Endocrine Abstracts

A 44 year old man was referred with a 3-week history of progressive visual failure without headaches. He had bitemporal hemianopia but no evidence of endocrine dysfunction. MR scanning revealed a large pituitary macroadenoma with evidence of intralesional haemorrhage and compression of the optic chiasm. Endocrine testing revealed no evidence of a hormone excess syndrome or hypopituitarism. Transphenoidal hypophysectomy was performed urgently in May 2000 and his vision improved. Histology indicated this to be a non-functioning pituitary adenoma. Two months later he complained of a rapid recurrence of his visual loss. A repeat MR showed a large recurrent/residual suprasellar tumour, and using a subfrontal approach the residual tumour was completely excised. Repeat MR imaging after the second operation showed good tumour clearance, with a small residue within the pituitary fossa but no suprasellar extension or optic nerve compression. Several months later however he re-presented and required removal of recurrent aggressive tumour growth, and then received external beam radiotherapy. After this third operation he complained of persisting visual impairment, increased appetite, and his short term memory was impaired. He was pan-hypopituitary, and was given thyroxine, testosterone, GH, DDAVP and hydrocortisone replacement. His headaches improved and an MR scan three months later showed no growth of residual tumour. One year later, in March 2002, he complained of severe headache, worsening visual loss and vomiting. MR imaging revealed a mass lesion in the right temporal area with midline shift and significant oedema. Brain biopsy confirmed metastatic spread of the pituitary tumour and he commenced chemotherapy with oral etoposide.
In summary this patient presented with what initially appeared to be a benign but locally aggressive non-functioning pituitary adenoma. The subsequent intracranial metastatic spread indicates that this was in fact a pituitary carcinoma.