PSTT is a rare neoplasm arising from the implantation site intermediate
trophoblast. It is a unique form of GTN and constitutes
1–2% of all GTN. Mostcases of PSTT are at least focally infiltrative
and myometrial smooth muscle cells are found in between
the clusters or sheets of tumour cells. Unlike choriocarcinoma,
which is immunoreactive for hCGand has a high Ki-67 proliferative
index, PSTT is only focally and weakly immunoreactive for
hCG and the mean Ki-67 is around 15%. PSTT can be preceded
by normal pregnancy, miscarriage or abortion,and less commonly
molar pregnancy and ectopic pregnancy. Most patients
present with vaginal bleeding, amenorrhoea and uterine enlargement.
Rarely, nephritic syndrome related to immunoglobulindeposits in the glomerular membranes, and virilisation due to
ovarian stromal hyperthecosis and paraneoplastic syndromes are
also seen. Serum hCG may be high and 79% of patients have
levels less than1000 IU/l and 58% less than 500 IU/l. Serum
human placental lactogen may be raised and this can be used as
a tumour marker. The diagnosis is often made in the hysterectomy
or curettage samples. Lungmetastasis, long interval from
antecedent pregnancy (5 years or more), mitotic count more than
5 per 10 high power fields, and advanced FIGO stage appear
to be the poor prognostic factors. Thecornerstone treatment
method is hysterectomy because PSTT is less sensitive to chemotherapy.
However, if fertility preservation is desired, conservative
management like uterine curettage,hysteroscopic resection
and chemotherapy may be considered if the lesion is localised in
the uterus, the mitotic count is low, there is no uterine enlargement
and close monitoring is available. The mostcommonly
used chemotherapy regimen is EMA-CO but EMA-EP (etoposide,
methotrexate, actinomycin- etoposide, and cisplatinum) can be
considered if patients are refractory to EMA-CO.
ETT is derived...