Partial mole occurs when an egg is fertilized by two sperm, resulting in a triploid fetus and placental abnormality. The fetus often dies early in gestation around 10-12 weeks. Partial mole is more common than complete mole. In complete mole, the egg is fertilized abnormally by one or two sperm without any maternal DNA, resulting in only placental tissue and no fetus. Diagnosis involves serum hCG levels, ultrasound, and histopathological examination of tissue. Elevated hCG levels can indicate gestational trophoblastic disease including molar pregnancies.

1. PARTIAL MOLE
 In this form of hydatidiform mole, embryo or fetus co-exist with placental abnormality.
 Though fetus tends to die at earlier gestation i.e at 10-12 weeks.
 Overall partial mole is more common then complete mole.
 0.5-1% partial mole require chemotherapy.
 Genetics:
 Partial moles are triploid with two sets of paternal and one set of maternal chromosomes i.e.
2 sperms fertilize an egg.
 This results in triploid. i.e. 69 Chromosomes.
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2. PARTIAL MOLE
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3. COMPLETE MOLE
 Abnormal pregnancy which consists of placental tissue only and there is no embyo in it.
 There is cytotrophoblastic and syncytiotrophoblastic hyperplasia.
 Bunch of graps/snow storn appearance on USG
 15% compete mole require chemotherapy.
 Genetics:
 In complete mole all of the genetic material is paternal in origin and results from
fertilization of an empty egg lacking maternal DNA.
 Chromosomes count is 46XX, 46XY.
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4. COMPLETE MOLE
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5. PARTIAL MOLE
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6. PATHOGENESIS AND CYTOGENETICS OF HM
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Genetic
Constitution
Diploid Triploid/ teraploid
Patho-genesis
4%
Fertilization
of an empty
ovum by two
sperms
“Diandric
dispermy”
90%
Triploid
fertilization of
a normal
ovum by two
sperms
“Dispermic
triploidy”
96%
Fertilization of
an empty ovum
by one sperms
that undergoes
duplication
“Diandric
diploidy”
10%
Tetraploid
fertilization of
a normal
ovum by three
sperms
“Dispermic
triploidy”
Karyotype
46XX
69XXX
69YXX
69YYX
46XX
46XY
Complete Partial

7. FEATURES OF COMPLETE AND PARTIAL MOLE
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8. CLINICAL PRESENTATION
 Clinical Presentation of Gestational Trophoblastic Diseases:
 Amenorrhoea
 Irregular bleeding
 Large for dates uterus
 Detection on routine USG
 Hyperemesis gravidarum
 Pre-eclampsia
 Hyperthyroidism
 DIC
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9. DIAGNOSIS
 History
 Clinical examination
 All base line investigations
 Serum β HCG
 USG
 CXR
 T3,T4,TSH
 Histopathological examination (Definitive Diagnosis)
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10. SERUM 𝛽 hCG
 hCG is a glycosylated heterodimer protein consisting of α and β units held together by non‐covalent bonds.
 Ideal tumour marker --- useful in tumour bulk, diagnosis and follow up.
 Produced by synchtiotrophoblastic cells of placenta.
 Its normal level is 0-4 mIU/ml in serum.
 Its half life is 24-36 hr.
 Expressed by all benign and malignant GTDs.
 β hCG level are higher in hydatidiform mole than in singleton pregnancy (levels > 2 multiples of the
median may be of value in the diagnosis often exceeding 105
IU/l.).
 hCG can be measured in serum (1mIU/ml) and urine (20mIU/ml).
 Raised T3 and T4 levels is seen in 3% cases and is due to the fact that subunits of both thyroid-stimulating
hormone (TSH) and hCG share a similar structure.
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