Gonadotropin-releasing hormone agonist-induced pituitary apoplexy. (8th June 2016)

• Record Type: Journal Article
• Authors: Keane, Fergus; Egan, Aoife M; Navin, Patrick; Brett, Francesca; Dennedy, Michael C
• Is Part Of: Endocrinology, diabetes & metabolism case reports. (2016)
• Publication Date: 2016-06-08
• Subjects: Adult -- Male -- White -- Ireland; Pituitary -- Pituitary -- GNRH -- Testosterone -- LH -- Gonadotropins -- FSH -- Pituitary apoplexy -- Pituitary adenoma -- Prostate cancer -- Gonadotrophic adenoma; Headache -- Ptosis -- Visual impairment -- Enlarged prostate -- FSH -- Gonadotrophins -- LH -- MRI -- Testosterone -- Cortisol -- ACTH stimulation -- Prostate-specific antigen -- Transsphenoidal surgery -- Resection of tumour -- Radiotherapy -- Hypophysectomy -- Fluid repletion -- GNRH antagonists -- Steroids -- Hydrocortisone; Urology; Insight into disease pathogenesis or mechanism of therapy -- June -- 2016; Endocrinology -- Periodicals; Diabetes -- Periodicals; Diabetes Mellitus; Endocrinology; Diabetes; Endocrinology; Case Reports; Periodicals; Periodicals; 616.4
• DOI: 10.1530/EDM-16-0021
• Languages: English
• ISSNs: 2052-0573

Abstract

Summary: Pituitary apoplexy represents an uncommon endocrine emergency with potentially life-threatening consequences. Drug-induced pituitary apoplexy is a rare but important consideration when evaluating patients with this presentation. We describe an unusual case of a patient with a known pituitary macroadenoma presenting with acute-onset third nerve palsy and headache secondary to tumour enlargement and apoplexy. This followed gonadotropin-releasing hormone (GNRH) agonist therapy used to treat metastatic prostate carcinoma. Following acute management, the patient underwent transphenoidal debulking of his pituitary gland with resolution of his third nerve palsy. Subsequent retrospective data interpretation revealed that this had been a secretory gonadotropinoma and GNRH agonist therapy resulted in raised gonadotropins and testosterone. Hence, further management of his prostate carcinoma required GNRH antagonist therapy and external beam radiotherapy. This case demonstrates an uncommon complication of GNRH agonist therapy in the setting of a pituitary macroadenoma. It also highlights the importance of careful, serial data interpretation in patients with pituitary adenomas. Finally, this case presents a unique insight into the challenges of managing a hormonal-dependent prostate cancer in a patient with a secretory pituitary tumour. Learning points: While non-functioning gonadotropinomas represent the most common form of pituitary macroadenoma, functioning gonadotropinomas are exceedingly rare. Acute tumour enlargement, with potential pituitary apoplexy, is a rare but important adverse effect arising from GNRH agonist therapy in the presence of both functioning and non-functioning pituitary gonadotropinomas. GNRH antagonist therapy represents an alternative treatment option for patients with hormonal therapy-requiring prostate cancer, who also have diagnosed with a pituitary gonadotropinoma.