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Endocrine Abstracts (2015) 37 EP1200 | DOI: 10.1530/endoabs.37.EP1200

ECE2015 Eposter Presentations Clinical Cases–Pituitary/Adrenal (95 abstracts)

New onset Graves' disease as a cause of an adrenal crisis in an unrecognised empty sella

Hela Marmouch 1, , Tasnim Slim 1 , Fadia Boubaker 1 , Sondes Arfa 1 , Hanene Sayadi 1, , Manel Jmal 1, & Ines Khochtali 1,


1Department of Internal Medecine-Endocrinology, MONASTIR, Tunisia; 2Faculty of Medecine, MONASTIR, Tunisia.


Introduction: A 66-year-old woman was admitted as an emergency with vomiting, hypotension and serum cortisol of 0.92 microg/dl indicative of adrenal failure. She was found to be hyperthyroid (fT4=72 pmol/l).

Case report: She had hypotension (blood pressure 80/40 mm/Hg) She was fit and well till the age of 65. Endocrine assessment revealed deficiency in ACTH-cortisol, growth hormone, and gonadotropin, as well as low-normal fT4. On the day of his emergency admission he looked ill and dehydrated, though was fully conscious and cooperative. Heart rate was 110 beats/min (sinus rhythm), blood pressure 85/60 mm/Hg. There were no obvious features of infection, but there was marked tremor and thyroid bruit. She received treatment with intravenous fluids and hydrocortisone. Administration of large dose of methimazole (40 mg per day) resulted in gradual decrease in fT4. Pituitary MRI showed empty sella. The patient was found to have increased titre of antithyroperoxidase (anti-TPO) and anti-TSH receptor (anti-TSHR) antibodies (2100 IU/l (ref. range <40) and 3.7 IU/l (ref. range <1.0), respectively). She was referred for radioactive iodine treatment. Iodine uptake scan performed prior to radioiodine administration confirmed uniformly increased iodine uptake consistent with Graves’ disease.

Discussion: We encountered a patient with unrecognised adrenocortical disease due to empty sella, in whom development of Graves’ hyperthyroidism caused an adrenal crisis. Empty sella syndrome in this case can be related to autoimmune hypophysitis.

Conclusion: Our case illustrates coexistence of hypopituitarism and clinically significant autoimmune thyroid disease. The presence of hypopituitarism does not preclude the development of autoimmune thyrotoxicosis.

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