A 21-year-old woman with a past medical history of poorly controlled type 1 diabetes mellitus (HbA1c=11.2%) was investigated at her local hospital after reporting amenorrhoea for 3 years following the birth of her child. In addition, she gave a history of lethargy and frontal headaches. Endocrinological investigations demonstrated anterior pituitary dysfunction with adrenal insufficiency, hypothyroidism, growth hormone deficiency, hypogonadotropic hypogonadism and hyperprolactinaemia with a prolactin level of 2207 mIU/l (Table 1). She was therefore commenced on hydrocortisone (11.8 mg/m2), T4 75 mug daily and cabergoline 0.25 mug twice weekly, which markedly improved her symptoms; she continued on oestrogen and progesterone hormone replacement therapy. She subsequently reported having a severe, sudden onset headache with transient loss of vision suggestive of pituitary apoplexy. Cranial MRI scan revealed an 18x14x19 mm pituitary lesion, with suprasellar extension and superior displacement of the optic chiasm (Fig. 2A and B). Despite compression of the optic tract, visual fields and visual acuity were unaffected. She was subsequently referred to the regional pituitary specialist team and a diagnosis of a non-functioning pituitary macroadenoma was made. She underwent endoscopic transsphenoidal surgery. Histological analysis of the resected lesion demonstrated areas of cholesterol cleft formation associated with multinucleate giant cells and numerous macrophages, highlighted by immunohistochemistry to CD68. Areas of necrotic tissue, fragments of fibrous tissue, and the residual compressed adenohypophysis were also present (Fig. 4B and C). Gram stain (for bacteria), Warthin-Starry stain (for treponemes) and Ziehl-Neelsen stain (for TB) were all negative. Histology did not demonstrate evidence of vasculitis or granuloma formation, therefore ruling out sarcoidosis and Wegener's granulomatosis as the other biochemical tests were not performed.
She made a full post-operative recovery and continued on hydrocortisone, T4 and HRT. She developed diabetes insipidus post-surgery. An MRI scan performed 6 months following surgery demonstrated normal pituitary gland, stalk and chiasm with no residual lesion (Fig. 2C).