B103-19 When Pregnancy Mimics Thyroid Storm, Hcg Mediated Hyperthyroidism From Molar Pregnancy

Abstract Introduction Human chorionic gonadotropin (hCG)-mediated hyperthyroidism is a rare cause of secondary thyrotoxicosis, mostly linked to gestational trophoblastic disease. Severe thyrotoxicosis in the intensive care unit (ICU) poses a diagnostic challenge, as overlapping findings such as tachycardia and respiratory distress may obscure recognition. Early identification is critical, definitive management requires addressing the underlying source—typically molar pregnancy. Case Presentation 36-year-old woman, gravida 4 para 3, with type 2 diabetes and no prior hypertension, presented at 14 weeks’ gestation with refractory hypertension despite maximal therapy. She denied headaches, visual changes, chest pain, or dyspnea. On arrival, blood pressure was 182/106 mmHg, heart rate 102 bpm, and exam revealed mild bilateral lower extremity edema. ECG showed sinus tachycardia. Labs revealed suppressed thyroid-stimulating hormone (TSH) 0.015 µIU/mL, free T4 1.25 ng/dL, and elevated transaminases suggesting evolving HELLP syndrome. β-hCG exceeded 270,000 mIU/mL, and urinalysis showed trace proteinuria.Ultrasound demonstrated a heterogeneous intrauterine mass without a viable fetus, consistent with partial molar pregnancy. Given thyrotoxicosis, persistent hypertension, and hemorrhage risk, she elected primary total hysterectomy after multidisciplinary consultation.Two hours postoperatively, rapid response was called for severe hypertension requiring ICU admission for nitroglycerin infusion and close monitoring. She received symptomatic therapy for blood pressure, tachycardia, and pain. Methimazole 20 mg daily was started with a taper plan. She remained stable on room air; point-of-care ultrasound showed no right ventricular strain. The infusion was discontinued as blood pressure improved, and she transitioned to a four-agent oral regimen.After surgical removal of the molar pregnancy, β-hCG declined from 270,000 to 36,000 mIU/mL, and free T4 improved from 1.25 to 1.02 ng/dL, She was discharged on tapering methimazole with close outpatient follow-up. Both were periodically monitored and continued to downtrend, confirming resolution of hCG-mediated thyrotoxicosis. Discussion This case illustrates a rare but critical condition—molar pregnancy leading to hCG-associated thyrotoxicosis. Excessive hCG mimics TSH, stimulating thyroid hormone production and precipitating cardiovascular instability. Multidisciplinary management enabled timely diagnosis, surgical treatment, and prevention of thyroid storm. Ongoing follow-up with serial β-hCG and thyroid testing ensures resolution and early detection of persistent trophoblastic disease. This abstract is funded by: None