Prolactin and prostate: an observational case-control study in men with prolactinoma under cabergoline treatment

Prolactin (PRL) exerts independent hypertrophic effects on prostate in in vivo and in vitro experimental models, and prostatic PRL receptors are known to activate cell proliferation pathways such as MAPK and STAT. Nevertheless, in men with hyperprolactinemia the risk of prostate cancer has been found reduced suggesting a role of concomitant hypogonadism. Chronic cabergoline treatment generally normalizes PRL treatment and improves gonadal function. The current study aimed at investigating prostate morphology in patients with prolactinoma under cabergoline treatment as compared to healthy control subjects. Twenty men with prolactinoma on chronic cabergoline treatment (CAB, 6–12 months, median dose 0.5 mg/week), including 6 (30%) on testosterone replacement therapy (TR, 6 months, median dose 30 mg/day) and 20 healthy age-matched controls entered the study. In patients and controls, hormonal levels (PRL, FSH, LH, testosterone) were evaluated and transrectal prostate ultrasound was performed. In patients, LH (P=0.04) and testosterone (P=0.026) levels were significantly lower than in controls, with no significant difference in PRL levels. Prostate volume was slightly but not significantly lower in patients than in controls. Prevalence of normal prostate morphology was significantly higher (P=0.05) in controls as compared to patients, whereas ultrasound signs of prostatitis resulted significantly more frequent in patients (P=0.027) as compared to controls. Prevalence of prostate adenoma and carcinoma was similar in patients and controls, with two cases being recorded in each group. PRL levels (r=−0.44, P=0.05), but not testosterone levels and CAB or TR dose, significantly and inversely correlated with prostate volume. In conclusion, in men with prolactinoma on chronic CAB treatment the risk of prostate hypertrophy is lower compared to healthy subjects, whereas prostatitis is more prevalent in patients than in controls. Concomitant testosterone deficiency, together with the known action of PRL as regulator of inflammation and autoimmune pathology, might represent potential mechanisms responsible for these findings. Further studies are required to better elucidate the burden and the role of PRL, hypogonadism, CAB and TR on prostate morphology in prolactinomas.