Gestational Trophoblastic Disease

Radiologic-Pathologic Correlation

Abstract Introduction Normal And Abnormal Trophoblast Epidemiologic Characteristics

Hydatidiform Mole Complete Hydatidiform Mole Invasive Mole Choriocarcinoma Partial Hydatidiform Mole

Placental Site Trophoblastic Disease Conclusions Source Information References

Normal And Abnormal Trophoblast

The trophoblast begins as the outer covering of the early blastocyst and provides the route of nourishment between the maternal endometrium and the developing embryo. Ultimately, trophoblast becomes the functional unit of the placenta. The villi of the placenta are covered with trophoblast and provide the surface for the exchange of oxygen and nutrients with the maternal circulation. The invasive and proliferative properties of the normal trophoblast account for some of difficulty in the microscopic assessment of the lesions that constitute GTD, because these features might suggest an aggressive tumor despite benign clinical behavior (5).

Three components make up the trophoblast: cytotrophoblast, syncytiotrophoblast, and the intermediate trophoblast. The cytotrophoblast is a stem cell with high mitotic activity but without hormonal synthesis. The syncytiotrophoblast, which constitutes the villous trophoblast, has low mitotic activity. The syncytiotrophoblast is responsible for the synthesis of the beta subunit of human chorionic gonadotropin (beta-hCG) (6) and can be identified with immunohistochemical stains. The intermediate trophoblast has features of the other two components and is responsible for endometrial invasion and implantation (5). A feature common to all types of GTD is abnormal proliferation of trophoblast, but different components predominate in different tumors.

The cytogenetic composition of GTD lesions is unusual. The most common situation, which is seen in nearly all cases of complete hydatidiform mole and invasive mole and in about half of cases of choriocarcinoma, consists of a diploid karyotype (46,XX) completely of paternal origin. This is thought to be the result of two incompletely explained mechanisms: First, the ovum loses its haploid (23,X) chromosomes, and, second, a subsequent fertilization by a 23,X sperm is followed by duplication of the chromosomes. (Although similar fertilization by a 23,Y sperm might occur, this event does not produce a viable zygote.) The end result is a zygote with a diploid 46,XX chromosomal makeup with no maternal contribution. Unusual zygotes with 46,XY karyotypes that are also completely paternal are thought to be due to fertilization of a chromosomally empty ovum by two different sperm.

Partial hydatidiform mole, on the other hand, usually occurs when an apparently normal (23,X) egg is fertilized by two sperm; the resultant triploid karyotype (69,XXX; 69,XXY; or 69,XYY) is thus two-thirds paternal (1). From a radiologic perspective, this distinction is of some practical usefulness in the management of a complete hydatidiform mole with a suspected normal twin gestation.

Abstract Introduction Normal And Abnormal Trophoblast Epidemiologic Characteristics

Hydatidiform Mole Complete Hydatidiform Mole Invasive Mole Choriocarcinoma Partial Hydatidiform Mole

Placental Site Trophoblastic Disease Conclusions Source Information References