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Endocrine Abstracts (2019) 62 P21 | DOI: 10.1530/endoabs.62.P21

1London North West University Healthcare NHS Trust, London, UK; 2West Middlesex University Hospital, London, UK.

Case history: A 34-year-old man attended the emergency department with a history of sudden onset severe headache associated with vomiting, neck stiffness mild photophobia not relieved with analgesia. He reported a past medical history of hypertension treated with angiotensin-converting enzyme inhibitor (ACEi). There was no focal neurology, and his observations were unremarkable - blood pressure 121/64 mmHg, heart rate 54 beats per minute, respiratory rate 14 breaths per minute. His visual acuity was well preserved - right eye 20/32 -3/7 and left eye 20/20 -2/9.

Investigations: Computed tomography (CT) head, magnetic resonance imaging (MRI) pituitary, routine biochemistry and haematology. His blood tests revealed an adrenocorticotropic hormone (ACTH) 417 ng/L, follicular stimulating hormone 4.8 IU/L (1.3 – 19.3), luteinising hormone 2.2 IU/L (1.2–8.6), insulin-like growth factor 1 22.8 nmol/L (13 – 50), serum prolactin (PRL) 9 miU/L (56 – 278), free thyroxine 3.8 pmol/L (8.4–19.1), thyroid-stimulating hormone 3.07 miU/L (0.38–5.33).

Results and treatment: Initial CT head reported an expanded sella turcica with the suggestion of an exogenous mass. A dedicated MRI pituitary confirmed a large supra-sellar mass lesion consistent with a pituitary macro-adenoma elevating and compressing the central part of the optic chiasm. There was bilateral mass effect on the cavernous sinuses with encasement of the cavernous portion of the internal carotid artery suggesting early invasion of the cavernous sinuses bilaterally with the possibility of a haemorrhagic component. The patient was initiated on oral hydrocortisone 10/5/5 mg which was later converted to prednisolone 5 mg once a day; levothyroxine 75 mcg once a day was also started. The patient was referred for urgent neurosurgical intervention as per the Society of Endocrinology guidance for management of Pituitary Apoplexy.

Conclusion and points for discussion: Spontaneous pituitary apoplexy (PA) typically presents with partial or complete pituitary hormone deficit (usually ACTH deficiency). As seen in our patient, isolated low serum prolactin might be the only manifestation. It is essential to exclude pituitary lesions in patients with borderline clinical signs and symptoms. Initial management involves the assessment of hypothalamic-pituitary-adrenal axis and indications for urgent surgical decompression. Spontaneous pituitary apoplexy is a rare and life-threatening endocrine emergency. It is caused by infarction of the pituitary gland (haemorrhagic or ischemic) and is most commonly associated with an existing macroadenoma. Early recognition and a high degree of suspicion are particularly important in patients with no known underlying pituitary adenoma. Timely identification of PA will reduce morbidity and mortality in these patients.

Volume 62

Society for Endocrinology Endocrine Update 2019

Society for Endocrinology 

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