Placental site trophoblastic tumor (PSTT) differs from other gestational trophoblastic neoplasias in its sensitivity to chemotherapy. The key distinguishing biomarker that is characteristically normal or minimally elevated in PSTT is:
- A β-hCG ✓
- B Human placental lactogen (HPL)
- C CA-125
- D Inhibin A
Explanation
PSTT consists predominantly of intermediate trophoblast cells that produce human placental lactogen (HPL) but relatively little β-hCG; therefore, β-hCG levels are characteristically low or minimally elevated despite potentially bulky disease. This makes hCG monitoring unreliable for PSTT, and HPL is the more characteristic marker. PSTT is relatively chemoresistant compared to choriocarcinoma; multi-agent chemotherapy (EP-EMA: etoposide, cisplatin/actinomycin-D, methotrexate) is used rather than EMA-CO. Hysterectomy is the cornerstone of treatment for localized disease. The interval from antecedent pregnancy is the most important prognostic factor—>2 years confers worse prognosis.
Reference: Williams Obstetrics, 26th ed.
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Written and medically reviewed by the StethoPrep medical team.