Session: MON 471-496-Thyroid Neoplasia & Case Reports
Poster Board MON-471
Clinical case: A 45 year-old male patient with metastatic MTC was referred to our institution after being treated unsuccessfully with two chemotherapy regimens. In addition to widespread and bulky metastatic disease (cervical, lung, liver and bones) the patient presented with severe diarrhea, muscle weakness and weight gain. Physical examination revealed plethoric facies, central obesity and profound proximal muscle weakness, which led to the suspicion of Cushing’s syndrome. Biochemical analysis revealed ACTH-dependent hypercortisolism suggestive of ectopic ACTH syndrome - basal serum ACTH 76 pg/mL (normal range 12-55) and 24 hr urinary cortisol 946 mcg/24hr (normal range 50-310). The calcinonin and CEA levels were 12456 pg/mL (normal range <8,4) and 210,4 ng/mL (normal range <10), respectively. As vandetanib or active clinical trials were not available at our institution, we opted to initiate the patient on off-label sorafenib 400 mg twice a day. After two weeks, laboratory evaluation revealed complete resolution of hypercortisolism associated with significant clinical improvement. The 24 hr urinary cortisol levels were 70,4 and 49 mcg/24 hr 15 and 21 days after initiating sorafenib therapy. Serum cortisol, ACTH and calcitonin levels also decreased significantly after 15 days of sorafenib therapy (7.2 mcg/dL, 23 pg/mL and 8057 pg/mL, respectively).
Conclusion: Despite a reduction of calcitonin and CEA levels, we question whether the rapid control of hypercortisolism was not only related to tumor mass reduction but possibly secondary to a direct effect of sorafenib on hormonal secretion. To date, the only well-defined hormonal abnormality observed in patients treated with TKI is hypothyroidism, which occurs in a substantial proportion of patients (5). The rapid correction of hypercortisolism was beneficial to this patient, however, it raises the question whether common side effects of TKI treatment such as fatigue, anorexia, nausea and vomiting are, at some extent, secondary to hypoadrenalism. Studies will be necessary to investigate the role of sorafenib and other TKIs in the pituitary-adrenal axis.
Nothing to Disclose: AOH, JEB, GC Jr., AML
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