Endocrine Abstracts

A 19-year-old man attended his optician with an 18-month history of decreased visual acuity. Formal visual field testing revealed significant bitemporal hemianopia. On further questioning in hospital, his voice had deepened only 6 months previously. He had no facial hair. He had no difficulty with erections or libido. He had felt fatigued for months, but had no headaches, weight loss or postural dizziness. There was no history of galactorrhoea, gynaecomastia, nocturia, or excessive thirst. Physical examination revealed normal height and weight. He had sparse axillary and pubic hair and decreased testicular volume. There were no features to suggest GH or glucocorticoid excess. Laboratory investigations revealed a normal gonadal axis. IGF-1 was suppressed (38 ng/ml). Free T4 was low for our assay (9.0 pmol/l), with normal TSH (2.29 mIU/l). A short Synacthen test demonstrated a blunted cortisol response. Serum osmolality was normal. Prolactin was markedly elevated (248,358 mIU/l). An MRI pituitary demonstrated a large (31 x 30 x 48 mm) solid and cystic pituitary mass with supra-sellar extension and chiasmal compression. An escalating regimen of cabergoline was commenced, in addition to hydrocortisone replacement. Prolactin levels dropped steadily, and the dose of cabergoline was up-titrated, targeting a prolactin level in the normal range. Over the following months there were steady improvements in serial visual field testing, correlating with MRI improvements. An insulin tolerance test (ITT) confirmed a blunted GH response and blunted cortisol response. A TRH stimulation test showed a normal TSH response. Free T4 remained inadequate, and levothyroxine was commenced. Twelve months after the initial presentation, a repeat ITT showed continued blunting of the GH axis, but recovery of the cortisol axis. Hydrocortisone was weaned. Growth hormone replacement was introduced. One month thereafter, the patient attended outpatients with a 3-week history of anorexia, vomiting, fatigue, postural dizziness, and decreased visual acuity. He was admitted emergently and hydrocortisone was re-commenced. MRI revealed a recurrent pituitary cyst with chiasmal compression and evidence of sub-acute intra-cystic haemorrhage, consistent with apoplexy. He underwent transsphenoidal adenomectomy soon thereafter. Currently, the patient has been stable for 8 years following TSS, and is maintained on cabergoline, hydrocortisone, and levothyroxine. Dynamic testing has demonstrated that the cortisol and GH axes have not recovered. There are no case reports in the literature describing pituitary apoplexy following commencement of GH replacement. The patient has declined to re-commence GH therapy and, nevertheless, enjoys a good quality of life.