Recommended Citation
Hawa SA, Tran K, Iyer M, Koh C. Hyperthyroidism in a Twin Pregnancy with a Complete Hydatidiform Mole and Coexisting Fetus: A Case Report. Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Abstract
Background/Significance:
Gestational Trophoblastic Disease (GTD) are tumors originating from trophoblastic cells of the placenta including premalignant hydatidiform moles and malignant gestational trophoblastic neoplasia. Incidence in the United States is from 1.1 to 1.2 per 1000 pregnancies. Rarer is pregnancy with a complete hydatidiform mole and coexisting fetus (CHMCF), from 1/22,000 to 1/100,000 pregnancies. GTD causes hyperthyroidism by cross-reactivity between the ɑ subunit of human Chorionic Gonadotropin (hCG) and Thyroid Stimulating Hormone (TSH), potentially resulting in devastating consequences.
Description:
A 23-year-old White Hispanic female presented with vaginal bleeding. hCG level was >248,400 mU/mL and an abdominal ultrasound (US) revealed a single, live intrauterine pregnancy of 15 weeks with a heterogeneous 11.7 cm echogenic mass. Week 18 US showed an area of mixed echogenicity with internal cystic structures up to 12.8 cm, possibly a partial mole. At 22 weeks, she developed palpitations. Beta-hCG exceeded 400,000 mU/mL; TSH was <0.008 mU/mL (0.4–5.5), and free T4 was 2.8 ng/dL (0.8–1.9). Hyperthyroidism was diagnosed, and methimazole and labetalol were initiated. At 26 weeks, she presented with chest pain, tremors, blood pressure of 197/101, uterine contractions with worsening labs. Magnetic Resonance Imaging confirmed CHMCF without invasion of adjacent structures. We started propylthiouracil, super-saturated potassium iodide, propranolol and cholestyramine. Two days later, she developed dyspnea with pulmonary edema, concerning for impending thyroid storm. She delivered a live female with normal anatomy via an urgent C-section. The mole was completely evacuated without complication. Labs began normalizing and anti-thyroid therapy was discontinued. At two weeks of post-partum, labs continued to normalize. The baby had a low TSH and normal fT4 at birth.
Discussion:
Molar pregnancies hypersecrete hCG, however, being 4000 times less potent than TSH, hyperthyroidism is rare with an incidence of 16% in those with complete molar pregnancy, with levels >400,000 IU/L posing greater risk. This case presented a unique challenge in its complexity due to comorbid pre-eclampsia. Prompt multimodal management prevents poor outcomes like neonatal hyperthyroidism, thyroid storm, eclampsia, maternal or fetal death or disability. We averted catastrophic consequences by aggressive management via a combination of synergistic thyroid hormone lowering strategies, culminating in an uncomplicated delivery.
Presentation Notes
Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Full Text of Presentation
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Document Type
Poster
Open Access
Available to all.
Hyperthyroidism in a Twin Pregnancy with a Complete Hydatidiform Mole and Coexisting Fetus: A Case Report
Background/Significance:
Gestational Trophoblastic Disease (GTD) are tumors originating from trophoblastic cells of the placenta including premalignant hydatidiform moles and malignant gestational trophoblastic neoplasia. Incidence in the United States is from 1.1 to 1.2 per 1000 pregnancies. Rarer is pregnancy with a complete hydatidiform mole and coexisting fetus (CHMCF), from 1/22,000 to 1/100,000 pregnancies. GTD causes hyperthyroidism by cross-reactivity between the ɑ subunit of human Chorionic Gonadotropin (hCG) and Thyroid Stimulating Hormone (TSH), potentially resulting in devastating consequences.
Description:
A 23-year-old White Hispanic female presented with vaginal bleeding. hCG level was >248,400 mU/mL and an abdominal ultrasound (US) revealed a single, live intrauterine pregnancy of 15 weeks with a heterogeneous 11.7 cm echogenic mass. Week 18 US showed an area of mixed echogenicity with internal cystic structures up to 12.8 cm, possibly a partial mole. At 22 weeks, she developed palpitations. Beta-hCG exceeded 400,000 mU/mL; TSH was <0.008 mU/mL (0.4–5.5), and free T4 was 2.8 ng/dL (0.8–1.9). Hyperthyroidism was diagnosed, and methimazole and labetalol were initiated. At 26 weeks, she presented with chest pain, tremors, blood pressure of 197/101, uterine contractions with worsening labs. Magnetic Resonance Imaging confirmed CHMCF without invasion of adjacent structures. We started propylthiouracil, super-saturated potassium iodide, propranolol and cholestyramine. Two days later, she developed dyspnea with pulmonary edema, concerning for impending thyroid storm. She delivered a live female with normal anatomy via an urgent C-section. The mole was completely evacuated without complication. Labs began normalizing and anti-thyroid therapy was discontinued. At two weeks of post-partum, labs continued to normalize. The baby had a low TSH and normal fT4 at birth.
Discussion:
Molar pregnancies hypersecrete hCG, however, being 4000 times less potent than TSH, hyperthyroidism is rare with an incidence of 16% in those with complete molar pregnancy, with levels >400,000 IU/L posing greater risk. This case presented a unique challenge in its complexity due to comorbid pre-eclampsia. Prompt multimodal management prevents poor outcomes like neonatal hyperthyroidism, thyroid storm, eclampsia, maternal or fetal death or disability. We averted catastrophic consequences by aggressive management via a combination of synergistic thyroid hormone lowering strategies, culminating in an uncomplicated delivery.
Affiliations
Advocate Lutheran General Hospital