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Gestational trophoblastic diseases
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Gestational trophoblastic diseases Chapter 20 from williams obstetrics.
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[Subject]Gestational trophoblastic diseasesGestational
trophoblastic diseases
DEFINITION 3. By a diploid sperm produced by failure of
Encompasses a heterogeneous group of either the first or second meiotic division
diseases form the benign to malignant type
It arises from the placental trophoblastic Partial Mole
epithelium after a normal or abnormal Derived from one maternal and two paternal
fertilization chromosomes, resulting to triploid genotype
MODIFIED WHO CLASSIFICATION Fertilization of Haploid Egg (23X)
Molar Lesions Non-Molar Lesions 1. By two haploid sperms (dispermy)
Hydatidiform Choriocarcinoma 2. By single diploid sperm which then
Mole Placental site trophoblastic replicates (monogenic diandric triploidy)
Complete, tumor 3. By a diploid sperm produced by failure of
Partial Epithelioid trophoblastic tumor either 1st or 2nd meiotic division
Invasive mole Miscellaneous trophoblastic
lesions Fetuses affected by triploidy in atrial moles gave
Exaggerated placental multiple congenital anomalies and mental
site retardation.
Placental site nodule
Clinicopathologic Features
HYDATIDIFORM MOLE Feature Partial Complete
An abnormal placenta characterized by Karyotype 69 XXX/69 46,X or 46,
edematous and vesicular chorionic villi XXY XY
accompanied by variable amount of Fetus Often present Absent
proliferative trophoblasts Amnion, RBC Usually Absent
Subtypes: present
o Complete Villous edema Variable Focal, diffuse
o Partial Trophoblastic Focal, slight Diffuse, slight
proliferation to moderate to severe
Risk factors Diagnosis Missed Molar
Age abortion gestation
o Extremes of age (<15 and >40 yo) Uterine size Small for Large for
Reproductive history dates dates
o H mole – risk of repeat Hmole is 1- Theca lutein cyst Rare 25-30% of
1.5% cases
o After 2nd molar pregnancy – 18% risk Medical Rare Less than
of recurrence complications 25%
Diet Postmolar <5% 6-32%
o Low animal fat and beta-carotene malignant
diet sequelae
Pathogenesis Diagnosis
Role of oncogenes Clinical presentation
Complete moles Sonographic picture
Overexpression of p53, cfms, c-myc, c-er Beta hCG titer
B2, bcl-2, p21, Rb, and MdM2 Histopathologic examination
Epidermal growth factor receptor (EGFR)
higher in molar pregnancies
Complete Mole
Derived from the paternal or androgenetic
origin Clinical Presentation
No maternal chromosomes Confirmed pregnancy
Classic “snowstorm” pattern Uterine size and date discrepancy
Exaggerated subjective symptoms of
Fertilization of an empty ovum pregnancy (nausea, vomiting)
1. By a SINGLE HAPLOID SPERM (23X) Painless second trimester bleeding
which duplicates itself to restore 46XX o With prevalence of early ultrasound,
karyotype called diandric diploidy moles are now diagnosed in the first
, 1. Anemia Discriminatory level of BHCG
2. Pre-eclampsia In normal pregnancy, GS visible
3. Hyperthyroidism o TVS at HCG 1000-2000 mIu/ml
4. Electrolyte imbalance o TAS at HCG 2400-3600 mIu/ml
5. Hyperemesis gravidarum o 90% of early moles correctly
6. Pulmonary insufficiency diagnoses when HCG level >
7. Disseminated Intravascular Coagulopathy 82,360mIu/ml and no FHT seen
Vaginal Bleeding Normal Pregnancy
Occurs in 89-97% of cases Serum HCG = 20000 to 100000 at 7-10
Occurs when molar chorionic villi disrupts weeks followed by gradual decline
maternal vessels by separating from the
deciduas GTD
Prune juice in character, and in some Any HCG level >1000000 at any time in
cases, vesicles are passed out pregnancy OR
>320000 miu/ml after 100 days of
Excessive Uterine Enlargement amenorrhea
Discrepancy between uterine size and AOG
Seen in 40-50% of patients with complete Immunostaining
mole The use of p57KIP2 during the early first
Due to retained blood and hydropic villi trimester
P57KIP2 is paternally derived and
Pre-eclampsia maternally expressed so that its absence
12-27% of patients on nuclear staining establishes the
Limited almost exclusively to patients with didagnosis of CHM;
markedly elevated hCG values A positive staining is seen in PHM and
Rare if the molar pregnancy is diagnosed hydropic abortus
before 10-12 weeks
Management: Familial recurrent molar pregnancy
o Control of hypertension Rare occurrence
o Prevention of convulsions Characterized by recurrent complete
o Prevention of end organ damage hydatidiform mole of biparental origin rather
than the more usual androgenetic origin
Hyperthyroidism Evaluation of families with recurrent molar
Clinically evident hyperthyroidism is seen in pregnancy suggests that dysregulation of
2-7% of patients normal parental imprinting of genes
Laboratory evidence of hyperthyroidism is Genetic mapping shows that in most
more common families the gene responsible is located in
Presenting symptoms include thyroid 1.1mb region on chromosome 19q13.4
enlargement, tachycardia Mutations in the gene result in dysregulation
Due to cross-stimulation of TSH receptor of normal parental imprinting of genes
with HCG
PTU and Propranolol given to inhibit Diagnostic CHM PHM Hydropic
peripheral conversion of thyroxine to test abortus
triiodothyronine Ultrasound Snowstor Cystic Cystic
Propranolol also blocks sympathetic m pattern spaces spaces
response to thyroid hormones – to prevent within within
thyroid storm placenta, placenta,
feuts, GS fetus, GS
Pulmonary Insufficiency Serial HCG Sustained, Sustained, Elevated,
Occurs in 2% of cases markedly markedly decline
Observed after molar evacuation in patients elevated elevated
with high βhCG levels, excessive uterine Karyotyping 46xx 69xxx, 69xxx
size and very large theca lutein cysts 69xxy oor
May result from pulmonary embolism, 69xyy
congestive heart failure due to
preeclampsia, severe anemia,
hyperthyroidism, and intravenous fluid Histopathologic examination
overload
Sonographic Picture
Theca Lutein Cysts
Multicystic, anechoic cysts
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