Transient Thyrotoxicosis in Molar Pregnancy

Abstract

Introduction: Thyroid function abnormalities commonly occur in pregnancy. Due to the structural homology between beta-human chorionic gonadotropin (beta-hCG) and thyrotropin (TSH), some of these changes may be physiologic, while others can be from pathologic causes. Molar pregnancies represent a unique etiology, as beta-hCG levels are often markedly elevated due to trophoblastic hyperplasia and can cause hyperthyroidism. Case Description: A 20-year-old pregnant female presented at 18 weeks estimated gestational age for persistent nausea and vomiting, which had worsened over the past one to two weeks. She also noted palpitations and heat intolerance. On initial presentation, her heart rate was 145 beats per minute, blood pressure was 135/86 mmHg, oxygen saturation was 98% on room air, and temperature was 98.3 F. Exam was notable for sinus tachycardia; no thyromegaly, palpable thyroid nodules, lower extremity edema, or tremors were appreciated. Transvaginal ultrasound was performed, and an approximately 17-week fetus with no cardiac activity was identified; an enlarged and hydropic placenta and bilateral theca lutein cysts were also seen on imaging, concerning for a partial molar pregnancy. Laboratory data revealed plasma beta-hCG >1,000,000 mIU/mL. Due to her symptoms and tachycardia that were refractory to intravenous hydration, thyroid function tests (TFTs) were assessed: TSH of 0.01 uIU/mL and free T4 (FT4) 6.85 ng/dL. She was started on methimazole and beta blockade in the pre-operative period. She received mifepristone and underwent dilatation and evacuation. Histopathology was consistent with a partial mole, given the presence of fetal somatic differentiation. Beta-hCG and FT4 levels rapidly trended down in the post-operative setting, and methimazole was discontinued. Levels were monitored closely after discharge. Atenolol was stopped when her TFTs normalized. Approximately six weeks after surgery, her TSH was 0.523 uIU/mL and FT4 was 0.70 ng/dL. Three months after surgery, the beta-hCG level had decreased to 4 mIU/mL. Discussion: In North America, the incidence of hydatidiform moles is approximately 100 per 100,000 pregnancies. Hydatidiform moles compromise two distinct entities: complete moles and partial moles, which are distinguishable based on karyotype and histopathological features. In molar pregnancies, the trophoblastic tissues, which produce hCG, are hyperplastic; thus, markedly elevated hCG levels can be seen. Due to its structural similarity to TSH, beta-hCG can activate TSH receptors and drive production of thyroid hormone, which can subsequently result in a thyrotoxic state. Surgical management of the mole is key, as the hyperthyroidism usually resolves with uterine evacuation, though hCG levels must be monitored closely afterwards to ensure gestational trophoblastic neoplasia does not develop.