Molar pregnancy

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Hydatidiform mole
Hydatidiform mole (1) complete type.jpg
Histopathogic image of hydatidiform mole (complete type). H & E stain.
Classification and external resources
ICD-10O01, D39.2
eMedicinemed/1047 med/866
NCIMolar pregnancy
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Hydatidiform mole
Hydatidiform mole (1) complete type.jpg
Classification and external resources
ICD-10O01, D39.2
eMedicinemed/1047 med/866
NCIMolar pregnancy
Hydatidiform mole on CT, sagittal view
Hydatidiform mole on CT, axial view

Molar pregnancy is an abnormal form of pregnancy in which a non-viable fertilized egg implants in the uterus and will fail to come to term. A molar pregnancy is a gestational trophoblastic disease[1] which grows into a mass in the uterus that has swollen chorionic villi. These villi grow in clusters that resemble grapes.[2] A molar pregnancy can develop when fertilized egg had not contained an original maternal nucleus. The products of conception may or may not contain fetal tissue. It is characterized by the presence of a hydatidiform mole (or hydatid mole, mola hydatidosa).[3] Molar pregnancies are categorized as partial moles or complete moles, with the word mole, being used to denote simply a clump of growing tissue, or a growth.

A complete mole is caused by a single (incidence is about 90%) or two (incidence is about 10%) sperm combining with an egg which has lost its DNA (the sperm then reduplicates forming a "complete" 46 chromosome set) [4] The genotype is typically 46,XX (diploid) due to subsequent mitosis of the fertilizing sperm, but can also be 46,XY (diploid).[4] 46,YY (diploid) is not observed. In contrast, a partial mole occurs when an egg is fertilized by two sperm or by one sperm which reduplicates itself yielding the genotypes of 69,XXY (triploid) or 92,XXXY (tetraploid).[4] Complete hydatidiform moles have a higher risk of developing into choriocarcinoma — a malignant tumor of trophoblast cells — than do partial moles.

The etymology is derived from hydatisia (Greek "a drop of water"), referring to the watery contents of the cysts, and mole (from Latin mola = millstone/false conception).[5] The term, however, comes from the similar appearance of the cyst to a hydatid cyst in an Echinococcosis.[6]

A hydatidiform mole conception may be categorized in medical terms as one type of non-induced (natural) "missed abortion"[7] - referred to colloquially as a "missed miscarriage", because the pregnancy has become non-viable (miscarried) but was not immediately expelled (therefore was "missed").

Natural history[edit]

An hydatidiform mole is a pregnancy/conceptus in which the placenta contains grapelike vesicles (small sacs) that are usually visible with the naked eye. The vesicles arise by distention of the chorionic villi by fluid. When inspected in the microscope, hyperplasia of the trophoblastic tissue is noted. If left untreated, a hydatidiform mole will almost always end as a spontaneous abortion (miscarriage).

Based on morphology, hydatidiform moles can be divided into two types: in complete moles, all the chorionic villi are vesicular, and no sign of embryonic or fetal development is present. In partial moles some villi are vesicular, whereas others appear more normal, and embryonic/fetal development may be seen but the fetus is always malformed and is never viable.


In rare cases a hydatidiform mole co-exists in the uterus with a normal, viable fetus. These cases are due to twinning. The uterus contains the products of two conceptions: one with an abnormal placenta and no viable fetus (the mole), and one with a normal placenta and a viable fetus. Under careful surveillance it is often possible for the woman to give birth to the normal child and to be cured of the mole.[9]


Parental origin[edit]

In most complete moles, all nuclear genes are inherited from the father only (androgenesis). In approximately 80% of these androgenetic moles, the most probable mechanism is that an empty egg is fertilized by a single sperm, followed by a duplication of all chromosomes/genes (a process called "endoreduplication"). In approximately 20% of complete moles, the most probable mechanism is that an empty egg is fertilised by two sperm. In both cases, the moles are diploid (i.e. there are two copies of every chromosome). In all these cases, the mitochondrial genes are inherited from the mother, as usual.

Most partial moles are triploid (three chromosome sets). The nucleus contains one maternal set of genes and two paternal sets. The mechanism is usually the reduplication of the paternal haploid set from a single sperm, but may also be the consequence of dispermic (two sperm) fertilization of the egg.[12]



Clinical presentation and diagnosis[edit]

Transvaginal ultrasonography showing a molar pregnancy.

Molar pregnancies usually present with painless vaginal bleeding in the fourth to fifth month of pregnancy.[3] The uterus may be larger than expected, or the ovaries may be enlarged. There may also be more vomiting than would be expected (hyperemesis). Sometimes there is an increase in blood pressure along with protein in the urine. Blood tests will show very high levels of human chorionic gonadotropin (hCG).[16]

The diagnosis is strongly suggested by ultrasound (sonogram), but definitive diagnosis requires histopathological examination. On ultrasound, the mole resembles a bunch of grapes ("cluster of grapes" or "honeycombed uterus" or "snow-storm"[17]). There is increased trophoblast proliferation and enlarging of the chorionic villi.[18] Angiogenesis in the trophoblasts is impaired as well.[18]



Hydatidiform moles should be treated by evacuating the uterus by uterine suction or by surgical curettage as soon as possible after diagnosis, in order to avoid the risks of choriocarcinoma.[19] Patients are followed up until their serum human chorionic gonadotrophin (hCG) level has fallen to an undetectable level. Invasive or metastatic moles (cancer) may require chemotherapy and often respond well to methotrexate. As they contain paternal antigens, the response to treatment is nearly 100%. Patients are advised not to conceive for one year after a molar pregnancy. The chances of having another molar pregnancy are approximately 1%.

Anesthesia Management: The uterine curettage is generally done under the effect of anesthesia, preferably spinal anesthesia in hemodynamically stable patients. The advantages of spinal anesthesia over general anesthesia include ease of technique, favorable effects on the pulmonary system, safety in patients with hyperthyroidism and non-tocolytic pharmacological properties. Additionally, by maintaining patient’s consciousness one can diagnose the complications like uterine perforation, cardiopulmonary distress and thyroid storm at an earlier stage than when the patient is sedated or is under general anesthesia. [20]


Carboprost (PGF2α) medication may be used to contract the uterus.



In 10 to 15% of cases, hydatidiform moles may develop into invasive moles. This condition is named persistent trophoblastic disease (PTD). The moles may intrude so far into the uterine wall that hemorrhage or other complications develop. It is for this reason that a post-operative full abdominal and chest x-ray will often be requested.

In 2 to 3% of cases, hydatidiform moles may develop into choriocarcinoma, which is a malignant, rapidly growing, and metastatic (spreading) form of cancer. Despite these factors which normally indicate a poor prognosis, the rate of cure after treatment with chemotherapy is high.

Over 90% of women with malignant, non-spreading cancer are able to survive and retain their ability to conceive and bear children. In those with metastatic (spreading) cancer, remission remains at 75 to 85%, although their childbearing ability is usually lost.

The prognosis of hydatidiform moles can be estimated by scoring systems such as the Modified WHO Prognostic Scoring System, wherein scores between 1 and 4 from various parameters are summed together:[21]

Modified WHO Prognostic Scoring System[21]
Antecedent pregnancymoleabortionterm
Interval months from index pregnancy<44–67–12>12
Pretreatment serum hCG (IU/L)<103103–104104–105>105
Largest tumor size (including uterus)<33–4 cm≥5 cm
Site of metastaseslungspleen, kidneygastrointestinalliver, brain
Number of metastases1–45–8>8
Previous failed chemotherapysingle drug≥2 drugs

Women with a score of 7 or greater are considered at high risk.

See also[edit]


  1. ^ Gestational Trophoblastic Disease at American Cancer Society. Last Medical Review: 04/14/2011
  2. ^ "hydatidiform mole". Merriam Webster. Retrieved May 7, 2012. 
  3. ^ a b Cotran RS, Kumar V, Fausto N, Nelso F, Robbins SL, Abbas AK (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. p. 1110. ISBN 0-7216-0187-1. 
  4. ^ a b c Kumar, Vinay, ed. (2010). Pathologic Basis of Disease (8th ed.). Saunders Elsevier. pp. 1057–1058. ISBN 1-4377-0792-0. 
  5. ^ Entries HYDATID n. (a.) and MOLE, n.6 in the Oxford English Dictionary online. ( — subscription required.)
  6. ^
  7. ^ Fine, Calliope; Bundy, Albert L; Berkowitz, Ross S; Boswell, Steven B; Berezin, Andrew F; Doubilet, Peter M (March 1989). "Sonographic diagnosis of partial hydatidiform mole". Obstet Gynecol 73 (3 Pt 1): 414–8. PMID 2644599. 
  8. ^ Di Cintio E, Parazzini F, Rosa C, Chatenoud L, Benzi G (1997). "The epidemiology of gestational trophoblastic disease". Gen Diagn Pathol 143 (2-3): 103–8. PMID 9443567. 
  9. ^ Sebire NJ, Foskett M, Paradinas FJ, et al. (June 2002). "Outcome of twin pregnancies with complete hydatidiform mole and healthy co-twin". Lancet 359 (9324): 2165–6. doi:10.1016/S0140-6736(02)09085-2. PMID 12090984. 
  10. ^ MedlinePlus Encyclopedia Hydatidiform mole
  11. ^ Paoloni-Giacobino A. (2007). "Epigenetics in reproductive medicine". Paediatr Res. May 61 (5 Pt 2): 51R–57R. doi:10.1203/pdr.0b013e318039d978. PMID 17413849. 
  12. ^ Monga, Ash, ed. (2006). Gynaecology by Ten Teachers (18th ed.). Hodder Arnold. pp. 99–101. ISBN 0-340-81662-7. 
  13. ^ Lawler SD, Fisher RA, Dent J (May 1991). "A prospective genetic study of complete and partial hydatidiform moles". Am J Obstet Gynecol. 164 (5 Pt 1): 1270–7. doi:10.1016/0002-9378(91)90698-q. PMID 1674641. 
  14. ^ Wallace DC, Surti U, Adams CW, Szulman AE (1982). "Complete moles have paternal chromosomes but maternal mitochondrial DNA". Human Genetics 61 (2): 145–7. doi:10.1007/BF00274205. PMID 6290372. 
  15. ^ Slim R, Mehio A (January 2007). "The genetics of hydatidiform moles: new lights on an ancient disease". Clin Genet. 71 (1): 25–34. doi:10.1111/j.1399-0004.2006.00697.x. PMID 17204043.  Review.
  16. ^ a b Ganong WF, McPhee SJ, Lingappa VR (2005). Pathophysiology of Disease: An Introduction to Clinical Medicine (Lange). McGraw-Hill Medical. p. 639. ISBN 0-07-144159-X. 
  17. ^ Woo J, Hsu C, Fung L, Ma H (1983). "Partial hydatidiform mole: ultrasonographic features". Aust N Z J Obstet Gynaecol 23 (2): 103–7. doi:10.1111/j.1479-828X.1983.tb00174.x. PMID 6578773. 
  18. ^ a b Oslo University - Eksamensoppgaver i barnesykdommer; 9
  19. ^ Cotran RS, Kumar V, Fausto N, Nelso F, Robbins SL, Abbas AK (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. p. 1112. ISBN 0-7216-0187-1. 
  20. ^ Ghanshyam Biyani and Pradeep Bhatia: Mortality in hydatidiform mole: Should we blame thyroid? Indian J Anaesth. 2011 Nov-Dec; 55(6): 628–29.
  21. ^ a b Stage Information for Gestational Trophoblastic Tumors and Neoplasia at The National Cancer Institute (NCI), part of the National Institutes of Health (NIH), in turn citing: FIGO Committee on Gynecologic Oncology.: Current FIGO staging for cancer of the vagina, fallopian tube, ovary, and gestational trophoblastic neoplasia. Int J Gynaecol Obstet 105 (1): 3-4, 2009

External links[edit]