Prolactin normally stimulates cell growth in the prostate gland (probably through direct as well as through androgen-mediated mechanisms), although it is unclear what impact hyperprolactinemia may have on the prostate gland in humans. In animal studies high prolactin results in prostate gland inflammation and abnormal cell growth (Reiter et al. 1999). In men benign prostatic hypertrophy is associated with increased prolactin in some but not all studies (Saroff et al. 1980). Prolactin levels normally increase with age, potentially confounding the results of these studies. Prolactin levels may be increased in men with prostate cancer, but the prostate itself may produce prolactin, making cause and effect difficult to determine (Goffin et al. 2002; Harper et al. 1976). One case-control study found no increased risk of prostate cancer in antipsychotic-treated patients (Mortensen 1992), but there are no studies of risk of prostate cancer in patients with sustained antipsychotic-induced hyper-prolactinemia.
Prolactin inhibits hypothalamic release of gonadotropin-releasing hormone (GRH), which in turn stimulates the pituitary to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH), both of which regulate testicular function, including normal production of testosterone, and spermatogenesis. In other disease states, high prolactin levels are associated with decreased testosterone and decreased sperm production (Winters and Troen 1984). However, usual doses of antipsychotics do not appear to be associated with changes in LH, FSH, or testosterone in men with schizophrenia (Kaneda and Fujii 2000; Markianos et al. 1999; Siris et al. 1980; Smith et al. 2002), although in one study very high doses of haloperidol (30-60 mg/day) were associated with low testosterone levels (Rinieris et al. 1989). Because men are less sensitive to the prolactin-elevat-ing effects of antipsychotic medications, there may be a risk for hypogo-nadism only with higher doses of prolactin-elevating antipsychotics. Longitudinal, prospective studies are needed before the impact of prolactin-elevating antipsychotics on the hypothalamic-pituitary-gonadal axis in men is understood.
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