Abstract #1404395: Metastatic Choriocarcinoma: A Rare Cause of Thyrotoxicosis

Abstract

Although Graves’ disease continues to be considered the most frequent cause of clinical hyperthyroidism in pregnancy, the disproportionately high production of human chorionic gonadotropin (HCG) as occurs in gestational trophoblastic disease (TSG), is another possible cause that should be considered when evaluating thyrotoxicosis in pregnancy. A 19-year-old female with unremarkable past medical history who was admitted for nausea, vomiting and abdominal pain for 2 weeks. Her last period was 4 weeks prior to her presentation and patient denied any vaginal bleeding. Her period had been irregular since her last miscarriage a year earlier. She denied being sick recently, and her last flulike illness was 4 months ago. Denied using any medication at home including herbal medication or OCPs. Review of systems was significant for fatigue, heat intolerance, palpitation, tremor, loss of appetite and unintentional weight loss over the last week. She denied diarrhea or anxiety. On presentation, Patient was hypotensive 90s/40s mmHg and tachycardic 140s bmp. EKG showed sinus tachycardia. Initial work-up was significant for HB 6.2, WBC 11.6 and B-hCG 9678 IU/ml. Liver enzymes were elevated. Transvaginal ultrasound showed empty uterus. Pan CT showed hemoperitonium and liver, lung and kidney lesions concerning for metastatic choriocarcinoma which was confirmed with positive liver biopsy. Work-up also showed suppressed TSH 0.01uIU/ml, high free T4 2.54ng/dl, and high free T3 5.1ng/dl, absent TSI, normal Tg level with negative Tg antibodies. There was no baseline TSH to compare. BHCG with dilution was 5,430,055IU/ml. Thyroid ultrasound was normal. Patient was diagnosed with metastatic choriocarcinoma and treated with 3 cycles of cisplatin/etoposide chemotherapy. Patient did not receive any antithyroid medication due to elevated liver enzymes and mild symptoms. B-HBG following the treatment was 3mIU/ml, TSH was 1.5 uIU/ml and FT4 was 1.1ng/dl. Hyperthyroidism has been reported in many patients with GTD. The beta subunit of β-hCG is structurally similar to TSH, allowing it to bind to the TSH receptor on thyroid follicular cells. It has been reported that β-hCG levels of greater than 200,000 m[IU]/ml sustained for several weeks are required to induce clinical hyperthyroidism. It is estimated that for every 10,000 m[lU]/ml increase in serum hCG, TSH decreases by 0.1 mlU/ml and free T4 increases by 0.1 ng/dL. No clear risk factors for hyperthyroidism in GTD were identified. Presentations can range from subclinical hyperthyroidism to thyrotoxicosis and thyroid storm. This case was challenging because the initial B-HCG was not high enough to cause thyrotoxicosis but delusional B-HCG confirmed our suspicion. While hyperthyroidism can be definitively managed with surgical evacuation of the uterus in GTD, hyperthyroidism secondary to metastatic choriocarcinoma could be successfully treated with chemotherapy with or without antithyroid medication. The increase in TSH usually parallel the reduction in BHCG.