SFEEU2025 Society for Endocrinology Clinical Update 2025 Workshop D: Disorders of the adrenal gland (17 abstracts)
Salford Royal Hospital, Manchester, United Kingdom
Introduction: Primary adrenal insufficiency and Graves disease both have an autoimmune aetiology with an incidence of 0.44 and 20 to 50 per 100,000 cases respectively 1, 2. An acute presentation with both conditions at the same time is rare We present a case of a male patient who presented to hospital with a recent diagnosis of Graves thyrotoxicosis who was found to be in adrenal crisis.
Case: A 37-year-old man presented to the emergency department with nausea, vomiting and hypotension. His GP had diagnosed hyperthyroidism two weeks previously and commenced carbimazole pending endocrinology review. His heart rate was 111 beats/min, blood pressure 82/48 mmHg, respiratory rate 28 breaths/min, oxygen saturation 97% on air and temperature 36.6 °C. Tanned skin with dark palmar creases were noted. He had tremor on outstretching his hands. Blood tests revealed low cortisol, hyponatraemia, and hyperthyroidism (see Table). Addisonian crisis was diagnosed, and he was commenced on intravenous hydrocortisone. A short Synacthen® test confirmed hypoadrenalism. Once stable, he was commenced on oral hydrocortisone and fludrocortisone.
Discussion: Simultaneous presentation with Addisons disease and Graves disease is rare. In thyrotoxicosis without adrenal insufficiency, both cortisol production and degradation are accelerated with circulating levels remaining normal. In hyperthyroidism and adrenal insufficiency, however, the ability to increase the synthesis of cortisol is impaired, leading to decreased levels. The loss of mineralocorticoid activity in primary adrenal insufficiency could also contribute to adrenal crisis in hyperthyroidism. Patients with Addisons disease have a 50% risk of developing a second autoimmune disease during their lifetime, such as hypothyroidism (range 4344%), vitiligo (910%), vitamin B12 deficiency (79%), type 1 diabetes (56%), coeliac disease (36%) and hyperthyroidism (45%).
| Test | Value | Reference range |
| On presentation | ||
| Sodium, mmol/l | 126 | 133 146 |
| Potassium, mmol/l | 5.0 | 3.5 5.3 |
| Calcium, mmol/l | 3.05 | 2.2 2.6 |
| Urea, mmol/l | 7.9 | 2.5 7.8 |
| Creatinine, µmol/l | 97 | 62 115 |
| Thyroid stimulating hormone (TSH), mU/l | 0.02 | 0.35 5.50 |
| Free thyroxine, pmol/l | 24.8 | 10.0 20.0 |
| Free triiodothyronine, pmol/l | 9.4 | 3.5 6.5 |
| Cortisol, nmol/l | 19 | 200 500 |
| Further investigations | ||
| Thyroid peroxidase antibody, IU/mL | 81 | 0 35 |
| TSH receptor antibody, U/l | 2.0 | 0.0 0.4 |
| Adrenocorticotropic hormone, ng/l | 437 | 0 46 |
| Anti-adrenal cortex antibody | Positive | |
| Short Synacthen® Test | ||
| Basal Cortisol, nmol/l | 42 | |
| 30-min Cortisol, nmol/l | 41 | |
| 60-min Cortisol, nmol/l | 33 |
Conclusion: It is rare for primary adrenal insufficiency to present simultaneously with another endocrine emergency. It should be suspected in patients who present to the hospital with hypotension, abdominal pain and vomiting. Treatment for adrenal crisis with glucocorticoids should not be delayed pending confirmatory investigations as it can be lifesaving.