Session: FP14-Thyroid Cancer: Insights into Diagnosis & Treatment
Room 103 (Moscone Center)
Poster Board SAT-418
Clinical Case: A 59 yo male with sporadic MTC with known bone, liver, and lung metastases treated previously with two multikinase inhibitors in clinical trials presented with progressive disease and new onset hypokalemia (2.3 mmol/L), metabolic acidosis (CO2 35 mmol/L), hyperglycemia (325 mg/dl), and hypertension (146/91)./ His physical appearance was suspicious for CS. Initial tests were consistent with ACTH-dependent CS: a 1-mg overnight dexamethasone suppression test (DST) showed a post-dexamethasone 8:00 am cortisol level of 13.86 ug/dl (<5 ug/dl), and an ACTH level of 103 pg/ml (9-50 pg/ml). The patient failed to suppress to 8-mg dex, with a pre-dex cortisol of 13.3 ug/dl and post-dex cortisol of 24.06 ug/dl .
The patient was started on insulin and potassium replacement therapy 120 mEq daily. He received ketoconazole for several weeks with minimal change in labs or signs and symptoms of CS. Once mifepristone was obtained, he was switched to this medication at a dose of 300 mg daily. After 2 weeks the dose was increased to 600 mg daily. Within approximately 1 month, his insulin requirements had decreased from 3-4 times per day to 5-6 times per week with all fasting BS <120. He had decreased facial edema and improved proximal muscle strength. He was increased to Mifepristone 900 mg daily. He was able to decrease potassium supplementation to 20 mEq daily and stop insulin. He was started on vandetanib for the progressive metastatic MTC with subsequent reduction in serum calcitonin and size and number of lesions. The mifeprostone was able to be decreased and eventually discontinued with persistent marked improvement in CS features, hypokalemia and hyperglycemia.
Conclusion: Mifepristone is a reasonable treatment option as an alternative to surgical adrenalectomy for patients with Medullary thyroid cancer producing ACTH and causing Cushing syndrome
Nothing to Disclose: SMB, MDR, MHS, LSK
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