Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P260

Pituitary

Solitary pituitary metastasis from carcinoma of the prostate: a case report

Seleena Farook, Kanna Gnanalingham, Pyali Pal & Tara Kearney


Royal NHS foundation Trust Manchester, UK.


Mr GC aged 67 presented to the ophthalmologists in December 2008 with blurring vision and headaches. Visual acuity was 6/9, 6/24 and reassured. Two weeks later he returned as an emergency with severe visual loss of left eye to finger movements and temporal field defect right eye.

Past history included cancer prostate, gleason score-7 (T2 N0). TURP performed in January 08 followed by hormonal therapy and external beam irradiation.

Neuroradiological studies confirmed a large enhancing mass arising from the pituitary focca with suprasellar extension and chiasmal compression suggesting a possible pituitary macro adenoma.

Initial pituitary function tests revealed a non-functioning tumour with slightly raised prolactin at 1059 suggesting a stalk effect. He was deficient of thyroxine, growth hormone and testosterone. Perioperative steroid cover and thyroxine was commenced. PSA was normal at 1.5.

Partial tumour resection was possible on the endoscopic transphenoidal approach. A further L frontal craniotomy was performed to access the suprasellar tumour. Good debulking was possible with minimal tumour residue and improvement in vision. Tumour histology and immunophenotyping reported metastatic adenocarcinoma of the prostate with areas of coexistent meningioma.

Follow-up imaging studies revealed no other secondary with a normal sized prostate. Postoperative pituitary radiotherapy was uneventful. Growth hormone and testosterone therapy was contraindicated with active prostate malignancy.

Pituitary metastasis from prostate cancer is unusual. Widespread metastasis is usually noted at the time of diagnosis. Pituitary lesion presenting as the solitary site of metastasis has never been reported. PSA levels which are usually a reliable marker of disease activity has remained normal throughout. Histology suggesting a coexistent meningioma could be explained by a tumour in tumour phenomenon where metastatic deposits shows a predilection to seed on pre-existent benign tumours in the region facilitating local spread. With improving life expectancy in cancer, the incidence of pituitary metastasis is on the rise.

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