Carmelia Cantika M.

C4

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Gestational Trophoblastic Disease The term gestational trophoblastic disease refers to pregnancy-related trophoblastic proliferative abnormalities. Past : classification based on histological criteria and clinical findings. Now: based on clinical findings and measurement of serum human chorionic gonadotropin (hCG) levels. Gestational trophoblastic disease is divided into two groups, hydatidiform mole and postmolar gestational trophoblastic neoplasia.

Hydatidiform Mole (Molar Pregnancy)

Molar pregnancy abnormalities of the chorionic villi that consist of trophoblastic proliferation and edema of villous stroma. Moles usually occupy the uterine cavity, develop in the oviduct and even the ovary. The absence or presence of a fetus or embryonic elements has been used to describe them as complete and partial moles. Table 112. Features of Partial and Complete Hydatidiform Moles Feature Karyotype Pathology Embryo-fetus Amnion, fetal red blood cells Villous edema Trophoblastic Clinical presentation Diagnosis Uterine size Theca-lutein cysts Medical complications Gestational trophoblastic neoplasia Missed abortion Small for dates Rare Rare <510% Molar gestation 50% large for dates 2530% Frequent 20% Often present Often present Variable, focal Variable, focal, slight to moderate Absent Absent Diffuse Variable, slight to severe Partial Mole Usually 69,XXX or 69,XXY Complete Mole 46,XX or 46,XY

Complete Hydatidiform Mole In complete hydatiform mole, the chorionic villi transform into a mass of clear vesicles(vary in size). The histological structure typically shows: 1. Hydropic degeneration and swelling of the villous stroma.

Carmelia Cantika M. C4

130110110100

Case 5

2. Absence of blood vessels in the swollen villi. 3. Proliferation of the trophoblastic epithelium to a varying. 4. Absence of fetus and amnion.

A complete or classical hydatidiform mole is characterized grossly by an abundance of edematous enlarged chorionic villi but no fetus or fetal membranes. There are theca-lutein cysts in both ovaries (arrows). The chromosomal composition of most complete molar pregnancies is 46,XX, with both chromosomes being of paternal origin androgenesis. Typically, the ovum has been fertilized by a haploid sperm, which then duplicates its own chromosomes after meiosis. The chromosomes of the ovum are either absent or inactivated. Occasionally, the chromosomal pattern in a complete mole may be 46,XY due to dispermic fertilization. Partial Hydatidiform Mole - partial hydatidiform mole when the hydatidiform changes are focal and less advanced, and some element of fetal tissue is seen;slowly progressive swelling within the stroma of characteristically avascular chorionic villi, whereas other vascular villi with a functioning fetal placental circulation are spared. - The karyotype typically is triploid69,XXX, 69,XXY, or 69,XYYthese are each composed of one maternal and two paternal haploid sets of chromosomes. A twin gestation of a complete mole and a normal fetus and placenta is sometimes misdiagnosed as a diploid partial mole . It is important to distinguish between the two, because twin pregnancies consisting of a normal fetus and a complete mole have a substantively increased risk of developing subsequent gestational trophoblastic neoplasia. Histological Diagnosis of Hydatidiform Moles Theca-Lutein Cysts It vary from microscopic size to 10 cm or more in diameter. Their surfaces are smooth, often yellowish, and lined with lutein cells. It come from overstimulation of lutein elements by large amounts of hCG secreted by proliferating trophoblastic cells.

Carmelia Cantika M. C4

130110110100

Case 5

Risk Factors 1)Age Highest in women aged 15 years or younger, and those aged 45 years or older 2)Previous Mole The clinical and diagnostic features of hydatidiform mole are: 1. Continuous or intermittent brown or bloody discharge evident by about 12 weeks and usually not profuse. 2. Uterine enlargement more rapidly,soft consistency. Ovarian theca lutein cells hard to be distinguished from enlargement uterine. 3. Absence of fetal parts and fetal heart motion. 4. Preeclampsiaeclampsia developing before 24 weeks. 5. Hyperemesis gravidarum 6. Thyrotoxicosis. Plasma thyroxine levels in women with molar pregnancy are often elevated, but clinically apparent hyperthyroidism is unusual. 7. Embolization. Variable amounts of trophoblastic cells with or without villous stroma escape from the uterus into the venous outflow at the time of molar evacuation 8. Characteristic ultrasonographic appearance(snow storm). Other structures may have an appearance similar to that of a mole, including uterine myoma and multifetal pregnancy. 9. Serum hCG level higher than expected for the stage of gestation. 10. Spontaneous expulsion is most likely around 16 weeks and is rarely delayed beyond 28 weeks. Treatment Hydatidiform mole treatment consists of two phasesimmediate evacuation of the mole, and the second is subsequent evaluation for persistent trophoblastic proliferation or malignant change. -Prophylactic Chemotherapy -Vacuum Aspiration -Oxytocin, Prostaglandins, and Hysterotomy -Hysterectomy Follow-Up Evaluation of Molar Pregnancy Close and consistent follow-up have aims: 1. Prevent pregnancy for a minimum of 6 months using hormonal contraception(Estrogen progestin contraceptives or depot-medroxyprogesterone) 2. Monitor serum hCG levels every 2 weeks. Serial measurement of serum hCG is important to detect trophoblastic neoplasia, and even small amounts of trophoblastic tissue can be detected by the assay. These levels should progressively fall to an undetectable level. 3. Chemotherapy is not indicated as long as these serum levels continue to regress. Once the hCG level falls to a normal level, test the patient monthly for 6 months; then follow-up is discontinued and pregnancy allowed.