Supplementary Material for: High-risk prostate cancer in a patient with untreated prolactinoma and castrate-level testosterone suppression: A case report

Introduction: Prolactinomas can induce castrate-level testosterone suppression by dysregulating the hypothalamic-pituitary-gonadal axis. While hypogonadism typically confers a reduced risk for prostate cancer (PCa), malignancy can still occur and may arise via non-classical pathways of carcinogenesis. Special consideration must be given when initiating treatment for patients with concurrent prolactinoma and PCa due to the complex hormonal interplay between prolactin and testosterone.

Case Presentation: A man in his 60s was diagnosed with localized high-risk PCa in the setting of castrate-level testosterone suppression mediated by an untreated prolactinoma. Following consistent treatment with a dopamine receptor agonist, testosterone levels normalized. PCa was managed with external beam radiotherapy and androgen deprivation therapy (ADT), initially with a gonadotropin-releasing hormone (GnRH) antagonist to avoid the flare phenomenon, and now with a GnRH agonist. Trends of prolactin, testosterone, and prostate-specific antigen (PSA) levels throughout his clinical course are illustrated alongside the case presentation.

Conclusion: Patients with prolactinoma-induced hypogonadism remain at risk for PCa. Dopamine agonists for treatment of prolactinoma may worsen PCa due to testosterone rebound; GnRH agonists for treatment of PCa may precipitate pituitary apoplexy (PA) in patients with preexisting pituitary adenoma. GnRH antagonists may be a theoretically safer alternative. Cautious and tailored selection of therapy alongside close clinical monitoring are essential to optimize care of this complex patient population.