Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2016) 44 EP4 | DOI: 10.1530/endoabs.44.EP4

SFEBES2016 ePoster Presentations (1) (116 abstracts)

Failure to suppress TSH in thyroid cancer – could it be Addison’s disease?

George E Fowler 1 , Jonathan Wadsley 2 , Jonathan Webster 3 & Sabapathy P Balasubramanian 4

1The Medical School, University of Sheffield, Sheffield, UK; 2Department of Oncology, Weston Park Hospital, Sheffield, UK; 3Department of Diabetes and Endocrinology, Northern General Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK; 4Sheffield Endocrine Surgical Unit, Directorate of General Surgery, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK.

Background: Papillary thyroid cancer is the commonest thyroid malignancy. Surgery is first-line treatment, followed by radioiodine and long-term, high dose levothyroxine to suppress TSH.

Cortisol is known to suppress TSH secretion by the pituitary, although the mechanism remains unclear. Correspondingly, hypocortisolism may raise TSH levels.

Case Summary: A 64 year old woman presented with a right-sided thyroid nodule, normal TSH and raised TPO antibodies (141 IU/ml). On conservative management, she developed biochemical evidence of hyperthyroidism and was commenced on carbimazole. A radionuclide scan showed the right-sided nodule to be cold. To treat her hyperthyroidism and remove the nodule, she underwent a near-total thyroidectomy a year after her initial presentation. Histology showed multinodularity, focal lymphoid infiltrate and multifocal papillary cancer (pT1m pN0 pMx, R0). Further treatment included radioiodine ablation and high dose thyroxine for TSH suppression.

TSH remained supressed at <0.1 mIU/L for 5 years following surgery (at ~250 mcg/day of thyroxine), but later started to rise. The thyroxine dose had to be increased gradually to 350 mcg/day (more than double her starting dose) to ensure a low TSH. Non-compliance to treatment was considered unlikely.

Five years later, her sister (non-medical background) suggested that she may have Addison’s disease following an online search based on symptoms. Subsequent examination demonstrated cutaneous and mucosal hyperpigmentation and a short synacthen test (basal and 30 minute cortisol of 61 and 66 respectively) confirmed the diagnosis. After commencing hydrocortisone her TSH levels suppressed using much lower doses of thyroxine (currently 225 mcg/day).

Conclusion: This case report highlights how the rare occurrence of Addison’s disease can be overlooked. In patients on long-term thyroxine, an increasing T4 requirement (either for replacement or TSH suppression) should raise the suspicion of Addison’s disease as a potential cause, in addition to the possibility of non-compliance.

Volume 44

Society for Endocrinology BES 2016

Brighton, UK
07 Nov 2016 - 09 Nov 2016

Society for Endocrinology 

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