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Gestational Trophoblastic Disease

Gestational Trophoblastic Disease. DI WEN M.D., Ph.D., Professor & Chairman Department Of Obstetrics & Gynecology Renji Hospital Affiliated to SJTU School of Medicine.

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Gestational Trophoblastic Disease

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  1. Gestational Trophoblastic Disease DI WEN M.D., Ph.D., Professor & Chairman Department Of Obstetrics & Gynecology Renji Hospital Affiliated to SJTU School of Medicine GTD

  2. introduction • Defination: • 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.

  3. introduction • Relations among the diseases: • Benign moleis considered to be abnormal formation of placenta accompanied by the special abnormal hereditary ; • Invasive moleresults from benign mole; • Choriocarcinoma and the trophoblastic cell tumor in placentamay result from benign mole, term pregnancy, abortion and ectopic pregnancy.

  4. Hydatidiform Mole

  5. 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

  6. Etiology • the etiology is not clear • Etiology of complete hydatidiform mole Epidemiology: the morbidity of hydatidiform mole is different in different area. 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. Genetic factors: 1.enucleate egg fertilization: chromosome karyotype of complete mole is diploid ,90% is 46XX,10% is 46XY.

  7. 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.

  8. Pathology Complete mole incomplete mole Embryotic or fetal tissue -+ Villus stromal edema diffuseed localized Trophoblastic hyperplasia diffuseed localized Villus outline regular irregular Villus stromal blood vessel -+ Karyotype diploid triploid or tetraploid

  9. Partial mole Complete mole

  10. Partial mole Complete mole

  11. Clinical manifestation • complete mole: • vaginal bleeding after amenorrhea • uterus is abnormally enlarged and become soft • hyperthyroidism • theca lutein ovarian cyst • gestational vomitting and PIH • Hyperthyroidism

  12. theca lutein ovarian cyst

  13. 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.

  14. 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. • 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

  15. Diagnosis • HCG measurement • ultrasound examination • detecting the fetal heart beat by ultrasound Doppler

  16. Differential diagnosis • abortion • twin pregnancy • polyhydramnios

  17. 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

  18. 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 • 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

  19. Follow up • HCG qw till normal • QW X 3m • Q2W X 3m • QM X 6m • Q6M X 2y

  20. Invasive mole

  21. introduction • Definition: Invasive molemeans 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 spread to the broad ligament or abdominal cavity.

  22. 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…… • Microexamination:villose structure and trophoblastic cells proliferation and differentiation deficiency.villose and trophoblastic cells can be found in most patients,and causevascular wall necrosis and bleeding

  23. Clinical manifestation • irregular vaginal bleeding • uterine subinvolution • theca lutein cyst does not disappear after emptying uterus • abdominal pain • metastatic focus manifestation

  24. Diagnosis • history and clinical manifestation • successive measurement of HCG • ultrasound examination • X-ray and CT • histologic diagnosis

  25. Choriocarcinoma GTD

  26. 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. • The most common metastatic site is lung ,then vagina,brain and liver • 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

  27. 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 cystmay be formed • histologic examination: under microscope the hyperplastic cytotrophoblastic cells and syntrophoblastic cells invade the myometrium and blood vessels accompanied by the bleeding and necrosis, so the cancer cells can notbe found in the center

  28. Clinical manifestation • Vaginal bleeding • Pain • Uterine enlargement • Mass

  29. Diagnosis • Clinical Features • Ultrasonography • Human Chorionic Gonadotrophin • CT • X-ray • Pathology

  30. Differential diagnosis • Hydatidiform mole • Invasive mole • Placental site trophoblastic tumors • Rudimental placenta

  31. Metastases • Lung • Vagina • Brain • Liver

  32. anatomic staging • Stage I disease confined to uterus • Stage II gestational trophoblastic tumor extending outside uterus but limited to genital structures (adnexa, vagina, broad ligament) • Stage III gestational trophoblastic disease extending to lungs with or without known genital tract involvement • Stage IV all other metastatic sites

  33. Management • Chemotherapy • Surgery

  34. Follow up • QM X 1 y • Q3M X 2 y • QY X 2y • Q2Y

  35. Thanks for Your Attention DI WEN M.D., Ph.D. Professor & Chairman Department of Obstetrics & Gynecology Renji Hospital Affiliated to SJTU School of Medicine GTD

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