tumor [1], [2]. The frequency of gestational trophoblastic lesions in Europe is low, with a reported incidence of 1.54/1000 live births [3], but higher in Asia with one case in 500 deliveries [4]. Moodley et al. [5] reported an incidence of molar pregnancy and choriocarcinoma of 1.2/1000 and 0.5/1000 deliveries for South Africa.
The most common form of GTD is the complete hydatidiform mole (CHM). It arises as a result of abnormal fertilisation with a genome that is almost entirely of paternal origin [6], [7], [8]. CHM most often arises from the fertilisation of an empty ovum by a haploid spermatozoon that subsequently duplicates without cytogenesis to restore the diploid number of chromosomes [9]. Occasional cases occur where the empty ovum is fertilised by a diploid spermatozoon (resulting from a failure of the second meiotic division in spermatogenesis). Both of these events result in a diploid karyotype (most often 46,XX); tetraploid CHMs are exceptionally rare [10]. Partial hydatidiform moles (PHM), in contrast, usually arise from the dispermic fertilisation of a haploid ovum, probably with a defective zona pellucida. This results in a triploid chromosomal constellation [6], [7].
The present study was performed to evaluate the clinicopathologic characteristics of CHM, the morphologic features associated with the development of gestational trophoblastic neoplasia [11], [12], [13] as well as the reproductive experience after treatment. Cases of PHM with a comparably low reported risk of less than 3% for persistent disease [14], [15] were not considered.
Section snippets
Material and methods
One hundred fifty-one cases of CHM were obtained from the files at the Department of Obstetrics and Gynecology, University of Leipzig. The study period covered all women who were treated between January 1985 and December 1996 at our department. Patients’ age, gestational week, last reproductive event, clinical presentation at admission and follow-up data were retrieved from the clinical charts. Subsequent pregnancy outcome was recognised.
All hematoxylin-eosin stained slides of the cases were
Results
In 12 cases, the diagnosis was changed during histopathologic re-evaluation into either hydropic abortion (n = 5) or partial hydatidiform mole (n = 5). Two cases showed marked regressive change, so definitive diagnosis was not possible. These cases were excluded from further evaluation. It is important to state that none of the excluded cases developed persistent disease or recurrence.
The overall study population consisted of 139 cases. During the study period, 73,498 deliveries occured. Therefore,
Discussion
Molar pregnancy is an unique disease and can be divided into partial and complete hydatidiform mole (CHM), based on genetic background and different risk of developing gestational trophoblastic neoplasia [6], [7], [16], [17]. While CHM represents a relative common disease in Asia, the incidence in the Western countries is quite low [3], [19]. The relatively high-incidence at our institution (one CHM in 530 deliveries) is probably due to selection bias and that most cases were referred from
References (41)
- et al.
Hytatidiform mole in England and Wales 1973–1983
Lancet
(1986) - et al.
Epidemiology and time trends of gestational trophoblastic disease in Korea
Int J Gynaecol Obstet
(1998) - et al.
Hydatidiform mole: two entities. A morphologic and cytogenetic study with some clinical considerations
Am J Obstet Gynecol
(1977) - et al.
Gestational trophoblastic disease following evacuation of partial hydatdiform mole: a review of 66 cases
Eur J Obstet Gynecol
(1997) The histological diagnosis of hydatidiform moles
Curr Diagn Pathol
(1994)- et al.
Gestational trophoblastic disease: update on new immunohistochemical findings
Curr Diagn Pathol
(2003) - et al.
Gestational trophoblastic disease: a study of mode of evacuation and subsequent need for treatment with chemotherapy
Gynecol Oncol
(2000) - et al.
Pregnancy outcomes of patients who conceived within 1 year after chemotherapy for gestational trophoblastic tumor: a clinical report of 22 patients
Gynecol Oncol
(2001) - et al.
Subsequent reproductive experience after treatment for gestational trophoblastic disease
Gynecol Oncol
(1998) How soon is it safe to undertake pregnancy after trophoblastic tumor?
Gynecol Oncol
(1999)
Pregnancy after EMA/CO for gestational trophoblastic disease. A report from The Netherlands
Br J Obstet Gynaecol
Risk of recurrent hydatidiform mole and subsequent pregnancy outcome following complete or partial hydatidiform molar pregnancy
Br J Obstet Gynaecol
Histologic classification and staging of gestational trophoblastic disease
Gen Diagn Pathol
Gestational trophoblastic disease
Gestational trophoblastic syndrome: an audit of 112 patients. A South African experience
Int J Gynecol Cancer
Complete and partial hydatidiform moles: cytogenetic and morphological aspects
Complete moles have paternal chromosomes but maternal mitochondrial DNA
Hum Genet
Mechanism of origin of complete hydatidiform mole
Nature
Clinicopathologioc differences between diploid and tetraploid complete hydatidiform moles
Int J Gynecol Pathol
The new FIGO 2000 staging and risk factor scoring system for gestational trophoblastic disease: description and critical assesssment
Int J Gynecol Cancer
Cited by (24)
Perinatal outcomes of first pregnancy after chemotherapy for gestational trophoblastic neoplasia: a systematic review of observational studies and meta-analysis
2022, American Journal of Obstetrics and GynecologyCitation Excerpt :The forest plots of the overall analysis are shown in Figures 2 to 5. Pooled data from 19 studies involving 2925 participants showed an incidence of spontaneous abortion of 15.28% (95% CI, 12.37–18.74) with substantial heterogeneity (I2=73%, t2=0.20, P<.01) (Figure 2).17,19,20,27–31,33–37,39–41,43–45 Among the 23 studies included in the systematic review, only 11 provided data for quantitative analysis,20,27–29,32–36,40,41 and 1693 participants showed a 3.30% incidence of malformation (95% CI, 2.27–4.79), with moderate heterogeneity between studies (I2=31%, t2=0.14, P=.14) (Figure 3).
Molar pregnancy after in vitro fertilization with euploid single embryo transfer
2021, F and S ReportsObstetrics outcomes after complete and partial molar pregnancy: Review of the literature and meta-analysis
2021, European Journal of Obstetrics and Gynecology and Reproductive BiologyCitation Excerpt :Conflicting results were obtained on the Cyclin E and the p57kip2 protein role in the CHM pathogenesis [26]. These proteins, through the cell cycle regulation, could influence not only the molar disease persistence but also the subsequent pregnancies [27]. However, cyclin E's role on subsequent pregnancies would be only a hypothesis, and further studies are needed to confirm these results.
Causative Mutations and Mechanism of Androgenetic Hydatidiform Moles
2018, American Journal of Human GeneticsCitation Excerpt :A new mechanism for the origin of AnCHMs was suggested: that dispermic fertilization of a haploid oocyte followed by postzygotic diploidization is more likely to be at the origin of the different genotypic types of sporadic HMs as well as of their association with mosaicisms and twin pregnancies consisting of one fetus with a normal placenta and a HM.4 Recurrent HMs (RHMs) affect 1.5%–9% of women with a prior HM.5–10 There are two genes, NLRP7 (MIM: 609661)11 and KHDC3L (MIM: 611687),12 responsible for RHMs.
Live births in women with recurrent hydatidiform mole and two NLRP7 mutations
2015, Reproductive BioMedicine Online