Endocrine Abstracts

Introduction: Dopamine agonists are the first line treatment for prolactinomas. However, some patients may develop dopamine-agonist-resistant hyperprolactinemia, leading to surgery and/or radiotherapy. The persistence of hypogonadism requires testosterone replacement therapy which could theoretically reduce the efficacy of dopamine agonists due to the conversion of testosterone to estradiol, thus, in turn, increasing the resistance to dopamine agonists. Consequently, in these patients an anti-estrogen treatment has been advocated, but, to date, very few cases have been reported on the use of the anti-estrogen treatment in patients with prolactinomas.

Case report: We present the case of a 23-year-old man who presented with headache and visual impairment with bitemporal hemianopsia. Magnetic resonance imaging (MRI) of the pituitary revealed a large invasive intra- and supra-sellar pituitary adenoma. Prolactin levels were significantly elevated (3258 µg/l, normal values, nv: 5-25 µg/l), with low levels of booth testosterone (1.3 ng/ml, nv 2.4-9 ng/ml) and FT4 (0.82 pg/ml, nv 0.8-2.2 pg/ml). Treatment with cabergoline was initiated and gradually increased to 3 mg/week, with reduction in prolactin levels and improvement in visual field. After 12 months of therapy, the prolactin levels decreased to 352 mg/l, and due to the persistence of central hypothyroidism and hypogonadotropic hypogonadism, a replacement therapy with levothyroxine and testosterone was started. After starting testosterone treatment and obtaining low-normal testosterone levels, the prolactin levels increased to 551 mg/l. In addition, there was no significant reduction in the size of the pituitary lesion and the patient experienced more frequent headaches with a slight deterioration in visual field. Surgical intervention was then performed. Following surgery, the prolactin levels decreased to 88 mg/l and the MRI showed the persistence of an infra – and supra-sella adenoma remnant. However, in the subsequent years, despite continuing the treatment with cabergoline (3 mg/week), the prolactin levels gradually increased to 132 mg/l. Anastrozole 1 mg/daily was initiated, and, consequently, it was possible to reduce the cabergoline dose to 2 mg/week (by reducing the dose by 0.5 mg/week after 3 months and then by a further 0.5 mg/week after 12 months). A further decrease in prolactin levels to 55 μg/l and a shrinkage of the pituitary adenoma was then observed.

Conclusion: In cases of dopamine-agonist-resistant hyperprolactinemia, alternative treatment strategies may be required. In this case, the addition of anastrazole proved beneficial, resulting in improved hormonal control, tumor shrinkage, and better patient tolerability.