Assistant Professor UNIVERSITY OF MIAMI Miami, Florida, United States
Background: Thyrotropin-secreting pituitary adenomas (TSH-omas) are a rare cause of central hyperthyroidism, accounting for less than 1% of pituitary adenomas. Timely diagnosis may be confounded by rote interpretation of elevated TSH as indicative of primary hypothyroidism, if clinical context is not taken into account. The recognition of historical symptoms of hyperthyroidism when faced with labs showing elevated free T4 and non-suppressed TSH is essential. A comprehensive clinical evaluation when interpreting discordant TFTs can prevent inappropriate thyroid hormone replacement and delays in definitive management.
Case Presentation: A 75-year-old woman was initially diagnosed with hypothyroidism one year prior to presentation at our institution based on an elevated TSH of 12 mcIU/L and was started on levothyroxine 25 mcg daily. Her TSH subsequently increased to 15 mcIU/mL and her levothyroxine dose was further increased to 50 mcg daily with ensuing development of palpitations, weight loss and anxiety. She was subsequently found to have elevated free T4 and levothyroxine was discontinued. Pituitary MRI showed a 11.9 × 9.5 mm pituitary adenoma. Pre-operative labs were notable for TSH of 8.870 (0.270-4.200 mcIU/mL) and free T4 of 2.03 (0.93-1.70 ng/dL), free T3 of 4.52 (2.0-4.4 pg/mL), ACTH of 21.9 (7.2-63.3 pg/mL), FSH of 50.9 (25.8-134.8 mIU/mL), LH of 14.4 (7.7-58.5 mIU/mL), IGF-1 of 126 (48-191 ng/mL) and prolactin of 18.9 (4.8-23.3 ng/mL). The pituitary adenoma was resected via Endoscopic Endonasal Approach 11 months after initial levothyroxine initiation. Post-operatively, TSH declined rapidly from 1.4 on post-operative day (POD) one to 0.861 on POD two and 0.114 on POD three while free T4 decreased from 2.09 on POD one to 1.95 on POD two and 1.83 on POD three supporting removal of a pituitary source of inappropriate TSH secretion. Final pathology demonstrated plurihormonal PIT-1 lineage pituitary neuroendocrine tumor with diffuse strong thyroid stimulating hormone immunoreactivity, weak diffuse growth hormone positivity, and strong somatostatin receptor 2A expression; collagen type IV staining showed loss of the acinar pattern. The Ki-67 labeling index was approximately 2%. Tumor cells were negative for adrenocorticotropic hormone, prolactin, follicle stimulating hormone, steroidogenic factor 1 and T-box transcription factor 19.
Conclusion: Although TSH-secreting pituitary adenomas are exceedingly rare ( < 1% of pituitary tumors), this case highlights a key diagnostic pitfall: elevated TSH does not universally indicate hypothyroidism. A comprehensive history and examination with re-evaluation of clinical response at follow-up provides vital context for TFT interpretation. Prompt recognition of central hyperthyroidism and pituitary-directed evaluation can prevent prolonged, inappropriate levothyroxine exposure and expedite definitive therapy.
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