Gestational Trophoblastic Disease

WANG XIN-YONG
Departmente of Gynecology
 PREFACE
 Whate is the happiest things for
a lady in the whole life ?

 ………..
To be a bride?
To get pregnent?
To be a mother ?
SUITABLE SPERMITY
 SUITABLE SPERMITY
 1 good sperm + 1 nice ovum =
wonderful
 Fertilizition…..1,2,3….babys
Defination:
Itroduction
• gestational trophoblastic
disease (GTD) is a group of
disease originated from
placental villose trophoblastic
cells, including hydatidiform
mole, invasive mole,
choriocarcinoma and a kind of
less common trophoblastic cell
tumor in placenta.(PSTT)
 Introduction
Relations among the diseases:
• Benign mole is considered to be
abnormal formation of placenta
accompanied by the special abnormal
hereditary ;
• Invasive mole results from benign mole;
• Choriocarcinoma and the trophoblastic
cell tumor in placenta may result from
benign mole, term pregnancy, abortion
and ectopic pregnancy.

Normal placenta choriocarcinoma Hydatidiform mole

Hydatidiform Mole
 Introduction
 The most common gestational
trophoblastic neoplasm
 The incidence varies worldwide from 1 in
125 deliveries in Mexico and Taiwan to 1
in 1500 deliveries in the U.S
 Introduction
 The incidence in higher women under
20 and over 40 , patients of low
economic status, and in those whose
diets are deficient in protein, folic
acid , and carotene.
 Molar pregnancy occurs in fewer than
2% of subsequent gestations in
women with a history of mole .
 Introduction
 Defination:
Hydatidiform mole means that
after pregnancy the placental
trophoblastic cells proliferate
abnormally, there is stromal
edema, and forms vesicula which is
like grape on its apparence.
 Classification :
Hydatidiform mole is divided
into complete and incomplete type.
Complete type
Complete type
incomplete type
 Etiology
 the etiology is not clear
 Etiology of complete
hydatidiform mole
Epidemiology: the morbidity of
hydatidiform mole is different in
different area.
 Etiology
 High risk factors:
1.nourishing status,social
economy.
2.age:over 35 and 40 years
old;below 20 years old.
3.hydatidiform mole history:if
a patient has the history of 1 or 2
times hydatidiform mole,then the
morbidity of the hydatidiform
mole when pregnant again is 1%
and 15~20% respectively.
 Etiology
Genetic factors:
enucleate egg fertilization:
chromosome karyotype of complete
mole is diploid ,90% is 46XX,10% is
46XY.
Etiology
 Etiology
Etiology of incomplete
hydatidiform mole:
• the morbidity of incomplete
mole is much lower than that of
the complete type, and it is not
associated with age.
• Genetic factors: chromosome
karyotype of 90% incomplete
mole is triploid. The most
common chromosome
karyotype is 69XXY, and then is
69XXX or 69XYY.
Etiology
 Pathology
Complete incomplete
mole mole
Embryotic or fetal - +
tissue
Villus stromal Diffused Localized
edema
Trophoblastic Diffused Localized
hyperplasia
Villus outline Regular Irregular
Villus stromal blood - +
vessel
Karyotype Diploid triploid or
FHB Absent tetraploid
HCG >50,000 Present
Symptoms Common <50,000
GTT 20-30% Rare
Normal and mole
 Pathology

Partial mole

Complete mole
 Pathology

Partial mole

Complete mole
 Clinical manifestation
complete mole:
• vaginal bleeding after
amenorrhea:3/4
• uterus is abnormally enlarged
and become soft
• Lack of fetus signs
• theca lutein ovarian cyst
• gestational vomitting and PIH
• Hyperthyroidism
Theca Lutein Ovarian Cyst
Theca Lutein Ovarian Cyst
 Clinical Manifestation
Partial mole:
• may have the major
symptoms of complete
mole but it is slightly
manifested. no luteinizing
cyst. The histologic
examination of curettage
sample may confirm the
diagnosis.
 Prognosis
 complete mole has the latent
risk of local invasion or
telemetastasis
 The high-risk factors includes
• β-HCG>100000IU/L
• uterine size is obviously
larger than that with
the same gestational
time.
 Prognosis
• the luteinizing cyst is >6cm
• If >40 years old,the risk of
invasion and metastasis may
be 37%, If >50 years old,the
risk of invasion and metastasis
may be 56%.
• repeated mole:the morbidity of
invasion and metastasis
increase 3~4 times
 Diagnosis
 HCG measurement : serum
urine
 Ultrasound examination
 Detecting the fetal heart beat by
ultrasound Doppler
Diagnosis
 Differential Diagnosis
 abortion
 twin pregnancy
 polyhydramnios
 Management
 Emptying uterine cavity
• once the diagnosis is confirmed
the uterine cavity should be
emptied as soon as possible
 Hysterectomy
• over 40 years old with high-risk
factors
• uterine size is over 14
gestational weeks
 Management of luteinizing cyst
 Management
Preventive chemotherapy
• over 40 years old
• the β-HCG is over
100kIU/L before
emptying mole
• the HCG regresion
curve is not
progressively declined
Preventive chemotherapy
• uterus is obviously larger than
the size of the amenorrhea
• luteinizing cyst is >6cm
• there is still over hyperplasia of
trophoblastic cells in the
second curettage
• no follow up conditions
 Follow up
 HCG qw till normal
 QW×3m
 Q2W×3m
 QM×6m
 Q6M×2y
Invasive Mole
 Introduction
 Definition:
Invasive mole means the
hydatidiform mole invade the
uterine myometrium or
metastasize to extrauterine
tissue.
 Biologic behavior:
Invasive mole villus may
invade myometrium or blood
vessels or both, at beginning it
spread locally,invade
myometrium, sometimes
penetrate the uterine wall and
 Pathology
 Macro examination:
Different size of
viscula in
myometrium,there may
be or may not be primary
focus in uterine
cavity.when the invasion
is near serosal layer……
Invasive Mole
 Pathology
 Microexamination:
Villose structure and
trophoblastic cells proliferation
and differentiation
deficiency.villose and
trophoblastic cells can be found
in most patients,and cause
vascular wall necrosis and
bleeding.
 Clinical Manifestation
 irregular vaginal bleeding
 uterine subinvolution

 theca lutein cyst does

not disappear after
emptying uterus
 abdominal pain

 metastatic focus
manifestation
 Diagnosis
 history and clinical
manifestation
 successive measurement of

HCG
 ultrasound examination

 X-ray and CT

 histologic diagnosis
Invasive Mole
 TREATMENT
 Same to choriocarcinoma.
 Discuss together
Choriocarcinoma
 Introduction
 Choriocarcinoma is a
highly malignant tumor,it
can metastasize to the
whole body through
blood circulation ,
damage tissues and
organs,cause bleeding
and necrosis.
 Introduction
 The most common metastatic
site is lung, then vagina,brain
and liver
 Introduction
 50% gestational
choriocarcinoma result from
hydatidiform mole (generally
occurs over 1 year after
emptying the mole), the rate of
occurrence after abortion or term
delivery is 25% and 25%
respectively, seldom occurs after
ectopic pregnancy.
 After hydatidiform mole one
 Pathology
 Macroexamination:
Most
choriocarcinoma occurs
in uterus, the tumor
diameter 2-10cm, its
color, section, cancer
embolus is often found in
parauterine veins,ovarian
luteinizing cyst may be
formed.
 Pathology
 Histologic examination:
Under microscope the
hyperplastic cytotro-phoblastic
cells and syntrophoblastic cells
invade the myometrium and
blood vessels accompanied by
the bleeding and necrosis, so the
cancer cells can not be found in
the center.
Pathology
 Clinical Manifestation
 Vaginal bleeding
 Pain

 Uterine enlargement

 Mass
 Diagnosis
 Clinical Features
 Ultrasonography
 Human Chorionic Gonadotrophin
 CT
 X-ray
 Pathology
 Differential Diagnosis
 Hydatidiform mole
 Invasive mole
 Placental site trophoblastic tumors
 Rudimental placenta
 Metastasis
 Lung
 Vagina
 Brain
 Liver
Metastasis （ Lung ）
 Anatomic Staging
Stage I disease confined to
Stage II uterus
gestational trophoblastic
tumor extending outside
uterus but limited to
genital structures
Stage (adnexa,
gestationalvagina, broad
trophoblastic
III ligament)
disease extending to
lungs with or without
known genital tract
Stage all other metastatic sites
IV involvement
Management
 Chemothera
py
 Surgery
 Good-prognosis Patients
 (1) metastases are confined to the
lungs or pelvis;
 (2) serum β-hCG levels are below
40,000 Miu/mL at the onset of
treatment; and
 (3) therapy is started within 4
months of apparent onset of disease.
 Poor-Prognosis Patients
 (1) serum β-hCG titers
greater than 40,000
 (2)disease diagnosed more

than 4 months after molar

pregnancy ;
 (3) brain or liver metastases;
 Poor-Prognosis Patients
(4) prior unsuccessful
chemotherapy ;
 (5)onset following term

gestation . These patients

respond poorly (<40%
response rate ) to single-
agent therapy .
 Follow up
 QM×1 y
 Q3M×2 y
 QY×2y
 Q2Y
PSTT
 PLACENTAL-SITE
TROPHOBLASTIC TUMOR
 derived from the intermediate
trophoblasts of the placental bed ,
with minimal or absent
syncytiotrophoblastic tissue
 local invasion occurs into the
myometrium and lymphatics.
 occur with any type of pregnancy
 Treatment of PSTT
 resistant to chemotherapy
 hysterectomy is the recommended
route of treatment . Partial uterine
resection
 Chemotherapy is indicated in cases
of metastatic disease . EP-EMA is the
preferred regiment over EMA/CO
 Prognosis of PSTT
 Early stage
 Late stage
 The greatest adverse outcomes are
associated with an inlerval > 2 years
from antecedent pregnancy to
diagnosis
Thanks for Your Attention