Poster Presentation Annual Meetings of the Endocrine Society of Australia and Society for Reproductive Biology and Australia and New Zealand Bone and Mineral Society 2016

Cavernous internal carotid artery ansurysm: a rare cause of marked hyperprolactinaemia (#394)

Emily J Meyer 1 , Sunita MC De Sousa 1 , Morton G Burt 2 , David J Torpy 1
  1. Royal Adelaide Hospital, North Adelaide, SA, Australia
  2. Flinders Medical Centre, Bedford Park, Adelaide, South Australia

Introduction: Hyperprolactinaemia can be caused by compression of the pituitary stalk by a non-functioning pituitary tumour. In this setting however, prolactin rarely exceeds 2000mU/L. Greater increases in serum prolactin are almost always secondary to a prolactinoma. We report two cases of marked hyperprolactinaemia secondary to a cavernous internal carotid artery (ICA) aneurysm. These cases highlight an extremely rare cause of marked hyperprolactinaemia and we speculate as to the underlying mechanism. 

Case 1: A 50 year-old man presented with headaches and bitemporal hemianopia. Hormonal evaluation demonstrated central hypocortisolism, hypothyroidism and hypogonadism and a prolactin of 97,780 mIU/L.  MRI revealed a 39 mm right cavernous ICA aneurysm, occupying the pituitary fossa and displacing the optic chiasm. No normal pituitary gland or adenoma was visible. A flow diverting stent was inserted and hydrocortisone and thyroxine commenced. However, prolactin remained elevated and two months later cabergoline 1 mg twice weekly was commenced.  After 10-months prolactin is 2070 mIU/L and central hypocortisolism has resolved.

Case 2: A 70 year-old man presented with headaches and a left temporal visual field defect. Hormonal evaluation demonstrated central hypogonadism and hypothyroidism with a prolactin of 70,355 mIU/L.  MRI revealed a 38 mm left cavernous ICA aneurysm, occupying the suprasellar space displacing the pituitary and optic chiasm. No pituitary adenoma was present. The aneurysm was conservatively managed. With regular cabergoline prolactin normalised and testosterone increased but did not normalise.

Conclusions: Cavernous ICA aneurysms are a rare cause of marked hyperprolactinaemia, with only four previous cases in the literature. We hypothesize that direct stimulation of pituitary lactotrophes by a putative aneurysmal-derived prolactin releasing factor via the superior hypophyseal arteries underlies the marked hyperprolactinaemia. Hypopituitarism is secondary to hyperprolactinaemia and aneurysmal compression of the pituitary and may, at least partially, recover during aneurysm remodeling.


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