MON-354 - Fetal Thyrotoxicosis in A Hypothyroid Mother with Ablated Graves Disease

Background:
Fetal thyrotoxicosis occurs in approximately 1-5% of pregnancies in women with Graves disease (GD), when maternal TSH receptor antibody (TRAb) crosses the placenta and stimulates fetal thyroid. Diagnosis is particularly challenging in patients previously treated with radioactive iodine (RAI) who may have elevated TRAb levels, as fetal hyperthyroidism may occur despite maternal euthyroidism on levothyroxine (LT4) replacement.


Case Presentation:
A 36-year-old woman with a history of GD and thionamide allergy, treated with RAI 16 years prior, presented at 30 weeks 6 days gestation with palpitations and abnormal fetal monitoring parameters. A previous pregnancy 3 years prior was complicated by neonatal GD. Throughout the current pregnancy, she was biochemically euthyroid on LT4 replacement, while TRAb levels remained >40 IU/L. Labs on admission showed TSH 0.22 mIU/L, free T4 1.41 ng/dL, and TRAb 39 IU/L. Fetal monitoring revealed fetal tachycardia (>200 bpm), oligohydramnios, and thyroid enlargement, concerning for fetal thyrotoxicosis. Management was coordinated among maternal-fetal medicine, adult and pediatric endocrinology, and allergy teams. The patient’s methimazole (MMI) allergy was challenged and tolerated, after which MMI was initiated and uptitrated from 5mg to 30mg daily over four days. Dosing was guided primarily by fetal HR response with improvement to the 170s by day 2, stabilization to 150–160 bpm, and normalization of amniotic fluid indices by day 10. The MMI dose was reduced to 20 mg daily, but recurrent fetal tachycardia required an increase to 30 mg. Maternal LT4 dosing was adjusted to maintain maternal euthyroidism. At 35 weeks, fetal thyroid circumference reached 6.6 cm (>90th percentile for gestational age). Labor was induced at 37 weeks 6 days due to decreased fetal movement, resulting in an uncomplicated vaginal delivery. Maternal MMI was then discontinued, and LT4 was reduced to the prepregnancy dose. Although clinically well at birth, the infant developed biochemical hyperthyroidism by day 3 and was treated with MMI, which was successfully discontinued at 4 months of age.

Conclusion
Fetal thyrotoxicosis occurs rarely in maternal GD but should be considered in patients with a history of RAI treatment and elevated TRAb levels. As maternal thyroid studies are not indicative of fetal thyroid status, serial fetal heart rate trends (target HR 130-160 bpm) and ultrasound-based assessments (thyroid size and amniotic fluid volume) are essential surrogate markers of fetal thyroid status that can guide treatment. Management relies on transplacental antithyroid treatment to the fetus, along with LT4 to maintain maternal euthyroidism. Additionally, in patients with a history of thionamide allergy, rechallenge may be an option with expert guidance.

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