Placental Site Trophoblastic Tumour
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Direct answer
Placental site trophoblastic tumour (PSTT) is the rarest gestational trophoblastic neoplasia, arising not from cytotrophoblast and syncytiotrophoblast like choriocarcinoma but from intermediate trophoblast at the implantation site. Its signature is a human chorionic gonadotropin level disproportionately low for the tumour burden, because the cells produce human placental lactogen rather than hCG — a solitary, minimally elevated beta-hCG in a woman with irregular bleeding years after a term delivery is the classic stem. Disease confined to the uterus is treated by hysterectomy, since PSTT is relatively chemoresistant; metastatic or recurrent disease warrants combination chemotherapy such as EMA/CO or EP/EMA, with prognosis worsening when the interval from the antecedent pregnancy exceeds two to four years.
What you must remember
- Cell of origin: intermediate trophoblast of the implantation site — the same family that gives the related epithelioid trophoblastic tumour, a variant arising from chorionic-type intermediate trophoblast.
- Marker discordance: hPL-positive, hCG-negative or trivially raised on immunohistochemistry; serum beta-hCG is a poor tumour marker, so monitoring relies on imaging as well.
- Presenting pattern: irregular bleeding, often amenorrhoea first, months to years after a term pregnancy, miscarriage or molar pregnancy — the long antecedent interval contrasts with choriocarcinoma's early metastasis.
- Histology: monomorphic proliferation of polygonal cells infiltrating myometrium, splitting muscle fibres, replacing vessel walls with fibrinoid material — no biphasic pattern, no widespread haemorrhage.
- Treatment: hysterectomy with pelvic node sampling is primary for localised disease; fertility-sparing local resection via hysterotomy is reported in highly selected young women with small tumours.
- Chemoradioresistance: PSTT responds poorly to single-agent methotrexate protocols used for low-risk GTN; metastatic disease needs multiagent regimens (EMA/CO, EP/EMA), and a FIGO/WHO score of 7 or more defines high risk in GTN generally.
- Prognostic divider: interval from antecedent pregnancy — an interval beyond about four years carries a markedly worse outlook, along with metastasis, older age and high mitotic index.
A worked diagnostic path
Picture a 34-year-old woman, three years after a normal vaginal delivery, with six months of brownish spotting and a mildly enlarged, boggy uterus. Urine pregnancy test is weakly positive; serum beta-hCG is 900 IU/L — far too low for the size of the uterus. Transvaginal ultrasound shows a heterogeneous myometrial mass breaching the endometrial interface, MRI confirms an infiltrative lesion without extrauterine spread, and chest imaging is clear. Dilatation and curettage yields sheets of large polygonal cells with prominent nucleoli invading between myometrial fibres; immunohistochemistry stains strongly for hPL and hCG only focally — the diagnosis of PSTT is secured.
Management follows the biology: because the tumour is chemoresistant and she has completed her family, total hysterectomy with intraoperative frozen-section assessment of margins is performed; pelvic lymphadenectomy or sampling adds staging value since PSTT can involve nodes. Serial beta-hCG is followed postoperatively as a crude surveillance marker alongside imaging. Had she been 26 years old, nulliparous and desperate for fertility, the rare option of hysteroscopically guided or hysterotomy-based local excision with surveillance could be discussed, accepting a higher recurrence risk. Had lung metastases been present at diagnosis, the pathway shifts to multiagent chemotherapy and the prognosis conversation changes entirely — driven chiefly by that three-year interval, sitting near the adverse threshold.
High-yield viva angles
Examiners anchor on the comparison with choriocarcinoma. Choriocarcinoma follows the antecedent pregnancy within weeks to months, secretes enormous quantities of hCG, metastasises early and haemorrhages dramatically, and melts with chemotherapy; PSTT follows a long interval, secretes little hCG, grows slowly, spreads late (lung, liver, brain), and stands up to chemotherapy. The second trap is using beta-hCG to gauge response: a "low" hCG can coexist with extensive disease, so hPL staining on tissue and imaging carry the monitoring load. Finally, remember that within the FIGO GTN scoring system the antecedent-pregnancy interval scores four points when it exceeds twelve months — which pushes most PSTT cases up the risk table — yet the decisive clinical distinction remains surgical fitness, because the first treatment is the hysterectomy itself.
Frequently asked questions
Which cell gives rise to placental site trophoblastic tumour?
Intermediate trophoblast of the implantation site, unlike choriocarcinoma which arises from cytotrophoblast and syncytiotrophoblast.
Why is beta-hCG unreliable in PSTT?
The tumour produces human placental lactogen preferentially, so serum hCG is disproportionately low relative to tumour volume and falls slowly even with residual disease.
What is the primary treatment of non-metastatic PSTT?
Hysterectomy, because the tumour is relatively resistant to the chemotherapy regimens effective in other gestational trophoblastic neoplasias.
Which factor predicts poor prognosis in PSTT?
An interval of more than about four years from the antecedent pregnancy, together with metastatic disease, deep myometrial invasion and high mitotic count.
Which chemotherapy is used for metastatic PSTT?
Multiagent regimens such as EMA/CO or EP/EMA, since single-agent methotrexate or actinomycin protocols used in low-risk GTN are inadequate.