Abstract

Gestational trophoblastic disease or neoplasia covers a spectrum of benign and malignant conditions arising from pregnancies with highly abnormal development of trophoblastic tissue. In this brief review, we discuss the different features of these different conditions and their origins and risk factors and introduce some of the more novel and controversial treatment options currently being explored.

Highlights

  • Gestational trophoblastic disease (GTD) or neoplasia (GTN) covers a spectrum of benign and malignant conditions arising from malformed pregnancies

  • We discuss the different features of these different conditions and their origins and risk factors and introduce some of the more novel and controversial treatment options currently being explored

  • At the tips of anchoring villi, proliferating CTB generates columns to attach to the maternal decidua and differentiating extravillous trophoblast (EVT) cells invade the maternal tissues, through the decidua and as far as the inner third of the myometrium[2]

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Summary

Introduction

Gestational trophoblastic disease (GTD) or neoplasia (GTN) covers a spectrum of benign and malignant conditions arising from malformed pregnancies. Gestational trophoblastic disease GTD is a heterogeneous group of pregnancy-associated growths, often termed tumors, including choriocarcinoma, invasive mole, hydatidiform mole (partial and complete), epithelioid trophoblastic tumor (ETT), and placental site trophoblastic tumor (PSTT)[7,8,9], that arise from placental villous and extravillous trophoblast cells[10]. Varying atypia of trophoblast, absence of fetal pregnancies tissue and villous capillaries, uterine enlarge , high hCG levels for gestational age, hypertension and hyperemesis gravidarum, abnormal bleeding, ovarian theca lutein cysts. Deep myometrial invasion, Villous trophoblast tumor size, molar pregnancy, smoking, spontaneous miscarriage, ectopic pregnancy, site of metastases, disease duration, hCG level, stage. Grant information The author(s) declared that no grants were involved in supporting this work

Shih IM
PubMed Abstract
24. Sebire NJ
26. Baltazar JC
Findings
39. McCormick JB
Full Text
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