Pituitary apoplexy in cabergoline-resistant macroprolactinoma

Ozlem Kanburoglu Meletli; Cigdem Birinci; M. Cuneyt Bilginer; Hulya Coskun; Irfan Nuhoglu; Ozge Ucuncu; Mustafa Kocak

doi:10.1530/endoabs.90.EP758

Introduction: Pituitary apoplexy is a life-threatening clinical syndrome that develops as a result of bleeding or infarction in a pituitary adenoma. Here, we aimed to present a case of cabergoline-resistant macroprolactinoma who developed pituitary apoplexy.

Case Report: A 40-year-old male patient presented to neurology 2 years ago with severe headache. Brain magnetic resonance imaging (MRI) revealed a 15.5×18×21 mm macroadenoma in the pituitary gland that did not compress the optic chiasm. Visual field examination was normal. He had loss of libido and erectile dysfunction. Endocrinological evaluation (Table 1) showed hyperprolactinemia and hypogonadism. With the diagnosis of macroprolactinoma, cabergoline 0.5 mg/week was started and it was planned to increase the dose gradually. He was informed about the side effects of cabergoline and the findings of pituitary apoplexy. After 3 months of treatment, the adenoma size was the same, but his complaints decreased, prolactin and testosterone were normal. Thereupon, the dose of cabergoline was increased to 3 mg/week. In the pituitary MRI performed at the end of 1 year, it was observed that the size of the adenoma remained constant, but the clinical and laboratory well-being continued. Adenoma-reducing transsphenoidal surgery was recommended for cabergoline-resistant macroprolactinoma. However, the patient did not accept surgical treatment. Six months later, he presented with severe headache, nausea, vomiting, weakness and blurred vision. Prolactin, cortisol, and testosterone levels were low (Table 1). Pituitary MRI revealed an increase in size of the adenoma and compression on the optic chiasm. Pituitary apoplexy and hypopituitarism were considered. No underlying predisposing factor was detected except for cabergoline use. Steroid replacement was started, adenoma resection was performed by transsphenoidal surgery and histologically confirmed as lactotroph adenoma. Visual field examination was normal in the postoperative follow-up, but hypopituitarism persisted.

Table 1: Laboratory findings
Parameter		Result	Reference Range
	First diagnosis	18th month
Prolactin (μg/l)	>200	<0,25	2,64–13,13
Diluted prolactin (μg/l)	3652		2,64–13,13
Follicle Stimulating Hormone (IU/l)	2,21	3,38	1,27–19,26
Luteinizing Hormone (IU/l)	1,39	0,97	1,24–8,62
Total Testosterone (μg/l)	0,97	<0,1	1,98–6,79
Cortisol (μg/dl)	14,3	1,91
Adrenocorticotrophic Hormone (ng/l)	27,9	18,4	<46

Conclusion: Pituitary apoplexy due to the use of dopamine agonists in macroprolactinoma is a rare complication. Because of the high mortality and morbidity rate of pituitary apoplexy, it should be known that patients with macroprolactinoma should be followed closely while using dopamine agonists. It should be kept in mind that when pituitary apoplexy occurs, timely surgical decompression should be the best treatment option for patients.

Endocrine Abstracts

EP758