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A 31-year-old woman with a 20-year history of type 1 diabetes presented with a 2-month history of recurrent disabling hypoglycaemia. Common causes of hypoglycaemia which included excess insulin, missing meals and unaccustomed exercise had been excluded. She did not have evidence of gastroparesis, her coeliac antibody screen was negative and her renal function was normal. However, a short synacthen test (SST) failed to show a cortisol response with a peak cortisol response of 166 nmol/L at 60 min. A static pituitary profile was subsequently performed showing an adrenocorticotropic hormone level of <5 ng/L indicating secondary hypoadrenalism and an inappropriately normal thyroid-stimulating hormone, low free T4 and T3 and low gonadotrophin, all pointing towards pituitary abnormality. MRI confirmed a pituitary adenoma with a high signal on T1, suggestive of recent bleeding into it (pituitary apoplexy) (figure 1). Since our patient had no neuro-opthalmic signs, she was managed conversatively1 with a plan to rescan the pituitary in 12 months’ time. She was established on hydrocortisone and thyroxine replacement.
Classical pituitary apoplexy refers to a clinical syndrome, characterised by sudden onset headache, vomiting, visual impairment and decreased consciousness caused by infarction or haemorrhage into a pituitary gland.1 However, not all patients with pituitary haemorrhage necessarily develop the apopletic syndrome.2 Furthermore, an abnormal SST does not differentiate between primary and secondary hypoadrenalism and should always be investigated further. The diagnosis of pituitary apoplexy in this patient would have been missed if a pituitary profile followed by an MRI pituitary was not performed.
Competing interests: None.
Patient consent: Obtained.
Provenance and peer review: Not commissioned; externally peer reviewed.