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| Hydatidiform Mole |
| Etiology • Unknown |
| Pathogenesis • Dispermic fertilization of an ovum with loss of maternal chromosome complement or duplication of paternal chromosome with loss of maternal genetic material • Results in diploid chromosome numbers that are usually paternal XX • No embryo formation • Excessive trophoblastic proliferation • Partial mole is usually triploid with dispermic fertilization of an ovum with retention of maternal chromosome., |
| Epidemiology • Prevalence varies in different populations with approximately 1-2/2000 gestations estimated in the U.S. • May give rise to invasive mole (chorioadenoma destruans) or provide substrate for the development of gestational choriocarcinoma |
| General Gross Description • Disorganized mass of massively dilated "grape-like" villi in complete mole • Partial mole with variably sized villi. |
| General Microscopic Description • Greatly enlarged avascular villi with central spaces (cisternae) • Surrounding stroma is relatively pale staining and acellular • Trophoblast may show abundant non-polar differentiation • Invasive mole determined by invasion of molar villi into underlying myometrium • Partial mole will show smaller villi lacking cisternae or prominent trophoblast • Partial moles will exhibit trophoblast inclusions, complex villus outlines, and be relatively devoid of vascularity. |
| Clinical Correlation • Usually cured by surgical evacuation of uterine contents • Followed with serial HCG's to monitor for persistent trophoblast • May treat with methotrexate |
| References • Benirschke K, Kaufmann P. Pathology of the human placenta, 3rd ed. New York: Springer-Verlag, 1995, pp. 655-653. |
| Hydatidiform Mole |
| Synopsis by: Melinda Sanders M.D. (T88100M91000)[426] |
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