Serum gonadotrophin pulsatile secretion in men with Prl-secreting and non-secreting pituitary tumours

Abstract

In order to investigate the possible influence of prolactin (Prl) at the hypothalamic level, serum LH and FSH pulsatility was studied in 16 male patients with prolactinomas, normally LH responders to GnRH (group A): 8 of them were untreated (group A1) and 8 had undergone previous unsuccessful pituitary treatments (group A2). In 7 patients the study was repeated when serum Prl was normalized by bromocriptine treatment (group B). For comparison the secretory pattern of LH and FSH was studied in 6 male patients with non\x=req-\ secreting pituitary tumours (group C). All parameters of LH pulsatile secretion (i.e. arithmetic mean of the single concentration, coefficient of variation from the mean value, frequency of peaks, amplitude of pulses expressed as either absolute or per cent value) were significantly lower in patients of groups A1, A2 and C than in normal subjects and no difference was found between the three groups. Furthermore the 7 patients with prolactinomas studied both before and after bromocriptine-induced Prl normalization showed no difference in all the parameters of LH pulsatility in both conditions. No significant abnormalities of FSH secretory pattern were found in the patients of groups A1, A2, B and C in comparison to normal subjects. In all groups of patients mean serum testosterone basal levels were significantly lower than in normals, while the mean oestradiol-17\g=b\ basal concentration was normal. The abnormalities in LH pulsatility found in untreated and bromocriptine-treated patients with prolactinomas and in patients with non-secreting tumours indicate an impairment of GnRH release in such patients; these findings suggest that Prl excess is not the only cause of the abnormalities in LH pulsatile secretion.

Impaired estrogen‐induced negative feedback on gonadotropin secretion in patients with gonadotropin‐secreting and nonfunctioning pituitary adenomas

“…In particular, ERβ mRNA and its variant missing exon 2 were found more frequently than ERα in NFPA and in Gn-omas [23]. In particular, reduced frequency and amplitude of gonadotropin peaks were observed in patients with untreated prolactinoma and NFPA, suggesting that GnRH deficiency may be at least in part secondary to anatomical or functional impairment of the hypothalamic-pituitary axis due to the tumoral mass per se [24]. Other possible mechanisms may be either an altered pituitary sensitivity to GnRH or a defective GnRH supply from the hypothalamus, both events preventing the estrogeninduced negative feedback on gonadotropin secretion.…”

“…Several studies indicate that almost all pituitary tumors express both ERα and ERβ, although the amounts of receptor isoforms and specific splice variants were found to be highly variable in the different tumor types [22]. Similarly, the spontaneous pulsatility of gonadotropins that reflects endogenous GnRH episodic release has been investigated in a small series of patients with pituitary tumors [24,25]. As these two receptor subtypes mediate different biological responses to estrogen receptor modulators, it is likely that the differential pattern of ER expression may influence the biological properties of these tumors, including the responsiveness to estrogen and antiestrogen agents [22].…”

“…Although all patients with Gn-omas in the present series showed a normal LH and FSH increase after GnRH administration, the test was performed with the maximally effective GnRH dose which is unable to discriminate subtle differences in gonadotroph sensitivity. Similarly, the spontaneous pulsatility of gonadotropins that reflects endogenous GnRH episodic release has been investigated in a small series of patients with pituitary tumors [24,25]. In particular, reduced frequency and amplitude of gonadotropin peaks were observed in patients with untreated prolactinoma and NFPA, suggesting that GnRH deficiency may be at least in part secondary to anatomical or functional impairment of the hypothalamic-pituitary axis due to the tumoral mass per se [24].…”

“…Similarly, the spontaneous pulsatility of gonadotropins that reflects endogenous GnRH episodic release has been investigated in a small series of patients with pituitary tumors [24,25]. In particular, reduced frequency and amplitude of gonadotropin peaks were observed in patients with untreated prolactinoma and NFPA, suggesting that GnRH deficiency may be at least in part secondary to anatomical or functional impairment of the hypothalamic-pituitary axis due to the tumoral mass per se [24]. Moreover, defective GnRH supply, together with gonadotroph cell loss, may be responsible for the low serum FSH and LH levels frequently observed in postmenopausal patients with NFPA [26].…”

Hypogonadism of male prolactinomas: Relation to pulsatile secretion of LH: Hypogonadisms des Mannes mit Prolaktinomen: Beziehungen zur pulsatilen LH-Sekretion

“…In most of them, LH pulsatility was absent or infrequent in the hyperprolactinemic patients, but LH pulsatility was recovered after transspenoidal operation (Koizumi et al, 1984) or bromocriptine (CB) treatment (Bohnet et al, 1975;Moult et al, 1982). On the other hand, there are rare reports of LH pulsatility in male prolactinoma (Ambrosi et al, 1985). Ambrosi et al (1985) described that the patients with prolactinoma showed significantly infrequent pulsation of LH compared with normal men.…”