Pituitary—Testicular Function of Prostatic Cancer Patients During Treatment with a Gonadotropin‐Releasing Hormone Agonist Analog I. Circulating Hormone Levels

Abstract

Eight patients with advanced prostatic carcinoma (ages 59 to 78 years) were treated with a potent gonadotropin-releasing hormone (GnRH) agonist analog (buserelin, Hoechst; 600 micrograms intranasally, 3 times daily) and orchiectomized after 6 months of treatment. Endocrine responses were followed by serum hormone measurements during agonist treatment and for 3 months after orchiectomy. Six other patients (65 to 86 years) with advanced prostatic cancer had been orchiectomized as the first therapeutic measure and their blood samples were used as controls. In the GnRH agonist-treated patients, serum immunoreactive luteinizing hormone (LH) and follicle stimulating hormone (FSH) decreased after initial stimulation by 70 to 80%, within 1 to 3 weeks (P less than 0.01). FSH partly recovered (P less than 0.05) after the first month of treatment. Serum prolactin (PRL) displayed a slight tendency to decline during buserelin treatment (P less than 0.05). Serum total and free testosterone (T) of the buserelin-treated patients decreased to the castrate range within 3 to 4 weeks after an initial 5-day increase (P less than 0.01). Serum progesterone and 17-hydroxyprogesterone (17-OHP-4) decreased to the castrate range (by 50 to 70%) in 1 week. Only minor changes were observed in sex hormone binding globulin (SHBG). Significant, acute elevations of LH, FSH, T, and 17-OHP-4 were observed only on day 1 after an injection of buserelin (500 microgram i.m.) and not when assessed between day 7 and month 6 of treatment. After 6 months of buserelin treatment, orchiectomy did not affect the serum steroids measured. After orchiectomy, immediate increases in serum LH, and somewhat later in FSH, were seen in the control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Intratesticular Testosterone Concentrations Comparable With Serum Levels Are Not Sufficient to Maintain Normal Sperm Production in Men Receiving a Hormonal Contraceptive Regimen

“…Treatment for 6 months with TE plus LNG suppressed ITT by 98% to levels that approximate normal serum T in normal young men (Figure 1). This degree of ITT suppression is similar to that seen in previous studies of gonadotropin withdrawal either through exogenous T administration (Morse et al, 1973) or through gonadotropin releasing hormone agonist treatment in prostate cancer patients (Huhtaniemi et al, 1987). Intratesticular T concentrations approximating normal serum T levels were coincident, with a dramatic decrease in sperm count from a mean of 65 to 1.3 million/mL.…”

“…Withdrawal of LH and FSH stimulation of the testis reduces sperm production. Suppression of LH levels results in a decrease in ITT (Morse et al, 1973; Huhtaniemi et al, 1987), which in turn suppresses sperm production in men (World Health Organization [WHO], 1990) and rats (Zirkin et al, 1989). ITT is believed to stimulate spermatogenesis directly in rats (Zirkin et al, 1989) and men (Matsumoto and Bremner, 1985) although not to quantitatively normal levels in men.…”

Effects of Benzo(a)pyrene on Intra-testicular Function in F-344 Rats

“…Withdrawal of LH and FSH stimulation of the testis reduces sperm production. Suppression of LH levels results in a decrease in ITT [19, 20], which in turn suppresses sperm production in men (World Health Organization; WHO, [21]) and rats [22]. Intratesticular testosterone is believed to stimulate spermatogenesis directly in rats [22] and men [17] although not to quantitatively normal levels in men.…”

Update on Male Hormonal Contraception: Is the Vasectomy in Jeopardy?

“…12,13 It is clear that in normal sperm-producing men, intratesticular testosterone levels are 100-fold higher than in serum. [14][15][16][17][18] Interestingly, LH-receptor-deficient mice can support some level of spermatogenesis, but use of an androgen receptor antagonist such as flutamide will suppress spermatogenesis completely. [19][20][21] The role of dihydrotestosterone, a potent metabolite of testosterone, in spermatogenesis appears to be less clear.…”