Gestational Trophoblastic Disease

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 hydatidiform mole:

incomplete

• 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 mole

incomplete mole

Embryotic or fetal tissue

-

+

Villus stromal edema Trophoblastic

Diffused

Localized

Diffused

Localized

Villus outline

Regular

Irregular

Villus stromal blood vessel

-

+

Karyotype FHB HCG Symptoms GTT

Diploid Absent >50,000 Common 20-30%

triploid or tetraploid Present <50,000 Rare

hyperplasia

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 QW×3m Q2W×3m QM×6m Q6M×2y

normal

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 vagina, broad Stage (adnexa, gestational trophoblastic ligament) III disease extending to lungs with or without known genital tract Stage all other metastatic sites involvement IV

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 singleagent 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