Gestational trophoblastic disease is uncommon (about 1/1000 pregnancies). There are several forms:
- Molar pregnancy (complete, partial)
- Persistent gestational trophoblastic neoplasia
- Gestational choriocarcinoma (as opposed to non-gestational choriocarcioma which is a germ cell tumour)
- Placental Site trophoblastic tumour
Hydatiform mole occur in about 1/1000 pregnancies. Of these, about 2/3rds are partial moles and 1/3rd are **complete moles. The are more common in older, fertile women.
Complete moles arise from fertilisation of an empty ovum:
- Most cases (80%) arise from fertilisation by a single 23X sperm which duplicates its haploid genome, forming a 46XX genome.
- A minority of cases arise from fertilisation of an empty ovum by two sperm (23X + 23X or 23X + 23Y)
- 46YY is not viable and does not develop into anything
Partial moles arise from fertilisation of a normal ovum by two sperm, leading to 69XXY, 69XXX or 69XYY.
It appears that presence of the Y chromosome in a complete mole is associated with increased risk of persistent and transformed disease.
Why does a mole develop?
The paternal component of the genome is mostly responsible for growth of the placental tissues; therefore presence of two paternal genomes causes abnormal overgrowth of the placenta.
Most molar pregnancies are detected at the 12 week ultrasound, or earlier due to hyperemesis.
In a complete mole there is no fetal tissue. The macroscopic appearance is of multiple villi with central cavitation, giving a 'grape like' appearance. Microscopically, there is central necrosis within atypical trophoblast.
Partial moles contain both abnormal and normal chorionic villi.
This has a similar appearance to non-gestational choriocarcinoma. The risk is highest after a complete mole, but it can occur after a normal pregnancy (1:150,000).
Staging is with TNM and FIGO, which match.
- T1: Confined to uterus
- T2: Invades pelvic structures
- M1a: Lung metastases
- M1b: Other metastases