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• W2093685655 abstract "Gestational trophoblastic disease includes hydatidiform mole (complete and partial) and gestational trophoblastic neoplasia (invasive mole, choriocarcinoma, placental site trophoblastic tumor, and epithelioid trophoblastic tumor). The epidemiology, pathology, clinical presentation, and diagnosis of each of these trophoblastic disease variants are discussed. Particular emphasis is given to management of hydatidiform mole, including evacuation, twin mole/normal fetus pregnancy, prophylactic chemotherapy, and follow-up. Gestational trophoblastic disease includes hydatidiform mole (complete and partial) and gestational trophoblastic neoplasia (invasive mole, choriocarcinoma, placental site trophoblastic tumor, and epithelioid trophoblastic tumor). The epidemiology, pathology, clinical presentation, and diagnosis of each of these trophoblastic disease variants are discussed. Particular emphasis is given to management of hydatidiform mole, including evacuation, twin mole/normal fetus pregnancy, prophylactic chemotherapy, and follow-up. Gestational trophoblastic disease (GTD) is a spectrum of cellular proliferations arising from the placental villous trophoblast encompassing 4 main clinicopathologic forms: hydatidiform mole (complete and partial), invasive mole, choriocarcinoma, and placental site trophoblastic tumor (PSTT) (Table). The term “gestational trophoblastic neoplasia” (GTN) has been applied collectively to the latter 3 conditions, which can progress, invade, metastasize, and lead to death if left untreated.For Editors' Commentary, see Table of ContentsTABLEClinicopathologic features of gestational trophoblastic diseaseGestational trophoblastic diseasePathologic featuresClinical featuresHydatidiform mole, complete46,XX (mainly); 46,XYAbsent fetus/embryoDiffuse swelling of villiDiffuse trophoblastic hyperplasia15-20% trophoblastic sequelaehCG often >100,000 mIU/mLMedical complicationsHydatidiform mole, partialTriploid (69, XXY; 69, XYY; 69 XXX)Abnormal fetus/embryoFocal swelling of villiFocal trophoblastic hyperplasia<5% trophoblastic sequelaehCG usually <100,000 mIU/mLRare medical complicationsInvasive moleMyometrial invasionSwollen villiHyperplastic trophoblast15% metastatic–lung/vaginaMost often diagnosed clinically, rather than pathologicallyChoriocarcinomaAbnormal trophoblastic hyperplasia and anaplasiaAbsent villiHemorrhage, necrosisVascular spread to distant sites–lung/brain/liverMalignant diseasePSTTTumor cells infiltrate myometrium with vascular/lymphatic invasionIntermediate cells/absent villiLess hemorrhage and necrosisTumor cells stain positive for hPLExtremely rarehCG levels less reliable indicatorRelatively chemoresistantMainly surgical treatmenthCG, human chorionic gonadotropin; hPL, human placental lactogen; PSTT, placental site trophoblastic tumor.Lurain. Gestational trophoblastic disease I. Am J Obstet Gynecol 2010. Open table in a new tab For Editors' Commentary, see Table of Contents hCG, human chorionic gonadotropin; hPL, human placental lactogen; PSTT, placental site trophoblastic tumor. Lurain. Gestational trophoblastic disease I. Am J Obstet Gynecol 2010. GTD was historically associated with significant morbidity and mortality. Hydatidiform moles were often accompanied by serious bleeding and other medical complications prior to the development of early detection and effective uterine evacuation means in the 1970s. The outcomes for GTN were likewise poor before the introduction of chemotherapy into their management 50 years ago. The mortality rate for invasive mole approached 15%, most often because of hemorrhage, sepsis, embolic phenomena, or complications from surgery. Choriocarcinoma had a mortality rate of almost 100% when metastases were present and approximately 60% even when hysterectomy was done for apparent nonmetastatic disease. Gestational trophoblastic neoplasms are now some of the most curable of all solid tumors, with cure rates >90% even in the presence of widespread metastatic disease.1Hancock B.W. Seckl M.J. Berkowitz R.S. Cole L.A. Gestational trophoblastic disease. 3rd ed. International Society for the Study of Trophoblastic Diseases, London, UK2009Google Scholar, 2Soper J.T. Gestational trophoblastic disease.Obstet Gynecol. 2006; 108: 176-187Crossref PubMed Scopus (121) Google Scholar, 3Berkowitz R.S. Goldstein D.P. Current management of gestational trophoblastic disease.Gynecol Oncol. 2009; 112: 654-662Crossref PubMed Scopus (217) Google Scholar The incidence and etiologic factors contributing to the development of GTD have been difficult to characterize. The problems in accumulating reliable epidemiologic data can be attributed to a number of factors, such as inconsistencies in case definitions, inability to adequately characterize the population at risk, no centralized databases, lack of well-chosen control groups against which to compare possible risk factors, and rarity of the diseases.4Bracken M.B. Incidence and etiology of hydatidiform mole: an epidemiological review.Br J Obstet Gyncol. 1987; 94: 1123-1135Crossref PubMed Scopus (100) Google Scholar Epidemiologic studies have reported wide regional variations in the incidence of hydatidiform mole.5Palmer J.R. Advances in the epidemiology of gestational trophoblastic disease.J Reprod Med. 1994; 39: 155-162PubMed Google Scholar Estimates from studies conducted in North America, Australia, New Zealand, and Europe have shown the incidence of hydatidiform mole to range from 0.57–1.1 per 1000 pregnancies, whereas studies in Southeast Asia and Japan have suggested an incidence as high as 2.0 per 1000 pregnancies.6Atrash H.K. Hogue C.J.R. Grimes D.A. Epidemiology of hydatidiform mole during early gestation.Am J Obstet Gynecol. 1986; 154: 906-909Abstract PubMed Google Scholar Investigations into possible ethnic and racial differences leading to an increased incidence of hydatidiform mole among American Indians, Eskimos, Hispanics, and African Americans as well as various Asian populations have not been able to attribute them to genetic traits, cultural factors, or simply differences in reporting.7Bagshawe K.D. Dent J. Webb J. Hydatidiform mole in England and Wales 1973-1983.Lancet. 1986; 2: 673-677Abstract PubMed Scopus (258) Google Scholar, 8Takeuchi S. Incidence of gestational trophoblastic disease by regional registration in Japan.Hum Reprod. 1987; 2: 729-734PubMed Google Scholar, 9Smith H.O. Gestational trophoblastic disease: epidemiology and trends.Clin Obstet Gynecol. 2003; 46: 541-556Crossref PubMed Scopus (95) Google Scholar Data with respect to choriocarcinoma incidence rates are even more limited. Collection of data on the incidence of choriocarcinoma has been more difficult not only for reasons similar to those encountered with hydatidiform moles, but also because of the rarity of choriocarcinoma and the difficulty in clinically distinguishing postmolar choriocarcinoma from invasive mole. In Europe and North America, choriocarcinoma affects approximately 1 in 40,000 pregnancies and 1 in 40 hydatidiform moles, whereas in Southeast Asia and Japan choriocarcinoma rates are higher at 9.2 and 3.3 per 40,000 pregnancies, respectively. The incidence rates of both hydatidiform mole and choriocarcinoma have declined over the past 30 years in all populations.10Brinton L.A. Bracken M.B. Connelly R.R. Choriocarcinoma incidence in the United States.Am J Epidemiol. 1986; 123: 1094-1100PubMed Google Scholar, 11Smith H.O. Qualls C.R. Prairie B.A. et al.Trends in gestational choriocarcinoma: a 27-year perspective.Obstet Gynecol. 2003; 102: 978-987Crossref PubMed Scopus (36) Google Scholar Several potential etiologic risk factors have been evaluated for the development of complete hydatidiform mole.12Parazzini F. Mangili G. LaVecchia C. et al.Risk factors for gestational trophoblastic disease: a separate analysis of complete and partial hydatidiform moles.Obstet Gynecol. 1991; 78: 1039-1045PubMed Google Scholar The 2 established risk factors that have emerged are extremes of maternal age and prior molar pregnancy. Advanced or very young maternal age has consistently correlated with higher rates of complete hydatidiform mole. Compared to women aged 21-35 years, the risk of complete mole is 1.9 times higher for women both >35 years and <21 years as well as 7.5 times higher for women >40 years.13Parazzini F. LaVecchia C. Pampallona S. Parental age and risk of complete and partial hydatidiform mole.Br J Obstet Gynecol. 1986; 93: 582-585Crossref PubMed Scopus (67) Google Scholar, 14Sebire N.J. Foskett M. Fisher R.A. et al.Risk of partial and complete molar pregnancy in relation to maternal age.Br J Obstet Gynecol. 2002; 109: 99-102Crossref Scopus (114) Google Scholar Prior hydatidiform mole predisposes to another molar pregnancy. The risk of repeat molar pregnancy after 1 mole is about 1%, or about 10-20 times the risk for the general population.15Sand P.K. Lurain J.R. Brewer J.L. Repeat gestational trophoblastic disease.Obstet Gynecol. 1984; 63: 140-144PubMed Google Scholar, 16Berkowitz R.S. Im S.S. Bernstein M.R. Goldstein D.P. Gestational trophoblastic disease: subsequent pregnancy outcome, including repeat molar pregnancy.J Reprod Med. 1998; 43: 81-86PubMed Google Scholar Familial clusters of biparental complete hydatidiform moles associated with novel missense NLRP7 gene mutations on chromosome 19q have also been identified.17Wang C.M. Dixon P.H. Decordova S. et al.Identification of 13 novel NLRP7 mutations in 20 families with recurrent hydatidiform mole; missense mutations cluster in the leucine-rich region.J Med Genet. 2009; 46: 569-575Crossref PubMed Scopus (120) Google Scholar Another reported obstetric risk factor for both complete and partial moles is a history of spontaneous abortion, giving women a 2- to 3-fold increased risk of a molar pregnancy compared to women without a history of miscarriage.12Parazzini F. Mangili G. LaVecchia C. et al.Risk factors for gestational trophoblastic disease: a separate analysis of complete and partial hydatidiform moles.Obstet Gynecol. 1991; 78: 1039-1045PubMed Google Scholar Although many possible environmental etiologies for complete mole have been studied, the only consistent association has been an inverse relationship between β-carotene and animal fat dietary intake and the incidence of molar pregnancy.18Berkowitz R.S. Cramer D.W. Bernstein M.R. et al.Risk factors for complete molar pregnancy from a case-control study.Am J Obstet Gynecol. 1985; 152: 1016-1020Abstract PubMed Google Scholar, 19Parazzini F. LaVecchia C. Mangili G. et al.Dietary factors and risk of trophoblastic disease.Am J Obstet Gynecol. 1988; 158: 93-99Abstract PubMed Google Scholar Ovulation induction for fertility may also be associated with an increase in pregnancies consisting of a normal fetus or fetuses and a molar gestation. Risk factors for choriocarcinoma include prior complete hydatidiform mole, ethnicity, and advanced maternal age. Choriocarcinoma is approximately 1000 times more likely after a complete mole than after another pregnancy event. The risk is also increased in women of Asian and American Indian descent as well as African Americans. Similar to molar pregnancies, the median age of women with choriocarcinoma is higher than that for normal pregnancies.11Smith H.O. Qualls C.R. Prairie B.A. et al.Trends in gestational choriocarcinoma: a 27-year perspective.Obstet Gynecol. 2003; 102: 978-987Crossref PubMed Scopus (36) Google Scholar There also seems to be an increased risk of choriocarcinoma in women with long-term oral contraceptive use and blood group A.5Palmer J.R. Advances in the epidemiology of gestational trophoblastic disease.J Reprod Med. 1994; 39: 155-162PubMed Google Scholar, 20Palmer J.R. Driscoll S.G. Rosenberg L. et al.Oral contraceptive use and the risk of gestational trophoblastic tumors.J Natl Cancer Inst. 1999; 91: 635-640Crossref PubMed Scopus (43) Google Scholar Molar pregnancies and gestational trophoblastic neoplasms all take their origin from the placental trophoblast. Normal trophoblast is composed of cytotrophoblast, syncytiotrophoblast, and intermediate trophoblast. Syncytiotrophoblast invades the endometrial stroma with implantation of the blastocyst and is the cell type that produces human chorionic gonadotropin (hCG). Cytotrophoblast functions to supply the syncytium with cells in addition to forming outpouchings that become the chorionic villi covering the chorionic sac. The villous chorion adjacent to the endometrium and basalis layer of the endometrium together form the functional placenta for maternal-fetal nutrient and waste exchange. Intermediate trophoblast is located in the villi, the implantation site, and the chorionic sac. All 3 types of trophoblast may result in GTD when they proliferate.21Moore K.L. Persaud T.V.N. The developing human–clinically oriented embryology. WB Saunders, Philadelphia (PA)1993Google Scholar, 22Bentley R.C. Pathology of gestational trophoblastic disease.Clin Obstet Gynecol. 2003; 46: 513-522Crossref PubMed Scopus (37) Google Scholar Hydatidiform mole refers to an abnormal pregnancy characterized by varying degrees of trophoblastic proliferation (both cytotrophoblast and syncytiotrophoblast) and vesicular swelling of placental villi associated with an absent or an abnormal fetus/embryo. Two syndromes of hydatidiform mole have been described based on both morphologic and cytogenetic criteria.23Szulman A.E. Surti U. The syndromes of hydatidiform mole, I: cytogenetic and morphologic correlations.Am J Obstet Gynecol. 1978; 131: 665-671Abstract Full Text PDF PubMed Scopus (427) Google Scholar, 24Szulman A.E. Surti U. The syndromes of hydatidiform mole, II: morphologic evolution of the complete and partial mole.Am J Obstet Gynecol. 1978; 132: 20-27Abstract Full Text PDF PubMed Scopus (355) Google Scholar Complete hydatidiform moles undergo early and uniform hydatid enlargement of villi in the absence of an ascertainable fetus or embryo, the trophoblast is consistently hyperplastic with varying degrees of atypia, and villous capillaries are absent (Figure 1). Approximately 90% of complete moles are 46, XX, originating from duplication of the chromosomes of a haploid sperm after fertilization of an egg in which the maternal chromosomes are either inactive or absent. The other 10% of complete moles are 46, XY, or 46, XX, as a result of fertilization of an empty ovum by 2 sperm (dispermy). Trophoblastic neoplasia (invasive mole or choriocarcinoma) follows complete mole in 15-20% of cases.23Szulman A.E. Surti U. The syndromes of hydatidiform mole, I: cytogenetic and morphologic correlations.Am J Obstet Gynecol. 1978; 131: 665-671Abstract Full Text PDF PubMed Scopus (427) Google Scholar, 24Szulman A.E. Surti U. The syndromes of hydatidiform mole, II: morphologic evolution of the complete and partial mole.Am J Obstet Gynecol. 1978; 132: 20-27Abstract Full Text PDF PubMed Scopus (355) Google Scholar, 25Berkowitz R.S. Goldstein D.P. Bernstein M.R. Evolving concepts of molar pregnancy.J Reprod Med. 1991; 36: 40-44PubMed Google Scholar, 26Mosher R. Goldstein D.P. Berkowitz R. et al.Complete hydatidiform mole: comparison of clinicopathologic features, current and past.J Reprod Med. 1998; 43: 21-27PubMed Google Scholar, 27Lage J.M. Mark S.D. Roberts D.J. et al.A flow cytometric study of 137 fresh hydropic placentas: correlation between types of hydatidiform moles and nuclear DNA ploidy.Obstet Gynecol. 1992; 79: 403-410Crossref PubMed Scopus (123) Google Scholar Partial hydatidiform moles demonstrate identifiable fetal or embryonic tissue, chorionic villi with focal edema that vary in size and shape, scalloping and prominent stromal trophoblastic inclusions, and a functioning villous circulation, as well as focal trophoblastic hyperplasia with mild atypia only (Figure 2). Most partial moles have a triploid karyotype (usually 69, XXY), resulting from the fertilization of an apparently normal ovum by 2 sperm. Less than 5% of partial moles will develop postmolar GTN; metastases occur rarely and a histopathologic diagnosis of choriocarcinoma has not been confirmed after a partial mole.23Szulman A.E. Surti U. The syndromes of hydatidiform mole, I: cytogenetic and morphologic correlations.Am J Obstet Gynecol. 1978; 131: 665-671Abstract Full Text PDF PubMed Scopus (427) Google Scholar, 24Szulman A.E. Surti U. The syndromes of hydatidiform mole, II: morphologic evolution of the complete and partial mole.Am J Obstet Gynecol. 1978; 132: 20-27Abstract Full Text PDF PubMed Scopus (355) Google Scholar, 27Lage J.M. Mark S.D. Roberts D.J. et al.A flow cytometric study of 137 fresh hydropic placentas: correlation between types of hydatidiform moles and nuclear DNA ploidy.Obstet Gynecol. 1992; 79: 403-410Crossref PubMed Scopus (123) Google Scholar, 28Paradinas F.J. Browne P. Fisher R.A. et al.A clinical, histopathological and flow of cytometric study of 149 complete moles, 146 partial moles and 107 non-molar hydropic abortions.Histopathology. 1996; 28: 101-110Crossref PubMed Scopus (146) Google Scholar, 29Sebire N.J. Fisher R.A. Rees H.C. Histopathologic diagnosis of partial and complete hydatidiform mole in the first trimester of pregnancy.Pediatr Dev Pathol. 2003; 6: 69-77Crossref PubMed Scopus (94) Google Scholar, 30Sebire N.J. Makrydimas G. Agnantis N.J. et al.Updated diagnostic criteria for partial and complete hydatidiform moles in early pregnancy.Anticancer Res. 2003; 23: 1723-1728PubMed Google ScholarFIGURE 2Partial hydatidiform moleShow full captionPartial hydatidiform mole with chorionic villi of varying size and shape with focal edema and scalloping, stromal trophoblastic inclusions, and functioning villous circulation, as well as focal trophoblastic hyperplasia.Lurain. Gestational trophoblastic disease I. Am J Obstet Gynecol 2010.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Partial hydatidiform mole with chorionic villi of varying size and shape with focal edema and scalloping, stromal trophoblastic inclusions, and functioning villous circulation, as well as focal trophoblastic hyperplasia. Lurain. Gestational trophoblastic disease I. Am J Obstet Gynecol 2010. Invasive mole is a benign tumor that arises from myometrial invasion of a hydatidiform mole via direct extension through tissue or venous channels (Figure 3). Approximately 10-17% of hydatidiform moles will result in invasive mole, and about 15% of these will metastasize to the lungs or vagina. Invasive mole is most often diagnosed clinically rather than pathologically based on persistent hCG elevation after molar evacuation and is frequently treated with chemotherapy without a histopathologic diagnosis.31Lurain J.R. Brewer J.I. Invasive mole.Semin Oncol. 1982; 9: 174-180PubMed Google Scholar Choriocarcinoma is a malignant disease characterized by abnormal trophoblastic hyperplasia and anaplasia, absence of chorionic villi, hemorrhage, and necrosis (Figure 4), with direct invasion into the myometrium and vascular invasion resulting in spread to distant sites, most commonly to the lungs, brain, liver, pelvis and vagina, kidney, intestines, and spleen. Choriocarcinoma has been reported to occur in association with any pregnancy event. Approximately 25% of cases follow abortion or tubal pregnancy, 25% are associated with term or preterm gestation, and the remaining 50% arise from hydatidiform moles, although only 2-3% of hydatidiform moles progress to choriocarcinoma.32Lurain J.R. Gestational trophoblastic tumors.Semin Surg Oncol. 1990; 6: 347-353Crossref PubMed Scopus (37) Google Scholar PSTT is an extremely rare disease that arises from the placental implantation site and consists predominantly of mononuclear intermediate trophoblasts without chorionic villi infiltrating in sheets or cords between myometrial fibers (Figure 5). PSTT is associated with less vascular invasion, necrosis, and hemorrhage than choriocarcinoma, and it has a propensity for lymphatic metastasis. Immunohistochemical staining reveals the diffuse presence of cytokeratin and human placental lactogen, whereas hCG is only focal. Cytogenic studies have revealed that PSTTs are more often diploid than aneuploid. Most PSTTs follow nonmolar gestations.33Baergen R.N. Rutgers J.L. Young R.H. et al.Placental site trophoblastic tumor: a study of 55 cases and review of the literature emphasizing factors of prognostic significance.Gynecol Oncol. 2006; 100: 511-520Crossref PubMed Scopus (153) Google Scholar Epithelioid trophoblastic tumor (ETT) is a rare variant of PSTT that simulates carcinoma. Based on morphologic and histochemical features, it appears to develop from neoplastic transformation of chorionic-type intermediate trophoblasts. Most ETTs present many years after a full-term delivery.34Shih I.M. Kurman R.J. Epithelioid trophoblastic tumor: a neoplasm distinct from choriocarcinoma and placental site trophoblastic tumor simulating carcinoma.Am J Surg Pathol. 1998; 22: 1393-1403Crossref PubMed Scopus (276) Google Scholar, 35Allison K.H. Love J.E. Garcia R.L. Epithelioid trophoblastic tumor: review of a rare neoplasm of the chorionic-type intermediate trophoblast.Arch Pathol Lab Med. 2006; 130: 1875-1877PubMed Google Scholar Complete hydatidiform mole most commonly presents with vaginal bleeding, usually occurring at 6-16 weeks of gestation in 80-90% of cases. The other classic clinical signs and symptoms, such as uterine enlargement greater than expected for gestational dates (28%), hyperemesis (8%), and pregnancy-induced hypertension in the first or second trimester (1%), occur less frequently in recent years because of earlier diagnosis as a result of widespread use of ultrasonography and accurate tests for hCG. Bilateral theca lutein cyst enlargement of the ovaries occurs in approximately 15% of cases, hCG levels are often >100,000 mIU/mL, and fetal heart tones are absent.36Curry S.L. Hammond C.B. Tyrey L. et al.Hydatidiform mole: diagnosis, management, and long-term follow-up of 347 patients.Obstet Gynecol. 1975; 45: 1-8PubMed Google Scholar, 37Kohorn E.I. Molar pregnancy: presentation and diagnosis.Clin Obstet Gynecol. 1984; 27: 181-189Crossref PubMed Scopus (44) Google Scholar, 38Soto-Wright V. Bernstein M.R. Goldstein D.P. et al.The changing clinical presentation of complete molar pregnancy.Obstet Gynecol. 1995; 86: 775-779Crossref PubMed Scopus (196) Google Scholar, 39Hou J.L. Wan X.R. Xiang Y. et al.Changes in clinical features in hydatidiform mole: analysis on 113 cases.J Reprod Med. 2008; 53: 629-633PubMed Google Scholar Partial mole does not have the same presenting features as complete mole. More than 90% of patients with partial moles have symptoms of incomplete or missed abortion, and the diagnosis is usually made after histologic review of curettage specimens. The main presenting symptom is vaginal bleeding, which occurs in approximately 75% of patients. Excessive uterine enlargement, hyperemesis, pregnancy-induced hypertension, hyperthyroidism, and theca lutein cysts develop infrequently. Preevacuation hCG levels are >100,000 mIU/mL in <10% of patients with partial moles.40Czernobilsky B. Barash A. Lancet M. Partial moles: a clinicopathologic study of 25 cases.Obstet Gynecol. 1982; 59: 75-77PubMed Google Scholar, 41Szulman A.E. Surti U. The clinicopathologic profile of the partial hydatidiform mole.Obstet Gynecol. 1982; 59: 597-602PubMed Google Scholar, 42Berkowitz R.S. Goldstein D.P. Bernstein M.R. Natural history of partial molar pregnancy.Obstet Gynecol. 1985; 66: 677-681PubMed Google Scholar GTN has a varied presentation depending on the antecedent pregnancy event, extent of disease, and histopathology. Postmolar GTN (invasive mole or choriocarcinoma) most commonly presents as irregular bleeding following evacuation of a hydatidiform mole. Signs suggestive of postmolar GTN are an enlarged, irregular uterus and persistent bilateral ovarian enlargement. Occasionally, a metastatic vaginal lesion may be noted on evacuation, disruption of which may cause uncontrolled bleeding. Choriocarcinoma associated with nonmolar gestation has no characteristic symptoms or signs, which are mostly related to invasion of tumor in the uterus or at metastatic sites. In patients with postpartum uterine bleeding and subinvolution, GTN should be considered along with other possible causes, such as retained products of conception or endomyometritis, primary or metastatic tumors of other organ systems, or another pregnancy occurring shortly after the first. Bleeding as a result of uterine perforation or metastatic lesions may result in abdominal pain, hemoptysis, melena, or evidence of increased intracranial pressure from intracerebral hemorrhage leading to headaches, seizures, or hemiplegia. Patients may also exhibit pulmonary symptoms, such as dyspnea, cough, and chest pain, caused by extensive lung metastases.32Lurain J.R. Gestational trophoblastic tumors.Semin Surg Oncol. 1990; 6: 347-353Crossref PubMed Scopus (37) Google Scholar PSTTs and ETTs almost always cause irregular uterine bleeding often distant from a preceding nonmolar gestation, and rarely virilization or nephrotic syndrome. The uterus is usually symmetrically enlarged, and serum hCG levels are only slightly elevated.33Baergen R.N. Rutgers J.L. Young R.H. et al.Placental site trophoblastic tumor: a study of 55 cases and review of the literature emphasizing factors of prognostic significance.Gynecol Oncol. 2006; 100: 511-520Crossref PubMed Scopus (153) Google Scholar, 34Shih I.M. Kurman R.J. Epithelioid trophoblastic tumor: a neoplasm distinct from choriocarcinoma and placental site trophoblastic tumor simulating carcinoma.Am J Surg Pathol. 1998; 22: 1393-1403Crossref PubMed Scopus (276) Google Scholar, 35Allison K.H. Love J.E. Garcia R.L. Epithelioid trophoblastic tumor: review of a rare neoplasm of the chorionic-type intermediate trophoblast.Arch Pathol Lab Med. 2006; 130: 1875-1877PubMed Google Scholar Ultrasonography plays a critical role in the diagnosis of both complete and partial mole, and it has virtually replaced all other means of preoperative diagnosis.38Soto-Wright V. Bernstein M.R. Goldstein D.P. et al.The changing clinical presentation of complete molar pregnancy.Obstet Gynecol. 1995; 86: 775-779Crossref PubMed Scopus (196) Google Scholar, 43Santos-Ramos R. Forney J.P. Schwarz B.E. Sonographic findings and clinical correlations in molar pregnancy.Obstet Gynecol. 1980; 56: 186-192PubMed Google Scholar, 44Benson C.B. Genest D.R. Bernstein M.R. et al.Sonographic appearance of first trimester complete hydatidiform moles.Ultrasound Obstet Gynecol. 2000; 16: 188-191Crossref PubMed Scopus (90) Google Scholar, 45Fine C. Bundy A.L. Berkowitz R.S. et al.Sonographic diagnosis of partial hydatidiform mole.Obstet Gynecol. 1989; 73: 414-418PubMed Google Scholar Because the chorionic villi of complete moles exhibit diffuse hydropic swelling, a characteristic vesicular ultrasonographic pattern can be observed, consisting of multiples echoes (holes) within the placental mass and usually no fetus (Figure 6). Ultrasonography may also facilitate the early diagnosis of a partial mole by demonstrating focal cystic spaces within the placenta and an increase in the transverse diameter of the gestational sac.45Fine C. Bundy A.L. Berkowitz R.S. et al.Sonographic diagnosis of partial hydatidiform mole.Obstet Gynecol. 1989; 73: 414-418PubMed Google Scholar hCG is a disease-specific tumor marker produced by hydatidiform moles and gestational trophoblastic neoplasms. It is easily measured quantitatively in both urine and blood, and hCG levels have been shown to correlate with the burden of disease. It is a placental glycoprotein composed of 2 dissimilar subunits: an α subunit resembling that of the pituitary glycoprotein hormones and a β subunit that is unique to placental production. Several forms of hCG exist, including at least 6 major variants that can be detected in serum: hyperglycosylated, nicked, absent C-terminal of the β subunit, free β subunit, nicked free β subunit, and free α subunit. The hCG molecules in GTD are more heterogenous and degraded than those in normal pregnancy, therefore, an assay that will detect all main forms of hCG and its multiple fragments should be used to follow up patients with GTD. Most institutions currently use rapid, automated radiolabeled monoclonal antibody sandwich assays that measure different mixtures of hCG-related molecules.46Cole L.A. hCG, its free subunits and its metabolites: roles in pregnancy and trophoblastic disease.J Reprod Med. 1998; 43: 3-10PubMed Google Scholar, 47Berkowitz R.S. Ozturk M. Goldstein D. et al.Human chorionic gonadotropin and free subunits' serum levels in patients with partial and complete hydatidiform moles.Obstet Gynecol. 1989; 74: 212-216PubMed Google Scholar, 48Ozturk M. Berkowitz R. Goldstein D. et al.Differential production of human chorionic gonadotropin and free subunits in gestational trophoblastic disease.Am J Obstet Gynecol. 1988; 158: 193-198Abstract PubMed Google Scholar Hydatidiform moles are commonly associated with markedly elevated hCG levels above those of normal pregnancy. Approximately 50% of patients with complete mole have preevacuation hCG levels >100,000 mIU/mL.49Menczer J. Modan M. Serr D.M. Prospective follow-up of patients with hydatidiform mole.Obstet Gynecol. 1980; 55: 346-349PubMed Google Scholar, 50Genest D.R. Laborde O. Berkowitz R.S. et al.A clinicopathologic study of 153 cases of complete hydatidiform mole (1980-1990): histologic grade lacks prognostic significance.Obstet Gynecol. 1991; 78: 402-409PubMed Google Scholar A single hCG determination, however, is seldom helpful in differentiating" @default.
• W2093685655 created "2016-06-24" @default.
• W2093685655 creator A5086072634 @default.
• W2093685655 date "2010-12-01" @default.
• W2093685655 modified "2023-10-11" @default.
• W2093685655 title "Gestational trophoblastic disease I: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole" @default.
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