Abstract
Hydatidiform mole (HM), a type of gestational trophoblastic disease (GTD), is a rare cause of clinical hyperthyroidism. The development of hyperthyroidism requires an elevation of HCG >100,000 mlU/mL for several weeks. Complete mole has a marked HCG elevation compared to partial mole thus presents with a higher incidence of thyrotoxicosis. Surgical uterine evacuation is the treatment of choice for HM. However, untreated hyperthyroidism can pose a risk for the development of thyroid storm and high-output cardiac failure in the perioperative period. To our knowledge, there are no specific guidelines for management at this time. We present a case of hyperthyroidism secondary to complete molar pregnancy successfully treated with propylthiouracil (PTU), potassium iodide (SSKI), and atenolol in the preoperative period.
A 42-year-old female with history of migraines presented to her gynecologist with a 3-week history of lower abdominal cramping, vomiting, loss of appetite, and abnormal vaginal bleeding. She also endorsed a 6-pound weight loss, intermittent tachycardia, exertional dyspnea, and increased anxiety. Pregnancy test was positive, and ultrasound was concerning for GTD. Laboratory work up was significant for HCG 797,747 mIU/mL (< 5mlU/mL), TSH <0.005 mIU/mL (0.4-4.0 mlU/mL), Free T4 3.09 ng/dL (0.9-1.9 ng/dL), and Free T3 11.48 pg/dL (1.76-3.78 pg/dL). The patient was admitted to the hospital and started on PTU 100 mg Q6H, SSKI 200 mg TID following the first dose of PTU, and atenolol 25 mg daily. She underwent an uncomplicated D & C the next day. On post-op day 1, HCG decreased to 195,338 mIU/mL and Free T4 to 2.39 ng/dL. The patient was discharged on the aforementioned doses of PTU and atenolol. One-week follow-up labs showed HCG 8,917 mIU/mL and Free T4 1.22 ng/dL. Surgical pathology confirmed a complete hydatidiform mole. PTU was decreased to 50 mg TID. On post-op day 14, HCG had risen to 15,395 mIU/mL with onset of nausea and vomiting. Repeat Free T4 remained within reference range. Patient was taken back to surgery for a laparoscopic total hysterectomy with bilateral salpingectomy. Pathology confirmed an invasive hydatidiform mole. Two-week follow-up lab work showed HCG 155 mIU/mL, TSH 1.5 mIU/mL, and Free T4 1.19 ng/dL. PTU and atenolol were then discontinued.
The development of hyperthyroidism in molar pregnancy is largely influenced by the level of HCG and usually resolves with treatment of GTD (1). However, it’s crucial to control thyrotoxicosis to avoid perioperative complications. This case also highlights the importance of monitoring HCG levels following a complete molar pregnancy due to an increased risk for invasive neoplasm.
1. Walkington, L et al. “Hyperthyroidism and human chorionic gonadotrophin production in gestational trophoblastic disease.” British journal of cancer vol. 104,11 (2011): 1665-9. doi:10.1038/bjc.2011.139
Genetic Screening of Susceptible Women to Recurrent Molar Pregnancy for Prevention of Gestational Choriocarcinomas
