Placental site trophoblastic tumour (PSTT) differs from other gestational trophoblastic neoplasias in its secretion and treatment. The unique characteristics are:
- A Secretes hCG predominantly; responds excellently to methotrexate monotherapy
- B Secretes inhibin B; is treated identically to gestational choriocarcinoma
- C Secretes human placental lactogen (hPL) predominantly; is relatively resistant to EMA-CO and requires surgery ✓
- D Secretes hCG and is treated with EMA-EP (high-dose etoposide-cisplatin)
Explanation
PSTT arises from intermediate trophoblast of the placental bed and characteristically secretes human placental lactogen (hPL) rather than hCG (which is minimally elevated). This means hCG is a poor tumour marker for PSTT. Critically, PSTT is relatively resistant to standard GTN chemotherapy including EMA-CO. Surgery (hysterectomy) is the primary treatment. When PSTT is metastatic or recurrent, EMA-EP (etoposide, methotrexate, actinomycin D alternating with etoposide-cisplatin) is used. The interval from antecedent pregnancy >48 months is a poor prognostic factor.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.