As in laboratory animals, long-term oestrogen treatment in the human male might induce prolactinomas. We here report on PRL levels in 142 male-to-female transsexuals, treated with 100 mg cyproterone acetate and 100 micrograms ethinyloestradiol per day for 6-108 months (median 52). PRL levels varied markedly between individuals. No relation with age and length of treatment period was found. In 42 subjects in whom PRL levels were followed serially, a slight fall was measured after 12-15 months of treatment. Galactorrhoea, present in 10 of 142 subjects, was unrelated to PRL levels. In 34 subjects in whom PRL levels were measured during treatment and 3 weeks after withdrawal, PRL levels fell significantly. Dopamine in doses of 0.1 microgram/kg/min and 1.0 microgram/kg/min was administered to six subjects with PRL levels greater than 1000 mU/l and six subjects with PRL levels less than 500 mU/l. No difference in the percentage decrease of PRL levels was found between these two groups. However, administration of monoiodotyrosine, an inhibitor of central dopamine synthesis, to these two groups, induced a significantly smaller release of PRL (expressed as percentage change) in subjects with PRL greater than 1000 mU/l than in those with PRL less than 500 mU/1 possibly indicating a loss of control of central dopaminergic regulation. These findings suggest that the risk of inducing prolactinomas through cross-gender hormone treatment is likely to be small.
The prolactin response to TRH in a group of patients with Kallmann's syndrome was found to be significantly lower compared to a group of hypergonadotrophic hypogonadal patients. Since levels of testicular products are comparably low in both groups, we hypothesize that high endogenous LHRH production might be associated with an increased prolactin response to TRH. In support of this, we were, indeed, able to establish a positive correlation between the magnitude of the prolactin response to TRH and basal and LHRH-stimulated LH/FSH levels (the latter serving as an index of endogenous LHRH production) in: (1) eugonadal men, (2) men with Kallmann's syndrome, (3) oestrogen-treated agonadal men, (4) men with severely impaired spermatogenesis and, (5) agonadal men. A direct relation between LHRH and the prolactin response to TRH was demonstrated in a group of eugonadal men, the prolactin response to TRH being greater after prolonged LHRH pretreatment. We speculate that an increase of endogenous or exogenous LHRH might be associated with decreased hypothalamic dopamine secretion which could directly increase prolactin synthesis. Indirectly, decreased dopamine secretion could augment the potency of TRH in releasing prolactin.
The present study investigated the effect of administration of somatostatin (SRIF) on the release of prolactin in men. No effect was observed when SRIF was administered to eugonadal men. Release of prolactin was inhibited, however, when SRIF was administered to oestrogen-treated agonadal subjects (male-to-female trans-sexuals) and to an even greater degree when subjects had been pretreated with a combination of oestrogen and cyproterone acetate. This is consistent with findings in the rat. Thus in man, as in the rat, SRIF can inhibit prolactin secretion, but only after treatment with oestrogen.
There is evidence that prolactin may be involved in testicular steroidogenesis, and we have therefore investigated whether there is feedback regulation of androgens/oestrogens on prolactin secretion in the human male. To assess this we have measured basal and TRH-stimulated prolactin levels in: Six eugonadal men before and after 2 weeks' administration of the aromatase inhibitor delta'-testolactone, which led to a fall in oestradiol levels with unchanged levels of testosterone. In these patients, prolactin levels decreased. Six eugonadal subjects before and after 6 weeks' administration of dihydrotestosterone undecanoate. In these subjects, prolactin levels decreased. Six agonadal subjects, tested after 12 weeks' treatment with dihydrotestosterone undecanoate and compared to: Six agonadal subjects who received no sex steroid treatment. Again, it was found that dihydrotestosterone treatment decreased prolactin levels in patients from Group C. Six eugonadal subjects were also studied before and after 6 weeks' administration of the androgen receptor antagonist, spironolactone, and this treatment increased Prl secretion. It is concluded that in the human male, endogenous oestrogens increase prolactin secretion whilst exogenous/endogenous androgens decrease prolactin secretion.
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