A 19-year-old with a complete hydatidiform mole at 14 weeks has a palpable thyroid, fine tremor, and suppressed TSH with FT4 above the upper limit of normal. What is the mechanism of her thyrotoxicosis?
- A Autonomous thyroid adenoma secreting T3 and T4
- B TSH receptor antibodies crossing from trophoblastic tissue
- C High concentrations of hCG stimulating the TSH receptor owing to structural homology of the alpha subunit ✓
- D Unique beta subunit of hCG acting directly on thyroid follicles
Explanation
hCG and TSH share an identical alpha subunit, and at very high titres, typically above 100,000 IU/L as seen in complete moles, hCG cross-stimulates the TSH receptor causing biochemical and sometimes clinical thyrotoxicosis. It resolves spontaneously after evacuation of the mole. The beta subunit is the hormone-specific portion responsible for hCG's biological uniqueness and does not mediate thyroid stimulation.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.