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Management of Gestational Trophoblastic Neoplasia Ansar Hussain*, Shiekh Aejaz Aziz, Gul Mohd

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Management of Gestational Trophoblastic Neoplasia Ansar Hussain*, Shiekh Aejaz Aziz, Gul Mohd Clinical Obstetrics, Gynecology and Reproductive Medicine Review Article Management of gestational trophoblastic neoplasia Ansar Hussain*, Shiekh Aejaz Aziz, Gul Mohd. Bhat, Lone AR DM Scholar medical Oncology, SKIMS, Srinagar, India Introduction Neoplasia(GTN). Hydatidiform mole is the most common form of GTN. While invasive mole and choriocarcinoma are malignant, a Gestational trophoblastic neoplasia is a success story in medical hydatidiform mole can behave in a malignant or benign fashion. oncology as it is associated with highest cure rates even in patients with high tumour loads and perhaps would be an excitement to the In histologic section of a complete hydatidiform mole stained practicing oncologist treating such cases. with hematoxylin and eosin, Villi of different sizes are present. The large villous in the center exhibits marked edema with a fluid- It is just 100 years since Marchand [1] identified choriocarcinoma as filled central cavity known as cisterna. Marked proliferation of the a tumour arising from placental villous trophoblast. Earlier description trophoblasts is observed. The syncytiotrophoblasts stain purple, while of similar tumours failed to identify their tissue of origin. Gestational the cytotrophoblasts have a clear cytoplasm and bizarre nuclei. No fetal Trophoblastic Disease (GTD) is the terminological umbrella now used blood vessels are in the mesenchyme of the villi. CHMs are usually to span the spectrum of cellular proliferations ranging from villous diploid and androgenetic in origin, 80% resulting from duplication forms of hydatiform mole through invasive mole and choriocarcinoma of the haploid genome of a single sperm while 20% arise by dispermic to placental site tumours [2]. Each form of GTD presents its own fertilisation of an ovum. In either case∼ maternal chromosomes are lost particular set of problems ranging from social to therapeutic. These before, or shortly after, fertilisation. However, while nuclear DNA is proliferations are unique in several aspects. In the first place there is entirely paternal in CHM, mitochondrial DNA remains maternal in no known homolog of hydatiform mole in any other species. The rare origin [15]. No methods exist to accurately predict the clinical behavior identification of choriocarcinoma like tumours remains restricted to a of a hydatidiform mole by histopathology. The clinical course is rhesus monkey [3] and an armadillo [4]. In the human, histologically defined by the patient’s serum human chorionic gonadotropin (hCG) characterized choriocarcinoma behaves in a broadly similar manner curve after evacuation of the mole. In 80% of patients with a benign whether it is genetically identical with the host as in germ cell origin, hydatidiform mole, serum hCG levels steadily drop to normal within or whether it arises from a normal conception or an androgenetic 8-12 weeks after evacuation of the molar pregnancy. In the other 20% hydatiform mole. of patients with a malignant hydatidiform mole, serum hCG levels It is now more than 35 years since the sensitivity of invasive mole either rise or plateau [16,17]. and choriocarcinoma to cytotoxic drugs was first recognized [5]. They Hydatidiform mole is considered malignant when the serum hCG remain the most sensitive and most curable of all human cancers. levels plateau or rise during the follow-up period and an intervening GTD is still an important reproductive health problem worldwide. pregnancy is excluded. This occurs in 15-20% of hydatidiform moles The problem is that much information of GTD has come from less [16,17]. developed countries, where proper diagnostic tools and up to date A hydatidiform mole with a fetus or fetal tissue and a triploid treatment cannot be employed. Maternal age, previous hydatiform karyotype is known as a partial or incomplete mole. Partial moles also mole, race and geographical region have been identified as clear risk have malignant potential, but only 2-3% become malignant [18-20]. factors for GTD. Etiological factors of GTD have long been studied but An invasive mole has the same histopathologic characteristics of a no definite causes have yet been found. hydatidiform mole, but invasion of the myometrium with necrosis and However, it can be speculated that during gametogenesis and hemorrhage occurs or pulmonary metastases are present. fertilization, the Risk factors may act synergistically. Genetic sub Histologically, choriocarcinomas have no villi, but they have sheets classification may be helpful in this context. Geographic variations of of trophoblasts and hemorrhage. Choriocarcinomas are aneuploid incidence exist but are inextricably linked with above mentioned risk and can be heterozygous depending on the type of pregnancy from factors. Important prerequisites for accurate evaluation are common which the choriocarcinoma arose. If a hydatidiform mole preceded the denominators, standard classification and definition of index cases. choriocarcinoma, the chromosomes are of paternal origin. Maternal The developments and improvements in suction curettage, termination and paternal chromosomes are present if a term pregnancy precedes of pregnancy, contraceptive techniques, diagnostic imaging and the choriocarcinoma. Of choriocarcinomas, 50% are preceded by a biochemical testing have been associated with not only fall in birth rate hydatidiform mole, 25% by an abortion, 3% by ectopic pregnancy, and but also with a reduction in trophoblastic disease [6-14]. the other 22% by a full-term pregnancy [16]. Gestational Trophoblastic Disease (GTD) can be benign or malignant. Histologically, it is classified into hydatidiform mole, invasive mole (chorioadenoma destruens), choriocarcinoma, and Correspondence to: Dr. Ansar Hussain, DM Scholar medical Oncology, SKIMS, Placental Site Trophoblastic Tumor (PSTT). Those that invade locally Srinagar, India, Tel: 9622717166; E-mail: [email protected] or metastasize are collectively known as Gestational Trophoblastic Received: April 15, 2015; Accepted: May 10, 2015; Published: May 13, 2015 Clin Obstet Gynecol Reprod Med, 2015 doi: 10.15761/COGRM.1000103 Volume 1(1): 5-11 Hussain A (2015) Management of gestational trophoblastic neoplasia Placental site trophoblastic tumor is a rare form of gestational However, where complete excision is possible this can provide useful trophoblastic neoplasia, with slightly more than 200 cases reported in the histological confirmation of the diagnosis and material for genetic literature [21,22]. In patients with PSTT, intermediate trophoblasts are analysis found infiltrating the myometrium without causing tissue destruction. Indications for treatment The intermediate trophoblasts contain human placental lactogen (hPL) [23]. These patients have persistent low levels of serum hCG (100-1000 1. Plateaued or rising hCG after evacuation mIU/mL). However, serum hCG levels as high as 108,000 mIU/mL Heavy vaginal bleeding or evidence of gastrointestinal or have been reported in patients with PSTT [24]. The most frequent sites 2. intraperitonealHaemorrhage of metastases of malignant gestational trophoblastic neoplasia are the lungs, lower genital tract, brain, liver, kidney, and gastrointestinal tract. 3. Histological evidence of choriocarcinoma Epidemiology 4. Evidence of metastases in the brain, liver or gastrointestinal tract, or radiological opacities of >2 cm on chest X-ray The incidence is estimated at 1-3: 1000 pregnancies for CHM and 3: 1000 pregnancies for PHM, respectively [15]. GTD appears to be more 5. Serum hCG of ≥20 000 IU/l >4 weeks after evacuation, because frequent in Asia than in North America or Europe. of the risk of uterine perforation. An increased risk of molar pregnancy is seen in the very young Staging investigations and treatment stratification after (<16 years), but is most associated with advanced maternal age (>45 a molar pregnancy years). Following a molar pregnancy, the risk of a further CHM or PHM increases to 1%. After two molar gestations, the risk of a third Most patients developing GTN post-HM are detected early via mole is 15%–20%. The frequency of CC and PSTT is less clear, since hCG monitoring and so extensive investigation is rarely required. these can arise after∼ any type of pregnancy. CC develops after around Information to determine therapy can be obtained from the clinical 1:50 000 deliveries, while recent data suggest that PSTT represents 0.2% history, examination, measurement of serum hCG and a Doppler of UK GTD cases [25]. GTN risk may also relate to hormonal factors pelvic ultrasound to confirm the absence of a pregnancy, to measure since women with menarche after 12 years of age, light menstrual flow the uterine size/volume, spread of disease within the pelvis and and prior use of oral contraceptives are at increased risk. its vascularity. The latter assessed by the Doppler pulsatility index is an independent prognostic factor for resistance to single-agent Diagnosis methotrexate MTX) therapy [30] and is now being evaluated in a prospective trial. Pulmonary metastases are most common, so a chest CHMs and PHMs most commonly present with vaginal bleeding radiograph is essential [31]. in the first trimester of pregnancy. Previously reported features such as anaemia, uterine enlargement, pre-eclampsia, hyperemesis, Computed Tomography (CT) of the chest is not required if the hyperthyroidism and respiratory distress are now rare [26] reflecting chest X-ray (CXR) findings are normal, since discovery of micro the introduction of routine ultrasonography in early pregnancy. metastases,
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