Gestational trophoblastic disease (gtd.version gao)
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Transcript of Gestational trophoblastic disease (gtd.version gao)
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Gestational Trophoblastic
Disease (GTD)
WAQAR ULLAH
08-207
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IntroductionWhat is GTD ?
It is a clinical term used to indicate closely
related conditions characterized by active
abnormal proliferation of trophoblastic cells
It is too among the rare human
malignancies that can be cured
even in the presence of widespread metastases
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Which does it include?
It includes a spectrum of interrelated tumors, including
hydatidiform mole (HM) 80 % of cases
invasive mole (IM) 12-15%
Choriocarcinoma (CH) 5-8%
Placental-site trophoblastic tumor (PSTT, borderline, very rare)
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Relationship of HM. IM. CH
hydatidiform therapeutic or
mole spontaneous abortion
term pregnancy
ectopic
invasion mole choriocarcinoma.
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Hydatidiform mole
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Hydatidiform mole
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Hydatidiform mole
It is a neoplastic proliferation of the trophoblast in which the terminal villiare transformed into vesicles filled with clear viscid material.
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It is usually benign but has malignant potentiality.
Incidence:
south east Asia is 1/500-600
the US and Europe:1/500-2000
China:1/1238
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Classification
It is divided into two classification
complete hydatidiform mole
partial hydatidiform mole
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complete hydatidiform mole(CHM):
the entire uterus filled with abnormal vesicles, no signs of fetus.
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partial hydatidiform mole
partial hydatidiform mole with evidence of a conceptus.
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Etiology
Though it is not known a number of associated factors have been noted:
age:>45 years women are 10 times more likely to develop HM than those younger.
Previous hx of HM
Previous misscarriage
Excessive smoking
Poor nutrion,esp vit A deficiency
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abnormal fertilization process:
the fertilization of a normal ovum with a duplicated haploid sperm:46XX
the fertilization of an empty egg by two sperms(dispermy):46XY
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Complete Mole, Pathogenesis
Duplication 46XX
Empty ovum
23X
Diandric diploidyAndrogenesis
Paternal chromosomes only
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Complete Mole, Pathogenesis
46XX
Empty ovum
23X
Dispermic diploidy
Paternal chromosomes only
23X 23X
23X
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Partial Mole, Pathogenesis
69XXY
Normal ovum
23X
Dispermic triploidy
Paternal extra set
23Y 23X
23Y 23X23X
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Pathologic findings
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complete hydatidiform mole
pathology
Complete moles lack identifiable embryonic or fetal tissues, and the chorionic villi exhibit generalized hydatidiform swelling and diffuse trophoblastic hyperplasia.
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Gross
we see a mass of vesicles, vary in size, grape-like with stems, blood and clot filling the inter-vesicle space
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Microscopic(complete mole)
Cytotrophoblast &
syncytiotrophoblast
hyperplasia(variable)
Avascularity
No fetal parts
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partial hydatidiform mole
It are characterized by the following pathologic features :
Chorionic villi if varying size with focal hydatidiform swelling and cavitation.
It contain identifiable embryonic or fetal tissues.
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Gross
we see a mass of vesicles, vary in size, grape-like and identifiable embryonic or fetal tissues.
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Microscopic(partial mole)
Vesicles have certain degree
of vascularity till fetal death
Fetal parts
Syncytiotrophoblast
hyperplasia
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Fetal hand demonstrating syndactyly. The fetus had a triploid karyotype, and the chorionic
tissues were a partial mole
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Feature Partial mole Complete mole
Karyotype
Most commonly
69, XXX or - XXY
Most commonly
46, XX or -,XY
Pathology
Fetus Often present Absent
Amnion, fetal RBC Usually present Absent
Villous edema Variable, focal Diffuse
Trophoblastic proliferation Focal, slight-moderate Diffuse, slight-severe
Clinical presentation
Diagnosis Missed abortion Molar gestation
Uterine size Small for dates 50% large for dates
Theca lutein cysts Rare 25-30%
Medical complications Rare 10-25%
Features Of Partial And Complete Hydatidiform Moles
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HYDATIFORM MOLE
CLINICAL FEATURES
Vaginal bleeding (anemia) 97%
Excessive uterine size 50%
Theco-lutein ovarian cysts 50%
Preeclampsia 27%
Hyperemesis 25%
Hyperthyroidism 7%
Trophoblastic embolization 2%
(respiratory distress)
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signs
1) abnormally enlarged and soft uterus
2) absence of braxton hicks contractions
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3) Bilateral ovarian enlargement
4) Absence of fetal parts on palpation
5) Pre eclampsia
6) Hyperthyrodism
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Diagnosis
suspicion:
abnormal bleeding after amenorrhea
inappropriately enlarged uterus;
absence of fetal heart sounds or could not feel fetal parts by palpation between 16-20th week
hyperemesis gravidarum
bilateral ovarian cysts
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Hydatidiform Mole
Diagnosis:
• Serum hCG levels:
Serum hCG levels of greater than 92 000 IU/l associated with absent fetal heart beat indicate a diagnosis of complete hydatidiform moles (Romero et al, 1985)
Serum hCG level decreases quickly if the patient has an abortion, but it does not in molar pregnancy
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Ultrasonography:
It is a reliable and sensitive technique for the diagnosis of complete molar pregnancy. Because the chorionic villi exhibit diffuse hydatidiformswelling. Complete moles produce a characteristic vesicular sonographic pattern, usually referred to as a “snowstorm” pattern.
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Ultrasonography may also
contribute to the diagnosis of
partial molar pregnancy by
demonstrating focal cystic spaces
in the placental tissues and an
increase in the transverse
diameter of the gestational sac.
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Differential diagnosis
abortion;
multiple pregnancy;
polyhydramnios
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Hydatidiform Mole
Management:
Complete history and physical examination
Investigations
Medical and surgical care
1
3
2
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Hydatidiform Mole Management:
• History and physcal examination:
Should aim to rule out the classic symptoms and signs that would lead to a diagnosis of:
• severe anemia
• dehydration
• preeclampsia
• thyrotoxicosis
The patient should be stabilized hemodynamically
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Hydatidiform Mole Management:
• Investigations:
Laboratory:
Pre-evacuation hCG
Complete blood count
Electrolytes, BUN, creatinine
Liver function tests
Thyroid function tests
Imaging:
Pelvic ultrasound
Chest x-ray
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Hydatidiform Mole
Management:
• Medical care:
Correction of:
Anemia
Dehydration
Hyperthyroidism
hypertension
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Hydatidiform Mole
Management: Surgical care:
Suction curettage (with
oxytocin or prostaglandin infusion)
Hysterectomy
•The method of choice
•Increased risk of medical complications
•Associated with a markedly decreased rate of malignant sequelae (3.5%) when compared with suction evacuation.
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Mangementsuction & curretage
Under GA.
Cervix dilation till 12mm.and S&C induced to the uterine cavity.
I.V oxytocin infusion is started .
S&C started by negative pressure of about 60 to 70cmHg.
The curette is genteelly rotated to ovoid perforation of the soft uterus, and the majority of the molar tissue is evacuated rapidly ,and the uterine size decreases
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F0llow-up
After the uterus has been evacuated :
About 90% of cases ,the trophoblastic tissue
die out completely.
About 10% of cases the trophoblastic tissue
does not die out completely and may persist
or recur as : invasive mole or
choriocarcinoma.
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Follow-up
So it is important that women who have had a hydatidiform mole:
should have close follow-up by serum hCG levels after the evacuation of the uterus,
To ensure early recognition of persistent
trophoblastic tissue .
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F0llow-up
After a molar pregnancy ,the hCG
levels will usually have returned to non
pregnant levels by 4 to 6 weeks after
evacuation.
The follow-up is recommended for 2
years in cases of complete moles, and 6
months of cases of partial moles after
the evacuation of uterus.
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F0llow-up
Serial quantitative measurement of serum hCG level at weekly intervals, after evacuation of moles till 4 to 5 weeks when the hCG become normal. Then every other week .When the titer gets negative the measurements are done every month fore 1 year.
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chemotherapy
Indication of chemotherapy after
the evacuation of the hydatidiform
mole in:
Serum hCG >20000 i.u/L , at any
time after evacuation of mole.
Raised hCG at 4 to 6 weeks after
evacuation of mole.
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F0llow-up
Evidence of metastases
,hepatic,brain,and pulmonary.
Persistent uterine hemorrhage
after evacuation of mole with
raised hCG levels.
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pregnancy
To achieve effective follow-up ,the
pregnancy is better to be avoided ,and also
the use of oral contraceptive pills until the
hCG levels returns to normal after the
evacuation of the mole.
Early diagnosis of persistent trophoblastic
disease ensures a good prognosis and an
effective system of follow-up.
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Invasion Mole
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Introduction
Invasion Mole arises from HM
it has malignant potentialities, invades the myometrium and penetrates the uterine wall, extends into the broad ligament or peritoneal cavity.
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in half or more of all cases invasive mole metastasizes through the peripheral circulation to distant sites, mostly to the lung.
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Pathologic findings
excessive trophoblastic proliferation and invasiveness
the degree of anaplasia is variable: completely benign---highly malignant
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differentiation between invasive mole and choriocarcinoma lies in whether the villous pattern is preserved:
if we see villi, it must be invasion mole;
if we can’t see villi, it is choriocarcinoma.
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Clinical course
Symptoms caused by primary lesions
vaginal bleeding
pelvic examination reveals delayed involution of the uterus, persisting cyst .
abdominal pain
intra-abdominal hemorrhage, penetration of the uterus .
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Metastatic symptoms
• cough, hemoptysis---positive X-ray signs
•profuse vaginal bleeding---vaginal or cervical metastasis, we can see bluish nodule in vaginal
•headache, nausea, vomit, paralysis or coma—it is caused by cerebral lesion.
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Diagnosis
history and clinical manifestation
hCG assay:
diagnosis suspected if hCG titers persist to be high 12 weeks after evacuation of a HM, or once regress to normal range but rise rapidly.
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possible reasons : retained HM
pregnancy
huge theca-lutein cyst persist
when we remove these reasons we can diagnosis invasive mole
other measurement
ultrasound
X-ray
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Prophylaxis
respond well to chemotherapeutic agents
main causes of death:hemorrhage, metastasis and infection
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Treatment:
Identical to that for choriocarcinoma
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Choriocarcinoma
It is highly malignant GTT
It may follow HM, invasion mole, abortion, normal pregnancy, ectopic pregnancy.
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Pathologic findings
Gross inspection
irregular or circumscribed hemorrhagic growth in the uterine wall
ulcerating surface opens into the endometrial cavity (rarely embedded in myometrium)
penetration into broad ligament or the peritoneal cavity
dark red blood:.it is filled metastatic nodules
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ulcerating surface opens into the endometrial cavity (rarely embedded in myometrium)
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Histologic findings
we see masses of anaplastic trophblastic cells in microscopy;
invasion into the uterine wall, destroying vessels, muscle tissue
prominent necrosis and hemorrhage
villi can not be recognized
spread through circulation
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Clinical Manifestations
irregular bleeding after preceding gestation;
malignant tumor cells enter the circulation through the open blood vessels and are transported to lungs, brain or to other distant sites.
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metastatic symptoms
pulmonary lesions
cerebral lesions
metastatic nodule in the vagina, vulva or cervix ,it is bluish nodule filled dark red blood.
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Diagnosis
Diagnosis must be suspected as a possible reason for continued (irregular) bleeding after any form of pregnancy.
we assay hCG , the time of hCG change into normal is different in various diseases.
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FIGO Staging
STAGE
I. Confined to the uterus
II. Outside of uterus, limited to genital structures
III. Extends to lungs +- genital tract involvement
IV. All other metastatic sites
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Who Orgnaization prognostic scoring system for gestational trophoblastic neoplasia
Prognostic factor 0 1 2 4
Age <39 >39 _ -
Antecedent pregnancy Hydatidiform Abortion , ectipic Term pregnancy -
Interval (months) <4 4-6 7-12 >12
hCG level (IU/liter) <10 10-10 10-10 >10
ABO blood groups
(female/male)
O/A B A/O AB
Largest tumor (cm) <3 3-5 >5 _
Site of metastasis _ Spleen, kidney Gastrointestinal tract, liver Brain
Number of metastases _ 1-3 4-8 >8
Prior chemotherapy _ _ Single drug Multiple
druge
The total score is obtained by adding the individual scores for each prognostic factor . Total score :<4 , low risk ; 5-7 , intermediate risk ;>8 , high risk .Interval :between antecedent pregnancy and start of chemotherapy.
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Treatment
highly sensitive to chemotherapy, which is invariably the treatment choice.
surgery has little place (because of the high vascularity and the effectiveness of chemotherapy). it is indicated for tumor resistant to chemotherapy and single metastases persisting despite chemotherapy.
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Chemotherapy
most often used drugs
methotrexate (MTX)
actinomycin D (Act-D)
5-fluorouracil (5-Fu)
vincristine (VCR)
cyclophosphamide (CTX)
chlo-ranbucil, etc
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principles low-risk patients are usually treated with a
single agent medium-risk patients are usually treated
with ABACA regimen with 80-90% survival rate. (Etoposide, Methotrexate,Hydroxyurea,6-mercaptopurine,Actinomycin-d,Folinic acid)
High-risk No. of regimens are used.mostcommon EMA/CO(etoposide,methotrexate,actinomycin-d,cyclophosphamide,vincristine)
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Operation
unresponsive or drug fails to reach the tumor;
if the tumor can be eradicated by drug therapy, esp.in young women, there is no reason to remove the uterus;
the ovaries need not be removed.
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Follow-up examinations
at 1-month interval for 1 year: at 3-month interval for 2 years
at 1-year interval for 3 years
at 2-year interval afterwards. pelvic examination
chest X-ray film
hCG
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Placental-Site Trophoblastic Tumor (PSTT)
Originate from intermediate cytotrophoblast cells
Secrete human placental lactogen (hPL) B-hCG often normal Less vascular invasion, necrosis and
hemorrhage than choriocarcinoma Lymphatic spread Arise months to years after term pregnancy
but can occur after spontaneous abortion or molar pregnancy
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Placental-Site Trophoblastic Tumor (PSTT)
Most common symptom is vaginal bleeding Tend to:
- Remain in uterus- Disseminate late- Produce low levels of B-hCG compared to other GTN- Be resistant to chemotherapy (treat with surgery)
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