Challenges in the management of prolactinomas: A case of partial resistance to high-dose cabergoline in a young male with an invasive giant prolactinoma

Larisa-Nicoleta Cheţan; Andreea Vladan; Dan Hortopan; Ionut Gobej; Serban Radian; Catalina Poiana

doi:10.1530/endoabs.90.EP762

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Endocrine Abstracts (2023) 90 EP762 | DOI: 10.1530/endoabs.90.EP762

ECE2023 Eposter Presentations Pituitary and Neuroendocrinology (234 abstracts)

Challenges in the management of prolactinomas: A case of partial resistance to high-dose cabergoline in a young male with an invasive giant prolactinoma

Larisa-Nicoleta Cheţan ¹ , Andreea Vladan ² , Dan Hortopan ³ , Ionut Gobej ⁴ , Serban Radian ^1,2 & Catalina Poiana ^1,2

Err

Author affiliations

¹C.I. Parhon National Institute of Endocrinology, Department of Pituitary and Neuroendocrine Diseases, Bucharest, Romania; ²C. Davila University of Medicine and Pharmacy, Bucharest, Romania, Department of Endocrinology, Bucharest, Romania; ³Gral Medical, Department of Imaging, Bucharest, Romania; ⁴Neurohope, Department of Neurosurgery, Bucharest, Romania.

Background: Giant prolactinomas are rare pituitary tumours larger than >40 mm in diameter, representing 2–3% of prolactin secreting tumours. Management is challenging especially in male patients, due to resistance to dopamine agonists (DA).

Methods: Clinical, hormonal and imaging evaluation and follow-up

Aim: To describe a case of partially resistant giant prolactinoma in a young male patient

Case report: A 17-years old adolescent with a 2 years history of progressive loss of vision and visual field defects (right eye blindness and left eye temporal hemianopia) presented following MRI identification of a 30×28×45 mm sellar mass, extending suprasellary, into the left cavernous sinus, compressing the left temporal cerebral lobe. Examination revealed left oculomotor palsy, delayed puberty (Tanner stage III), without other signs of hypopituitarism. Laboratory workup demonstrated severe hyperprolactinemia (6739.8 ng/ml), normal IGF1 and thyrotroph and gonadotrop insufficiency. Family history was negative for MEN1 and FIPA and hyperparathyroidism screening was negative. Our MDT considered surgery for rapid visual pathways decompression, but a 2 week course of cabergoline lead to significant improvement of vision and visual fields, obviating the need for surgery. Continued cabergoline in escalating doses produced a steady reduction of prolactinemia and further visual improvement and a great reduction in tumour size. The evolution was complicated by an episode of pituitary apoplexy and transient hypocortisolism, managed conservatively. Gradual testosterone replacement led to induction of puberty, accompanied by a plateauing of prolactinemia to 33.5 ng/ml, despite escalation of cabergoline to 8 mg/week. Prolactinemia showe no response to added anastrozole, and then began rising slowly. Tumour control was maintained. Initial and follow-up echocardiograms were unremarkable.

Conclusion: Our case illustrates partial biochemical resistance to high-dose DA, despite excellent tumour response. Anastrozole did not improve the biochemical response. We are closely monitoring the patient, who continues to have an excellent clinical status.