BES2005 Poster Presentations Clinical (51 abstracts)
Department of Endocrinology, Imperial College Faculty of Medicine, Charing Cross Hospital, London, UK.
A 25 year old female presented with a two year history of secondary amenorrhoea and expressible galactorrhoea. There was no history of headache or visual disturbance, and the patient took no regular medication. Examination, including formal perimetry, was normal. Investigations revealed a moderately elevated prolactin 1,029 (NR 59-619 mU/ml), 9am cortisol 366 nmol/L, remainder of pituitary profile normal. An MRI pituitary revealed a macroadenoma with stalk deviation and bowing of the optic chiasm. The diagnosis was of non-functioning adenoma with hyperprolactinaemia secondary to stalk compression.
The patient was commenced on bromocriptine (intolerant of cabergoline) and referred for neurosurgical opinion, which advised medical management unless the patient developed deterioration in visual fields associated with tumour growth.
One month later, the patient conceived, bromocriptine was discontinued and the plan was to monitor closely with regular perimetry. At 11 weeks gestation, the patient presented with headache. Perimetry was normal, random cortisol 13 nmol/L and CT scan excluded pituitary haemorrhage. The patient was commenced on regular hydrocortisone and her symptoms resolved.
At 30 weeks the patient developed a mild bitemporal hemianopia, prolactin 2,524. An MRI reported increase in size of the pituitary with adenoma causing optic chiasm compression. The patient was recommenced on bromocriptine, prolactin 740, but there was further deterioration in the field defect. At 37 weeks a LSCS was performed and a healthy boy was delivered. Post-partum the patient was continued on bromocriptine and hydrocortisone and visual fields returned to normal. The patient is due for further MRI and pituitary assessment 6 months post-partum.
This case illustrates that pituitary expansion in normal pregnancy due to lactotroph hyperplasia can cause a macroadenoma to compress the optic chiasm with an associated visual field defect that is reversible post-partum. In addition, the patient was probably cortisol deficient at the time of presentation and it would have been of value formally to assess this at presentation.