FRI311 GnRH Agonist Induced Pituitary Apoplexy In A Patient With Gonadotropinoma

FRI311 GnRH激动剂诱发促性腺激素瘤患者垂体卒中

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Abstract

Disclosure: I. Madahar: None. S. Khan: None. L. Hergenroeder: None. B. Skaff: None. A. Haider: None. Introduction: GnRH therapy is commonly employed in patients with advanced prostate cancer. It acts as an agonist that binds to pituitary GnRH receptors. It acts via desensitization, downregulating FSH and LH production, and ultimately decreasing testicular steroidogenesis. Initial administration leads to transient stimulation of the pituitary which leads to elevated FSH and LH levels and increased production of estrogen and testosterone with eventual downregulation of the overall pathway. Case description: 80-year-old male with a past history of atrial fibrillation and OA was diagnosed with prostate cancer. Prostate adenocarcinoma Gleason score 7 (4+3) grade 3 was diagnosed by needle core biopsy five months prior to presentation. CT chest, abdomen, pelvis, and bone scan did not show evidence of metastatic disease. A week prior to starting Lupron therapy he was started on bicalutamide therapy. He received a dose of leuprolide (Elligard) as part of his chemoradiation therapy for his cancer. The patient went golfing after the treatment and within four hours he started noticing headaches and retroorbital pain. Headaches were sharp in quality, intensity 9 out of 10, and associated with nausea and vomiting. He later developed right-sided ptosis and double vision which progressively worsened after the next few hours. An initial CT scan of the head showed an enlarging pituitary mass which was followed MRI of the brain with and without contrast showed an enlarged pituitary mass and right cavernous sinus effacement of the optic chiasm. Anterior pituitary hormone functions were ordered, and the patient was started on stress-dose steroids. Transsphenoidal pituitary resection was done which the patient tolerated well pathology showed pituitary adenoma with pituitary apoplexy and the immunoprofile was compatible with gonadotroph adenoma. The adenoma cells were positive for synaptophysin, cam 5.2, GATA3, and FSH. A repeat MRI of the Sella three months after surgery showed a 9 mm nodule in the right aspect of the Sella. Anterior pituitary hormone levels done prior to surgery showed an IGF- 1 level of 204 ng/ml (Z score 1.5 SD). TSH and free T4 were in the normal range. Hydrocortisone was tapered and stopped 6 weeks after transsphenoidal surgery. Discussion: Lupron levels reach maximum concentration four hours after intramuscular administration. Initial pituitary stimulation by leuprolide administration causes the increased metabolic activity of the underlying adenoma which outgrows its blood supply, thus developing ischemic necrosis and subsequent hemorrhage. The majority of pituitary apoplexy develops in patients with previous undiagnosed pituitary adenomas. Should patients get central imaging to screen for pituitary macroadenoma before Lupron treatments to prevent this potentially life-threatening complication? Presentation: Friday, June 16, 2023

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