eMedicine Specialties > Obstetrics and Gynecology > Gynecologic Oncology

Hydatidiform Mole

Author: Lisa E Moore, MD, FACOG, Assistant Professor, Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of New Mexico Health Sciences Center
Coauthor(s): Enrique Hernandez, MD, FACOG, FACS, Chairman, Department of Obstetrics and Gynecology, Director of Gynecologic Oncology, Abraham Roth Professor of Obstetrics, Gynecology and Reproductive Science, Professor of Pathology, Temple University Hospital, Temple University School of Medicine
Contributor Information and Disclosures

Updated: Sep 24, 2008

Introduction

Background

Gestational trophoblastic disease encompasses several disease processes that originate in the placenta. These include complete and partial moles, placental site trophoblastic tumors, choriocarcinomas, and invasive moles.

Almost all women with malignant gestational trophoblastic disease can be cured with preservation of reproductive function. The following discussion is limited to hydatidiform moles (complete and partial).

Pathophysiology

A complete mole contains no fetal tissue. Ninety percent are 46,XX, and 10% are 46,XY.1,2 Complete moles can be divided into 2 types:

  • Androgenetic complete mole
    • Homozygous
      • These account for 80% of complete moles.
      • Two identical paternal chromosome complements, derived from duplication of the paternal haploid chromosomes.
      • Always female; 46,YY has never been observed.
    • Heterozygous
      • These account for 20% of complete moles.
      • May be male or female.
      • All chromosomes are of parental origin, most likely due to dispermy.
  • Biparental complete mole: Maternal and paternal genes are present but failure of maternal imprinting causes only the paternal genome to be expressed.3
    • The biparental complete mole is rare. 
    • A recurrent form of biparental mole, which is familial and appears to be inherited as an autosomal recessive trait, has been described. Al-Hussaini describes a series of 5 women with as many as 9 consecutive molar pregnancies.4,5
    • A candidate region of chromosome arm 19q13.4 has been identified.6,7

With a partial mole, fetal tissue is often present. Fetal erythrocytes and vessels in the villi are a common finding. The chromosomal complement is 69,XXX or 69,XXY.8 This results from fertilization of a haploid ovum and duplication of the paternal haploid chromosomes or from dispermy. Tetraploidy may also be encountered. As in a complete mole, hyperplastic trophoblastic tissue and swelling of the chorionic villi occur.

Frequency

United States

By studying elective pregnancy terminations, hydatidiform moles were determined to occur in approximately 1 in 1200 pregnancies.9

International

The reported frequency of hydatidiform mole varies greatly. Some of this variability can be explained by differences in methodology (eg, single hospital vs population studies, identification of cases). The reported frequencies range from 1 in 100 pregnancies in Indonesia to 1 in 200 pregnancies in Mexico to 1 in 5000 pregnancies in Paraguay.10 The study of pathologic material from first- and second-trimester abortions established a frequency of complete and partial hydatidiform moles in Ireland of 1 per 1945 pregnancies and 1 per 695 pregnancies, respectively.11

Mortality/Morbidity

A hydatidiform mole is considered malignant if metastases or destructive invasion of the myometrium (ie, invasive mole) occurs, or when the serum hCG levels plateau or rise during the period of follow-up and an intervening pregnancy is excluded. Malignancy (see eMedicine's article Gestational Trophoblastic Neoplasia) is diagnosed in 15-20% of patients with a complete hydatidiform mole and 2-3% of partial moles.12,13 Lung metastases are found in 4-5% of patients with a complete hydatidiform mole and rarely in cases of partial hydatidiform moles.14,15

Race

Differences in the frequency of hydatidiform moles between ethnic groups have been reported internationally.10,16 In the United States, comparison of frequency of hydatidiform moles in African Americans and Caucasians have yielded conflicting results.16 If differences exist, whether they are due to genetic differences or environmental factors is not clear.

Sex

Hydatidiform mole is a disease of pregnancy and therefore a disease of women.

See Medscape's Pregnancy Resource Center.

Age

Hydatidiform mole is more common at the extremes of reproductive age. Women in their early teenage or perimenopausal years are most at risk.17,18,19,10,16 Women older than 35 years have a 2-fold increase in risk. Women older than 40 years experience a 5- to 10-fold increase in risk compared to younger women. Parity does not affect the risk.

Clinical

History

  • Complete mole: The typical clinical presentation of complete molar pregnancies has changed with the advent of high-resolution ultrasonography. Most moles are now diagnosed in the first trimester before the onset of the classic signs and symptoms.20,21
    • Vaginal bleeding: The most common classic symptom of a complete mole is vaginal bleeding. Molar tissue separates from the decidua, causing bleeding. The uterus may become distended by large amounts of blood, and dark fluid may leak into the vagina. This symptom occurs in 50% of cases.
    • Hyperemesis: Patients may also report severe nausea and vomiting. This is due to extremely high levels of human chorionic gonadotropin (hCG).
    • Hyperthyroidism: Signs and symptoms of hyperthyroidism can be present due to stimulation of the thyroid gland by the high levels of circulating hCG or by a thyroid stimulating substance (ie, thyrotropin) produced by the trophoblasts.22
  • Partial mole: Patients with partial mole do not have the same clinical features as those with complete mole. These patients usually present with signs and symptoms consistent with an incomplete or missed abortion.
    • Vaginal bleeding
    • Absence of fetal heart tones

Physical

  • Complete mole
    • Size inconsistent with gestational age: A uterine enlargement greater than expected for gestational age is a classic sign of a complete mole. Unexpected enlargement is caused by excessive trophoblastic growth and retained blood. However, patients present with size-appropriate enlargement or smaller-than-expected enlargement at a similar frequency.
    • Preeclampsia: Pelvic ultrasonography has resulted in the early diagnosis of most cases of hydatidiform mole and preeclampsia is seen in less than 2% of cases.21
    • Theca lutein cysts: These are ovarian cysts greater than 6 cm in diameter and accompanying ovarian enlargement. These cysts are not usually palpated on bimanual examination but are identified by ultrasonography. Patients may report pressure or pelvic pain. Because of the increased ovarian size, torsion is a risk. These cysts develop in response to high levels of beta-hCG. They spontaneously regress after the mole is evacuated, but it may take up to 12 weeks for complete regression.
  • Partial mole
    • Uterine enlargement and preeclampsia is reported in only 5% of patients.23
    • Theca lutein cysts, hyperemesis, and hyperthyroidism are extremely rare.
  • Twinning
    • Twinning with a complete mole and a fetus with a normal placenta has been reported. Cases of healthy infants in these circumstances have been reported.24,8
    • Women with coexistent molar and normal gestations are at higher risk for developing persistent disease and metastasis25 . Termination of pregnancy is a recommended option.
    • The pregnancy may be continued as long as the maternal status is stable, without hemorrhage, thyrotoxicosis, or severe hypertension. The patient should be informed of the risk of severe maternal morbidity from these complications.26
    • Prenatal genetic diagnosis by chorionic villus sampling or amniocentesis is recommended to evaluate the karyotype of the fetus.

Causes

A diet deficient in animal fat and carotene may be a risk factor.16,17

More on Hydatidiform Mole

Overview: Hydatidiform Mole
Differential Diagnoses & Workup: Hydatidiform Mole
Treatment & Medication: Hydatidiform Mole
Follow-up: Hydatidiform Mole
Multimedia: Hydatidiform Mole
References
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References

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  6. Hodges MD, Rees HC, Seckl MJ, et al. Genetic refinement and physical mapping of a biparental complete hydatidiform mole locus on chromosome 19q13.4. J Med Genet. Aug 2003;40(8):e95. [Medline].

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  15. Menczer J, Girtler O, Zajdel L, Glezerman M. Metastatic trophoblastic disease following partial hydatidiform mole: case report and literature review. Gynecol Oncol. Aug 1999;74(2):304-7. [Medline].

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  32. Batorfi J, Vegh G, Szepesi J, et al. How long should patients be followed after molar pregnancy? Analysis of serum hCG follow-up data. Eur J Obstet Gynecol Reprod Biol. Jan 15 2004;112(1):95-7. [Medline].

  33. Feltmate CM, Batorfi J, Fulop V, et al. Human chorionic gonadotropin follow-up in patients with molar pregnancy: a time for reevaluation. Obstet Gynecol. Apr 2003;101(4):732-6. [Medline].

  34. Garner EI, Lipson E, Bernstein MR, Goldstein DP, Berkowitz RS. Subsequent pregnancy experience in patients with molar pregnancy and gestational trophoblastic tumor. J Reprod Med. May 2002;47(5):380-6. [Medline].

  35. Sebire NJ, Fisher RA, Foskett M, et al. Risk of recurrent hydatidiform mole and subsequent pregnancy outcome following complete or partial hydatidiform molar pregnancy. BJOG. Jan 2003;110(1):22-6. [Medline].

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Further Reading

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Keywords

gestational trophoblastic disease, placental site trophoblastic tumor, molar pregnancy, complete mole, partial mole, cystic mole, hydatidiform mole, choriocarcinoma, invasive mole, trophoblastic hyperplasia, nonmetastatic trophoblastic disease, theca lutein cysts, diet deficient in animal fat, diet deficient in carotene, hyperemesis, trophoblastic malignancy, vaginal bleeding, hyperthyroidism, absence of fetal heart tones, preeclampsia, toxemia, proteinuria, edema with hyperreflexia

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Contributor Information and Disclosures

Author

Lisa E Moore, MD, FACOG, Assistant Professor, Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of New Mexico Health Sciences Center
Lisa E Moore, MD, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Enrique Hernandez, MD, FACOG, FACS, Chairman, Department of Obstetrics and Gynecology, Director of Gynecologic Oncology, Abraham Roth Professor of Obstetrics, Gynecology and Reproductive Science, Professor of Pathology, Temple University Hospital, Temple University School of Medicine
Enrique Hernandez, MD, FACOG, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, American College of Surgeons, American Medical Association, American Society for Colposcopy and Cervical Pathology, Association of Professors of Gynecology and Obstetrics, Johns Hopkins Medical and Surgical Association, Pennsylvania Medical Society, Philadelphia County Medical Society, and Society of Gynecologist Oncologists
Disclosure: Nothing to disclose.

Medical Editor

Jordan G Pritzker, MD, Assistant Professor of Obstetrics, Gynecology, and Women's Health, Women's Comprehensive Health Center, Albert Einstein College of Medicine; Physician-In-Charge, Dept of Obstetrics and Gynecology, Long Island Jewish Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

A David Barnes, MD, PhD, MPH, FACOG, Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital, Mammoth Lakes, California, Pioneer Valley Hospital, Salt Lake City, Utah, Warren General Hospital, Warren, Pennsylvania and Mountain West Hospital, Tooele, Utah
A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association, Association of Military Surgeons of the US, and Utah Medical Association
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

David Chelmow, MD, Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Program Director, Tufts University Affiliated Hospitals OB/GYN Residency Program; Chair, Tufts University Health Sciences Campus Institutional Review Board
David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical Decision Making
Disclosure: Nothing to disclose.

 
 
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