GESTATIONAL TROPHOBLASTIC

DISEASE
PREPARED BY:
NIKITA PATEL
 DEFINITION
• Gestational trophoblastic disease (GTD)
encompasses a spectrum of proliferative
abnormalities of trophoblasts associated with
pregnancy. Persistent GTD (persistently raised
b-hCG) is referred as gestational trophoblastic
neoplasia (GTN).
 CLASSIFICATION
• Hydatidiform mole: – Complete – Partial
• Invasive mole
• Placental site trophoblastic tumor
• Choriocarcinoma
Non metastatic disease (confined to the uterus)
Metastatic disease:
A. Low risk (good prognosis)
• Disease is present < 4 months duration
• Initial serum hCG level < 40,000 mIU/mL
• Metastasis limited to lung and vagina
• No prior chemotherapy
• No preceding term delivery
B. High risk (poor prognosis)
• Long duration of disease (> 4 months)
• Initial serum hCG > 40,000 mIU/mL
• Brain or liver metastasis
• Failure of prior chemotherapy
• Following term pregnancy
• WHO score > 7
HYDATIDIFORM MOLE (Syn: Vesicular mole)

TYPES:
• Complete
• Incomplete (partial)
• DEFINITION: It is an abnormal condition of the
placenta where there are partly degenerative
and partly proliferative changes in the young
chorionic villi. These result in the formation of
clusters of small cysts of varying sizes. Because
of its superficial resemblance to hydatid cyst,
it is named as hydatidiform mole. It is best
regarded as a benign neoplasia of the chorion
with malignant potential.
 ETIOLOGY
• The cause is not definitely known, but it appears to be related
to the ovular defect as it sometimes affects one ovum of a twin
pregnancy. However, the following factors and hypotheses have
been forwarded:
• Its prevalence is highest in teenage pregnancies and in those
women over 35 years of age.
• The prevalence appears to vary with race and ethnic origin.
• Faulty nutrition caused by inadequate intake of protein, animal
fat could partly explain its prevalence in the Oriental Countries.
Low dietary intake of carotene is associated with increased risk.
• Disturbed maternal immune mechanisms suggested by—(a)
Rise in gamma globulin level in absence of hepatic disease. (b)
Increased association with AB blood group which possesses no
ABO antibody.
• Cytogenetic abnormality—In general, complete moles
have a 46XX karyotype (85%), the molar chromosomes
are derived entirely from the father. The ovum nucleus
may be either absent (empty ovum) or inactivated which
has been fertilized by a haploid sperm. It then duplicates
its own chromosomes after meiosis. This phenomenon is
known as androgenesis. Infrequently, the chromosomal
pattern may be 46XY or 45X.
• The higher the ratio of paternal: maternal chromosomes,
the greater is the molar change. Complete moles show 2:0
paternal/maternal ratio whereas partial mole shows 2:1
ratio.
• History of prior hydatidiform mole increases the chance of
recurrence (1–4%).
PATHOLOGY OF HYDATIDIFORM MOLE
• It is principally a disease of the chorion. Death of the
ovum or failure of the embryo to grow is essential to
develop complete (classic) hydatidiform mole.
• Microscopic appearance : The basic findings are-
There is marked proliferation of the syncytial and
cytotrophoblastic epithelium.
• Ovarian changes: Bilateral lutein cysts are present in
about 50%. These are due to excessive production of
chorionic gonadotropin and they are also observed in
multiple pregnancy. These regress spontaneously
within 2 months after expulsion of mole.
 CLINICAL FEATURES
• Abnormal vaginal bleeding
• Lower abdominal pain
• Hyperemesis gravidarum
• Features of early onset preeclampsia < 20 weeks
• Uterus > dates (50%)
• Absent fetal parts and FHS
• Expulsion of vesicular tissues (Fig. 16.17)
• Theca lutein cyst of ovaries (25%) > 6 cm
• Hyperthyroidism (rare)
• Serum hCG > 100,000 mIU/mL
• USG: snowstorm appearance
SIGNS
• Features suggestive of early months of
pregnancy are evident.
• The patient looks more ill than can be
accounted for.
• Pallor
• Features of preeclampsia
• The size of the uterus is more than that
expected for the period of amenorrhea
• The feel of the uterus is firm elastic (doughy).
This is due to the absence of the amniotic fluid
sac.
• Fetal parts are not felt, nor any fetal
movements. External ballottement cannot be
elicited.
• Absence of fetal heart sound which cannot be
detected even by the Doppler effect
cardioscope.
Vaginal examination:
• Internal ballottement cannot be elicited.
• Unilateral or bilateral enlargement (theca
lutein cyst) of the ovary may be palpable in
25–50% of cases. The enlarged ovary may not
be palpable due to the enlarged uterus.
• Finding of vesicles in the vaginal discharge is
pathognomonic of hydatidiform mole.
• If the cervical os is open, instead of the
membranes, blood clot or the vesicles may be
felt.
 INVESTIGATIONS
• Full blood count, ABO and Rh grouping.
• Hepatic, renal and thyroid function tests are
carried out.
• Sonography: Characteristic feature of molar
pregnancy is “snowstorm” Appearance
• Estimation of chorionic gonadotropin:
• X-ray abdomen
• CT and MRI
 DIFFERENTIAL DIAGNOSIS
• Threatened abortion
• Fibroid or ovarian tumor with pregnancy
• Multiple pregnancy
COMPLICATIONS OF MOLAR PREGNANCY

• Hemorrhage and shock

• Sepsis
• Perforation of the Uterus
• Preeclampsia
• Acute pulmonary insufficiency due to
pulmonary embolization of the trophoblastic
cells
• Late: The development of choriocarcinoma
 MANAGEMENT
• Flow chart in DC dutta book
PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT)
• It is a rare histological diagnosis.
Syncytiotrophoblastic cells are generally
absent. So there is persistent low level of
serum or urinary hCG. The tumor arises from
the intermediate trophoblasts and is composed
mainly of cytotrophoblastic cells. Patient
presents with vaginal bleeding. Local invasion
into the myometrium occurs. PSTT is not
responsive to chemotherapy. Hysterectomy is
the preferred treatment.
PERSISTENT GESTATIONAL TROPHOBLASTIC DISEASE
• DEFINITION: Persistent GTD is defined where there
is persistence of trophoblastic activity as evidenced
by clinical, imaging, pathological and/or hormonal
study following initial treatment. This may be
following treatment of hydatidiform mole, invasive
mole, choriocarcinoma or placental site
trophoblastic tumor.
• A postmolar GTD may be benign or malignant. But
a GTD after nonmolar pregnancy is always a
choriocarcinoma.
• Treatment: Hysterectomy