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Hubaishi, Cherifi, Mohsen, Binashoor, Al Sayari, and Mehdipour: Partial molar pregnancy resulting in a healthy newborn


Partial molar pregnancy is a trophoblastic disease caused by a genetic disorder, such as an additional haploid set of chromosomes, which results in a total of 69 chromosomes.

Excluding molar pregnancy cases resulting from multiple conceptions and therefore co-existing fetuses, partial molar pregnancy in which a living fetus is carried to term is very rare. When molar changes exist alongside the living fetus, the patient can be offered close observation.1

We describe a case of partial molar pregnancy that was managed throughout at Dubai Hospital in the United Arab Emirates (UAE) and resulted in a live and healthy baby delivered at 36 weeks.

Case report

A 32-year-old Emirati woman, gravida 3, para 1, with no family history of genetic abnormalities, was initially assessed at 9 weeks' gestation in the gynaecology clinic at Dubai Hospital for management of early threatened miscarriage. Clinical examination was normal and ultrasonography revealed a live embryo consistent with 9 weeks' gestation.

The patient's obstetric history detailed that her first pregnancy, during 2007, was complicated by partial molar pregnancy and resulted in miscarriage; her second pregnancy, during 2009, resulted in the delivery of a live newborn by emergency caesarean section at full term.

Serum beta-human chorionic gonadotropin (β-HCG) was given to the patient at 9 weeks' gestation in view of her previous history of molar pregnancy. It was suggested to the patient that she should attend an antenatal clinic follow-up at 13 weeks' gestation and at regular intervals thereafter. At these follow-up sessions, the patient complained of vaginal spotting.

The patient's clinical and gynaecological examination was normal and ultrasonography showed a single live fetus corresponding to the 13 weeks' gestation stage. However, multiple cystic changes, of differing sizes, suggestive of partial molar degeneration, were noted in the placenta (Figure 1).


Ultrasound image of the fetus at 13 weeks' gestation.


The result of the β-HCG test was > 200 000 iu/l and the results of renal, liver and thyroid function tests were all normal.

The patient was advised to undergo karyotyping to analyse the chromosomes in a sample of the fetal cells at 13 weeks' gestation and again at 20 weeks' gestation; however, she refused any medical intervention.

The patient was kept under observation at regular antenatal clinic sessions and growth of the fetus, placental size and the placental mass were monitored every 2 weeks. The patient did not develop pre-eclampsia, thyrotoxicosis or anaemia; however, vaginal spotting persisted throughout the pregnancy.

At 32 weeks' gestation, the patient presented with antepartum haemorrhage and was admitted to the Department of Obstetric Gynecology at Dubai Hospital for assessment. Following an examination, the patient's vital signs were normal. Fundal height of the uterus corresponded to the gestational age of the fetus and the cervix was closed; however, bleeding was detected at the cervical os.

Ultrasonography revealed a single and viable fetus in cephalic presentation whose measurements were consistent with gestational age and there were no obvious gross anomalies. An umbilical artery Doppler assessment was conducted and the results were normal. The placenta was positioned posterior to the fundus of the uterus and was 50 mm in thickness, with hyperechoic and cystic changes visible but no signs of placental separation (Figure 2). The result of the umbilical artery Doppler assessment can be seen in Figure 3 where the colour shows the hypervascularized nature of the placenta.


Changes in the resulting ultrasound image at 32 weeks' gestation.


The result of the placenta hypervascularization assessment.


The bleeding caused by the antepartum haemorrhage lessened 2 days after admission and as a result the patient was discharged and and asked to return for weekly follow-up appointments at the antenatal clinic. As the pregnancy continued, the rate of growth of the fetus decreased and a symmetrical intrauterine gestational retardation was identified. However, the results of the umbilical artery Doppler assessment remained normal; thus, the observation continued and cardiotocography and biophysical profiling were carried out twice a week.

The patient was readmitted with spontaneous labour pain at 36 weeks' gestation, which resulted in a normal vaginal delivery of a live and healthy baby girl who weighed 1710 g. Despite this low birthweight, the baby had a good Apgar score of 9 and 10 at 1 and 5 minutes, respectively, and was admitted to the neonatal intensive care unit for close observation.

The subsequent pathological analysis of the placental tissue was consistent with the diagnosis of partial molar placenta.

The patient was discharged in fit and healthy condition and was followed up in the gynaecology clinic. The patient's β-HCG concentration levels were repeatedly checked until three negative results were obtained (Figure 4). Oral contraceptive pills were offered for family planning.


β-HCG level during pregnancy and after delivery.



Partial hydatidiform mole is a histopathological entity characterized by a focal trophoblastic hyperplasia that is associated with hydropic villi along with identifiable fetal tissue.2 This usually results in a fetus displaying a triploid karyotype, resulting from the fertilization of a normal ovum with two sperm.

Partial molar pregnancy resulting in a live and healthy child is rare and estimated to occur in 1 in 20 000 to 1 in 100 000 pregnancies.2 It is even rarer for the resulting child to be born with a normal karyotype. There are few cases reported in the literature; however, some studies do report on this rare condition.1,36

Several studies5,7 have reported cases of a single normal fetus associated with partial molar placenta and stated that the fetus must have a normal karyotype to survive in utero, although the placenta can show some variation, from diploidy of the amnion to triploidy of the chorionic villi,7 which is similar to the patient in the case discussed above. From this clinical perspective, there are two different types of gross pathology that can affect the placenta: focal degeneration and diffuse partial degeneration.5,810

Previously, most partial molar pregnancies identified early were terminated8,11,12 with or without medical complications, but especially when pre-eclampsia was also present.13 However, termination of the pregnancy is not always the only option as the pregnancy can be managed conservatively if the fetus appears normal and healthy on ultrasound, and if there are no maternal complications. Patients who develop partial molar placenta may find the pregnancy complicated by intrauterine growth restriction and oligohydramnios, which were both observed in the case discussed above.14

Some studies11,15,16 have questioned whether patients with partial hydatidiform mole require follow-up observation and assessment of serum β-HCG concentration. However, patients can develop choriocarcinoma if not followed up correctly, and one study by Seckl et al.16 reported the death of one such patient.

Szulman and Surti17 reviewed 86 cases of partial hydatidiform mole and reported that the overall prevalence of the disease was 4%; however, Berkowitz et al.15 reported a higher prevalence (9.9%) among patients who had developed persistent gestational trophoblastic disease.6

The patient in the case discussed above did not show any persistent trophoblastic disease after the birth and her serum β-HCG concentration returned to normal within 4 weeks.

A single assessment of a patient's serum β-HCG concentration after the termination of pregnancy is sufficient to confirm remission in these patients.18


Partial molar pregnancy resulting in a live and healthy baby is rare and is usually associated with numerous maternal complications, including persistent gestational trophoblastic disease, which is diagnosed by histopathological examination. It is important that a diagnosis of partial molar placenta, which may be only suspected during pregnancy, is confirmed after delivery as the result may affect the future of both the mother and her baby.



Walker S, Andrews J, Gregson NM, Gault W. Three further cases of triploidy in man surviving to birth. J Med Genet 1973; 10:135–41.


Korego M, Bellad M, Malapati C. Case report: partial hydatiform Mole with a live fetus- a rare entity. South Asian Federation of Obstetrics and Gynecology 2009; 1:77–9.


Zhang P, McGinniss MJ, Sawai S. Bernirschke K. Diploid/triplod mosaic placenta with fetus. Towards a better understanding of partial moles early. Hum Dev 2000; 60:1–11.


Parveen Z, Bashir R, Jadoon T, Qayum I. Case report: partial hydatiform mole along with term gestation and alive baby. J Ayub Med Coll Abbottabad 2004; 16:84–5.


Jones WB, Lauerson NH. Hydatiform mole with coexistant fetus. Am J Obstet Gynecol 1975; 72:485–8.


Hsieh CC, Hsieh TT, Hsueh C, Kuo DM, Lo LM, Hung TM. Delivery of a severely anaemic fetus after partial molar pregnancy: clinical and ultrasonographic findings. Hum Reprod 1999; 14:1122–6.


Sarno Jr AP, Moorman AJ, Kalousek DK. Partial molar pregnancy with fetal survival: an unusual example of confined placental mosaic. Obstet Gynecol 1993; 82:716–19.


Deaton JL, Hoffman JS, Saal H, Allred C, Koulos JP. Molar pregnancy coexisting with a normal fetus: a case report. Gynecol Oncol 1989; 32:394–7.


Vejerslev LO. Clinical management and diagnostic possibilities in hydatiform mole with coexistant fetus. Obstet Gynecol Surv 1991; 46:577–88.


Nwosu EC, Ferriman E, McKormack MJ, Williams JH, Gosden CM. Partial hydatiform mole and hyperetension associated with alive fetus – variable presentation in 2 cases. Hum Reprod 1995; 10:2459–62.


Szulman AE, Surtu U. The syndrome of hydatiform mole. (ii). morphologic evolution of the complete and partial mole. Am J Obstet Gynecol 1978; 132:20–7.


Teng NNH, Ballon SC. Partial hydatiform mole with diploidy karyotype. report of three cases. Am J Obstet Gynecol 1984; 150:961–4.


Berkovitz RS, Goldstein DP. Gestational Trophoblastic Disease. In Berek JS. Berek & Novack's Gynecology, 14th edn. Philadelphia: Lippicott Williams & Wilkins; 2007. pp. 1581–602.


Chen FP. Molar pregnancy and living normal fetus coexisting until term. Prenatal biochemical and sonographic diagnosis. Hum Reprod 1997; 12:442–4.


Berkowitz RS, Goldstein DP, Bernstein MR. Natural history of partial molar pregnancy. Obstet Gynecol 1985; 66:677–81.


Seckl MJ, Fisher RA, Saermo G, et al. Choriocarcinoma and partial hydatiform moles. Lancet 2000; 356:36–9.


Szulman AE, Surti U. The clinicopathologic profile of the partial hydatiform mole. Obstet Gynecol 1982; 159:597–602.


Felmate CM, Bartorfi J, Fulop V, Goldstein DP, Doszpod J, Berkovitz RS. Human chorionic gonadotropin follow up in patients with molar pregnancy: a time for reevaluation. Obstet Gynecol 2003; 101:732–6.

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