Endocrine Abstracts

A 54 year old gentleman presented to the eye services with reduced vision on the right attributed to a cataract. Following cataract surgery there was no improvement and his vision declined further with reducing vision also on the left. He was reviewed in Neuro-ophthalmology clinic 29/10/21 and clinical suspicion of a pituitary lesion based on binasal retinal ganglion cell layer loss and bilateral optic atrophy prompted urgent imaging. His right eye visual acuity was to hand movements only with a relative afferent pupil defect and left 6/9. Visual fields were grossly restricted on the right and showed a temporal hemianopia and reduced nasal sensitivity in the left. An urgent MRI orbit on 02/11/21 showed a homogeneous enhancing mass within the sella with bi-lobulated suprasellar extension elevating the optic chiasm and with marked compression of the right pre-chiasmatic optic nerve. He was referred urgently to neurosurgery and endocrinology. His co-morbidities include CKD3, obstructive sleep apnoea, hypertensive heart failure, bronchiectasis, and rheumatoid arthritis for which he was taking prednisolone 12.5 mg daily. Pre-surgical bloods on 08/11/21showed TSH 1. /l, T4 10.6 pmol/l, Testosterone 2.1 nmol/l, IGF-1 17.7 nmol/l and peak GH and cortisol levels during a GST of 0.2 mg/l and 248 nmol/l respectively. He underwent elective endoscopic endonasal trans-sphenoidal debulking of pituitary tumour on 16/11/21 with an uneventful post-operative course without evidence of hypo/hypernatraemia, polydipsia or polyuria. He continued a double dose of prednisolone for three days. Ophthalmology review showed mild improvement. Both eyes continued to show optic atrophy. Visual acuity improved to 6/36 and 6/9 in the right and left eye respectively. Post-operative bloods on 10/12/21 revealed a peak cortisol 248 nmol/l and peak growth hormone of 0.2 mg/l on repeat GST; Testosterone 3.8 nmol/l, LH 4.3 iu/l, FSH 0.2 iu/l, TSH 2.0 miu/l, Free T4 10.4 pmol/l, IGF1 17.7 (6.3-27.2) nmol/l. Histopathology confirmed a null cell pituitary adenoma positive for synaptophysin with a high proliferative index (Ki67 10%) and P53 in sparse cells suggesting possible future aggressive biological behaviour. Post surgically he developed hypopituitarism (GH, LH/FSH and ACTH deficiencies). He has been tired and lethargic. He is to be initiated on testosterone replacement and we will consider levothyroxine replacement in view of his low Free T4. He is currently on hydrocortisone 10 mg/5 mg/5 mg following reduction of his prednisolone dose to 5 mg OD.