REVIEW

The Obstetrician
& Gynaecologist
2003;5:130-5

Keywords
gestational
trophoblastic disease
(GTD),
human chorionic
gonadotropin (hCG),
hydatidiform mole,
trophoblastic
tumour

Trophoblastic diseases and

pregnancy
Eric Jauniaux
Gestational trophoblastic disease (GTD) is a term commonly applied t o
a spectrum of interrelated disorders originating from the placental
trophoblast. These include complete, partial and invasive moles,
placental site trophoblastic tumours and choriocarcinomas. Modern
genetic and molecular biology techniques enable rapid and accurate
diagnosis and have contributed t o a better understanding of the
pathophysiology of GTD. As a result most women can be treated
before they develop severe complications. This review addresses the
perinatal diagnosis of GTD and focuses on the roles of ultrasound and
Doppler examination in prenatal diagnosis and the importance of
histopathology in the postnatal diagnosis of GTD.
Introduction

Author details

Gestational trophoblastic diseases result from

abnormal proliferation of the trophoblast. They
include a wide spectrum of disorders, ranging
from molar pregnancy at the benign end to
neoplastic placental site trophoblastic tumours.'
Estimates of the incidence of the different forms
of GTD throughout the world vary, mainly
because few countries have registries and, rather
than being population based, incidence figures
are often based on hospital cases. Furthermore,
the vast majority of complete and partial moles
miscarry during the first trimester of pregnancy.
The incidence of molar pregnancies has been
estimated to be as high as one per 41
miscarriages.'With the advent of a sensitive assay
for human chorionic gonadotropin (hCG) for
monitoring trophoblastic tumours and new
approaches to chemotherapy, most women
diagnosed with a GTD are efficiently followed
up and can be treated before the development of
severe complications.

Pathophysiology of gestat iona I

troDhoblastic disease

the demise of an embryo or early gestational age

fetus. However, gross waterlogging and villous
cistern formation are only found in complete
hydatidiform moles (CHM) and partial hydatidiform moles (PHM). The process of
hydatidiform transformation in CHM is rapid,
but not instantaneous, and a small proportion of
the villi retain a prehydatidiform, still solid, core
complete with remnants of villous capillaries.'
Since the embryo only partially forms or dies
early in development, well before the establishment of an embryo-placental circulation, the
vestigial villous vessels contain no embryonic
erythrocytes and usually disappear by the sixth
week following conception. In delayed
miscarriage, independent of chromosomal
abnormality, the progressive disappearance of the
villous vasculature after embryonic death (before
seven to eight weeks menstrual age) leads to
villous hydrops. However, this does not
necessarily lead to a PHM.
Biochemical analysis of the molar fluid suggests
that it is derived from maternal plasma by
diffusion and/or synthesis by the trophoblast and
that it is unchanged by fetal rnetaboli~m.~
The
high levels of sodium, potassium and chloride
found in molar fluid are most probably
secondary to the absence of villous drainage, as
the trophoblast continues to transfer water and
electrolytes for a few weeks following embryonic demise. However, a-fetoprotein, which is
synthesised by the secondary yolk sac and the
fetal liver but not by the villous trophoblast, is
found in all molar fluid samples. Analysis of
concanavalin A affinity molecular variants of afetoprotein in molar vesicle fluid indicates that ;

Departments of Obstetrics and

Gynaecology, Royal Free and
University College London Medical
School, University College London,
86-96 Chenies Mews, London
WClE 6HX UK.
ernail: e.jauniaux@ucl.ac.uk

Although there is a well established clinical

association between molar changes of the villi
and trophoblastic hyperplasia, hydropic villous
changes can be found in conditions that are not
related to GTD. Hydropic (hydatidiform)
transformation of the villous mesenchyme, by
either a lack, maldevelopment or regression of
the villous vasculature, prevents the drainage of
fluid supplied by the trophoblast. Mild to
moderate generalised villous oedema can follow

130

0 2003 Royal College of Obstetricians and Gynaecologists

Eric Jauniaux MD PhD MRCOG.

Professor
in Obstetrics
and
Gynaecology,
Academic

originates from the yolk sac.3This suggests that

in CHM the conceptus develops at least up to
the blastocyst stage and, even if the embryo does
not form, cellular differentiation in the primary
and secondary yolk sac is sufficient to start the
synthesis of a-fetoprotein molecules.

miscarriages has confirmed that the majority of

cases are diandric in origin; but that only a
proportion of these paternally derived triplodies
develop a partial molar phenotype.8This suggests
that the mere presence of two paternal genomes
is not sufficient for molar development.

The investigation of reconstituted mouse eggs

suggests that the maternal contribution to the
zygote is essential for normal growth and
development of the embryo; whereas the
paternal contribution is crucial in the development of extra-embryonic tissues,in particular the
placenta and its tr~phoblast.~

Diagnosis of gestational
trophoblastic disease during
pregnancy

Complete hydatidiform moles are diploid with

chromosomes totally derived from the paternal
genome, probably resulting from the fertilisation
of an empty oocyte. The oocyte, devoid of the
maternal X chromosome, is instead fertilised by
a single spermatozoon whose chromosomes
double without cell cytokinesis.These moles are
characterised by generalised trophoblastic
hyperplasia and rapidly developing villous
oedema with central cistern formation, giving
the macroscopic appearance of a bunch of
grapes. The fluid, at first uniformly distributed
in the core of the villi, collects in several loculi to
coalesce into a central cistern.

REVIEW

The Obstetrician
& Gynaecologist
2003;5:130-5

Angiography was first used in both the diagnosis

of molar pregnancy in utero and the follow up of
women at risk of persistent trophoblastic disease.
In women with persistent trophoblastic disease,
or with chemotherapy-resistant disease, angiography has been of value in the diagnostic workup of myometrial invasion and surgical
management. Because of associated costs,
maternal discomfort and morbidity it was
progressively replaced by ultrasound imaging in
the 1960s. Ultrasonography has now also
replaced all other methods in early screening and
in establishing the differential diagnosis of molar
pregnancies in utero.

Partial hydatidiform moles are almost always

triploid, having inherited two sets of
chromosomes from the father (diandric) and one
from the mother.. Early cytogenetic studies
have suggested that the majority of triploidies
are of paternal-diandric origin, resulting from
the fertilisation of a haploid ovum either by two
single sperm or a single diploid sperm.6Less than
one-third of triploidies encountered in the first
trimester are of digynic origin, resulting from a
double maternal haploid contribution when the
ovum fails to undergo the first or second meiotic
division before fertilisation. A single paternal
haploid set imparted to the ovum gives a total of
69 chromosomes. A study of 91 cases of triploid

Singleton complete hydatidiform

moles
Classically, patients with singleton CHM present
with vaginal bleeding, abnormally high levels of
maternal serum P-hCG and uterine enlargement that is greater than expected for the
gestational age (Table 1). Medical complications
include pregnancy-induced hypertension, hyperthyroidism, hyperemesis, anaemia and the
development of ovarian theca lutein cysts.
Ovarian hyperstimulation and enlargement of
both ovaries may subsequently lead to ovarian
torsion or rupture of theca lutein cysts. Earlier
diagnosis has led to a reduction in the incidence
of these complication^.^ Molar changes can now
be detected from the second month of
pregnancy by ultrasound, which typically reveals
a uterine cavity filled with multiple sonolucent

Table 1 . Clinical features and maternal complications (%) of complete and triploid partial
hydatidiform moles. (modified from Jaunauix)
Features

Complete hydatidiform mole

KaVotyPe
Maternal serum P-hCG
Vaginal bleeding
Bilateral multicystic ovaries
Hyperemesis gravidarum
Pre-eclampsia
Hyperthyroidism
Uterine enlargement
Anaemia
Postmolar GTD
_

46 XX (90%)
1G200 MOM
84-97%
15-25%
8-26%
12-27%
<l%
28-51%
5520%
1429%

Triploid partial hydatidiforrn mole

69 XXX (70%)
1 M 0 MOM
25-50%
9%
5%
1WO%
<I%
9%
<1%

1-1 1%

MOM=mulnples of the meman

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areas of varying size and shape ('snow storm'

appearance) without associated embryonic or
fetal s t r u c t ~ r e . ~Large
~ ' ~ sonolucent areas
resulting from stasis of maternal blood in
between the molar villi are often found. Theca
lutein cysts, secondary to the high serum P-hCG
levels, may be diagnosed in up to 50% of secondtrimester cases of CHM, but their prevalence in
early pregnancy is much lower." Elevated serum
P-hCG levels combined with these specific
sonographic features are highly indicative of the
presence of a hydatidiform mole, even before the
final histopathological diagnosis is confirmed."
Within this context the role of Doppler, which
almost always demonstrates high velocities and
low resistance to flow in the uterine arterial
circulation, is limited and will only be of clinical
interest in the diagnosis of an invasive mole."

Diagnosis of a CHM with a coexisting fetus is

usually made at a later gestational age (around
15-20 weeks) than with a singleton CHM. As
CHMs produce a characteristic vesicular
sonographic pattern, their association with a
normal gestational sac can be accurately
determined at the end of the first trimester.'"^"

Partial hydatidiform moles

Partial hydatidiform moles refer to the

combination of a fetus with localised placental
molar degenerations.l6Histologically PHM are
characterised by focal swelling of the villous
tissue, focal trophoblastic hyperplasia and
embryonic or fetal tissue.The abnormal villi are
scattered within macroscopically normal
placental tissue, which tends to retain its shape.
In around 90% of cases PHM are triploid, the
remaining 10% includes tetraploidies and rare
Complete hydatidiform moles in
cases of placental diploid or triploid mosaics.'6
multiple pregnancies
O n ultrasound, PHM present as an enlarged
A CHM may coexist with a normal fetus and placenta (thickness >4cm at 18-22 weeks)
placenta in cases of molar transformation of one containing multicystic avascular sonolucent
ovum in a dizygotic twin pregnan~y."~'~~'~
As triploidy is a highly lethal
~paces.'~~''
Mothers with this condition are at a higher risk chromosomal abnormality most embryos
of persistent trophoblastic tumour, requiring affected by this defect die within a few weeks of
multiple cycles of chemotherapy, than patients conception. Diandric PHM triploidies are
with a classic molar pregnancy, 5040% versus associated with a higher miscarriage rate than
10-1 5% respectively, (Table 2).VaginaI bleeding digynic triploidies; probably because the excess
from the second month of pregnancy is the most of paternal contribution to the zygote has a
common presenting symptom and is found in deleterious effect on placental implantation and
90% of cases.The mother must be informed that
development. This can explain why PHM are
if she wishes to continue with the pregnancy she only observed in about one-third of all
will be at a high risk of developing the severe triploidies diagnosed after 11 weeks of
medical complications associated with a CHM. gestation.I6 Furthermore, in PHM the hydatiPregnancy induced hypertension is observed in diform transformation is slower and before 1250-60% of cases of continuing pregnancy. These weeks gestation some partial moles may present
complications are often related to high maternal as an enlarged placenta without obvious
serum P-hCG levels. In women deciding to macroscopic vesicular changes.Vaginal bleeding
in the first or second trimester is the most
continue with the pregnancy serum P-hCG
common maternal symptom reported in both
levels can be used to monitor the growth of the
molar mass until fetal viability is reached. types of triploidies (Table 1).The phenotypic
expression of both diandric and digynic
triploidies includes growth restriction and
disturbance of organogenesis, it becomes
obvious in fetuses surviving into the second
Table 2. Outcome of multiple pregnancies combining a complete
hydatidiform mole and normal fetus and placenta*'
trimester. From 16 weeks of gestation almost all
triploid fetuses have a least one measurement
Variables
I
I1
I11
(n=22)
(n=18)
(n=7)
below the normal range and more than 70%
Mean gestational age at diagnosis (weeks)
21
N/A
14
present with severe growth restriction.l6It must
Termination of pregnancy
12
8
1
be highlighted that more than 80% of fetuses
Complications of ongoing pregnancies
with triploid PHM present with symmetrical
Vaginal bleedmg
21
N/A
6
growth restriction, which is important from a
Pregnancy-induced hypertension
6
5
2
Theca lutein cyst
6
N/A
2
differential diagnosis point of view. Structural
Outcome
fetal defects are observed antenatally in about
Term delivery
2
2
2
93% of all cases. The most common are
5
1
3
Preterm delivery
abnormalities of the hands, bilateral cerebral
2
1
3
Intrauterine death
ventriculomegaly, heart
anomalies and
I = USA" and the world,""' I1 =Japan," I11 = U K (author's database).
micrognathia."
(Pregnancy Induced Hypertension occurred in 13 out of21 (62%)ongoing pregnancies)

132

Aneuploidies, and in particular trisomy 13 and

21 (but also mesenchymal dysplasia of the
placenta in Beckwith-Wiedemann syndrome),
can present with vesicular transformation of
some villous trunks. However, they are without
trophoblastic abnormalities and so cannot be
classified as 'true' PHM. The combined use of
ultrasound features, maternal serum proteins and
fetal cytogenetic findings enable early differential
diagnosis in utero and perinatal management of
those molar pregnancies that often present with
an anatomically normal fetus.l*

Persistent trophoblastic disease

Following uterine evacuation, 18-29% of
patients with a CHM and 1-11% of patients
with a PHM will develop a persistent trophoblastic disease.',16 While the incidence of
maternal complications has been reduced by
early diagnosis, the incidence of persistent
trophoblastic disease has remained unchanged
since the introduction of routine ultrasound
examination during pregnancy.'*" This suggests
there is a similar risk of post-molar tumour after
a first-trimester spontaneous molar miscarriage
than after the therapeutic abortion of a secondtrimester molar pregnancy. Serial hCG levels are
the standard method used for diagnosing and
monitoring therapeutic response of persistent
trophoblastic disease. Before the development of
transvaginal sonography, transabdominal sonography was used for the assessment of
trophoblastic uterine involvement in patients
with non-metastastic GTD. Transabdominal
sonography is only capable of detecting massive
uterine involvement.All studies have shown that
transvaginal sonography is a more accurate
method for the assessment of the depth of
myometrial invasion than transabdominal
sonography." The use of colour Doppler
imaging, with its added capability of displaying
bloodflow data, has improved the accuracy of
transvaginal sonography. Newly formed vessels
with frequent arteriovenous anastomosis, which
produce a characteristic ultrasound pattern,
surround nodules of residual GTD. The most
frequent feature is hypoechoic areas (blood
lacunae) surrounded by irregular echogenic areas
(trophoblastic
nodules)
and
numerous
intramyometrial signals (vascular shunts). In these
cases Doppler investigation of the uterine
vasculature and of small intratumoural vessels has
consistently shown a low resistance to flow and
high peak systolic velocities.

Invasive hydatidiforin moles

An invasive mole is defined as the penetration of
molar villi from a complete or partial hydatidi-

form mole into the myometrium or the uterine

vasculature.' Rarely, the molar tissue may
penetrate the whole thickness of the myometrium (percreta) leading to uterine
perforation and/or local pelvic extension. In
contrast to a choriocarcinoma, an invasive mole
contains villus structures with a variable degree
of trophoblastic proliferation and produces a
lower level of hCG. An invasive mole usually
becomes clinically apparent after the evacuation
of a molar pregnancy, the patient usually
presenting with heavy vaginal bleeding. The
tumour appears sonographically as a focal area of
increased echogenicity within the myometrium.
These nodules usually appear several weeks after
evacuation of a mole but may occur concurrently with a mole. The sonographic features
of the nodules are similar to the lesions found in
cases of placental-site trophoblastic tumours.

REVIEW
The Obstetrician
& Gynaecologist
2003;5:130-5

Placental site trophoblastic

tumours
Placental site trophoblastic tumours are the rarest
form of GTD. This particular variant of
malignant trophoblastic tumour is composed of
intermediate trophoblastic cells from the
extravillous trophoblast of the placental bed.' In
more than 90% of the cases placental site
trophoblastic tumours develop after a normal
pregnancy. Rare cases have been reported
following a diploid or triploid mole and in
postmenopausal women. Common presenting
symptoms include amenorrhoea of up to one
year or irregular vaginal bleeding of varying
duration.' Placental site trophoblastic tumours
invade the myometrium by separating muscle
bundles and fibres. Around 15-20% of them
behave in a malignant fashion with metastases to
the lungs, liver, abdominal cavity and brain. The
principal protein produced by the intermediate
trophoblast is human placental lactogen.'
Relatively low hCG levels and high human
placental lactogen levels should be found in the
serum of patients with placental site
trophoblastic tumours. Maternal biology can be
an important parameter in the differential
dagnosis since on ultrasound these tumours
appear as small heterogeneous echogenic areas
with fluid filled cysts," representing haemorrhagic areas, similar in appearance to an invasive
mole or persistent GTD.

Choriocarcinomas
Choriocarcinomas are highly malignant
tumours that arise from the trophoblastic
epithelium; they metastasise readily to the lungs,
liver and brain.9 Many women with a
choriocarcinoma will present with dyspnoea,

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neurological symptoms and abdominal pain.

These symptoms usually appear a few weeks or
months following pregnancy, but can sometimes
appear up to 10-15 years after the last
pregnancy's9 Around 50% of choriocarcinomas
follow a molar pregnancy, 30% occur after a
miscarriage and 20% after an apparently normal
pregnancy.' Seckl et al. demonstrated that
choriocarcinomas can also occur after a triploid
PHM.I9 There have been a few well documented examples of choriocarcinoma arising
from villous tissue in an otherwise normally
developed placenta; suggesting that most
choriocarcinomas that follow an apparently
normal pregnancy are in reality metastases from
a small intraplacental choriocarcinoma.' The
primary tumour is usually small in size, ranging
from 2.5-8 mm, and an extensive search of the
entire placenta is often required to find the
lesion. In most cases of intraplacental
choriocarcinoma the mother presents with
multiple metastases during the course of
pregnancy, but the infant is usually free of
disease. In sittr choriocarcinomas can also arise in
association with a chorioangioma."

Histopathological diagnosis
Most triploid placentas, between 7-12 weeks of
gestation, have no noticeable macroscopic
features of molar change, suggesting that molar
transformation becomes more pronounced as
pregnancy advances.*' In early pregnancy, molar
changes are often identified by histopathological
examination only; suggesting that most triploidy
will escape clinical detection in cases of firsttrimester miscarriage. The histological diagnosis
of hydatidiform moles depends on the presence
of trophoblastic hyperplasia.' In the vast majority
of PHM the trophoblastic hyperplasia is often
focal, involving the syncytiotrophoblast alone.'6.20
The hydatidiform changes are also focal,
resulting in an irregular patchwork of seemingly
normal and affected areas. Unusually conspicuous trophoblastic anomalies and insufficient
placental sampling may cause errors. Most
authors found that the atypical pattern of
trophoblastic hyperplasia is the important
diagnostic histological feature of a partial
mole.Z.lb,ZOHowever, most histopathologists have
difficulties in differentiating pseudomolar
pregnancies presenting with hydropic villous
changes from PHM. We found that the positive
predictive value and sensitivity of histology for
the detection of triploidy in first-trimester
miscarriages was high." Discordant results were
mainly found for specimens with histological
alterations due to prolonged placental postmortem retention where the trophoblastic
hyperplasia was not apparent. Delayed fixation

134

can also alter the results of microscopic

examination.To minimise the rate of histological
examination failure, it has been our policy to
request the whole specimen from the referring
physician and to process the samples
immediately upon arrival at the laboratory.
Pathological examination, in some cases, may
also be complicated by the fact that the molar
placental tissue may come from a resorbed twin.
Within this context, many diploid PHM
previously reported in the literature were
probably complete hydatidiform moles with a
coexisting fetus and placenta.16 Ploidy
determination by flow cytometry allows further
classification of molar gestations, even if villous
tissue has been embedded in paraffin. This
procedure is easier, faster and cheaper than cell
culture and can provide useful information that
may serve as an adjunct to equivocal histological
diagnosis. New techniques such as fluorescent in
situ hybridisation can also be readily used in
determining the ploidy of placental tissues from
partial moles, but are more expensive than flow
cytometry. Furthermore, the latter technique
enables the investigation of large cell
populations and is able to discover molar
mosaicism.

Recommendations and follow up

It is important to record the occurrence of
gestational trophoblastic diseases. The R C O G
along with the Departments of Health for
England, Scotland and Wales recommend that
women with either a CHM, PHM, twin
pregnancy with CHM or PHM, or macroscopic
or microscopic molar change that requires
follow up should be registered." Information on
registering patients is available through the
Hydatidiform Mole & Choriocarcinoma UK
Information and Support Service webi~te.'~
Although the risk of having a further molar
pregnancy is low, the RCOG recommends that
women considering future pregnancy should be
advised to avoid conceiving until their hCG
levels have been normal for six months. Women
should also avoid taking the oral contraceptive
pill or hormone replacement therapy until their
serum hCG levels are considered normal."
Modern methods of diagnosis and treatment
have led to improved outcomes for women diagnosed with trophoblastic diseases. But because of
the diagnostic and management difficulties for
women, in the second trimester of pregnancy,
with ultrasonic features that are suggestive of
molar transformation, it is important to refer
them to a specialised fetal medicine unit.

REVIEW

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