<scp>d</scp>-Trp<sup>6</sup>-Luteinizing Hormone-Releasing Hormone Inhibits Sulpiride-Induced Hyperprolactinemia in Normal Men

Rubio, Miguel A.; Torres‐Alemán, Ignacio; Calle, José Ramón Caballero de la; Cabranes, José A.; Charro, Aniceto

doi:10.1210/jcem-65-2-368

Cited by 10 publications

(7 citation statements)

References 14 publications

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“…This finding might be explained by the possibility that dopaminergic drugs preferentially affect pure lactotropes, which in part constituted the adenoma. Although it has been recently shown that a GnRH agonist can reduce PRL secretion by a paracrine action (28), the observed decrease in serum PRL during buse¬ relin administration might be explained by an effect of the analogue on the cells co-secreting go¬ nadotropins and PRL.…”

Section: Discussionmentioning

confidence: 90%

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: Hormonal and immunocytochemical studies.

Ambrosi

Bassetti²,

Ferrario³

et al. 1990

Acta Endocrinologica

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The case of a 7-year-old boy affected with precocious puberty and a large intra-and suprasellar pituitary tumour is described. He had hyperprolactinemia and elevated serum LH, FSH and testosterone concentrations. Pre-operative dynamic hormonal studies showed a rise of PRL, LH and FSH levels after TRH (200 \g=m\giv) and a rise of LH and FSH after GnRH (100 \g=m\giv). Dopamine infusion (4 \g=m\g \ m=. \ kg\ m=-\ 1 \ m=. \min\m=-\1 for 180 min) did not affect gonadotropins and greatly reduced serum PRL. GnRH analogue (buserelin, 0.5 mg sc t.i.d. for 10 days) administration inhibited both LH and FSH, but did not affect PRL concentration. Serum LH and FSH increased after ethinyl-estradiol (0.5 mg orally) administration, and were not affected by bromocriptine (5-7.5 mg/day for 10 days), which decreased serum PRL levels. The patient underwent transfrontal neurosurgery and a large tumour mass was completely removed. Morphological study of the excised tumour, by electron microscope double label immunotechnique, revealed that a large number of tumour cells (70-85%) were positive for PRL, LH and FSH, co-localized in the same secretory granule. After neurosurgery, serum PRL, LH, FSH and testosterone levels fell to within the normal limits. Two months later the patient was well and signs of precocious puberty had partially regressed; hormone levels were in the normal range and MR imaging control did not demonstrate any residual lesion in the sellar region.True precocious puberty in boys is an uncommon disorder. When an organic cause is identifiable, the most common ones are hypothalamic lesions (craniopharyngioma, astrocytoma, hamartoma) or pineal tumours (1). Pituitary tumours rarely occur in childhood and adolescence and they are usually associated with delayed onset of puberty and hypogonadism (2): these features have been particu¬ larly described in young patients with prolactinomas (3) and in one girl with LH-and PRL-secreting pituitary tumour (4). So far, precocious pu¬ berty in patients with pituitary adenomas has been described, to our knowledge, in only two patients, one with a prolactinoma (5) and one with a LH-and PRL-producing tumour (6).In this paper we describe a 7-year-old boy with precocious puberty and a large pituitary tumour who had hyperprolactinemia and slightly elevated LH and FSH levels. Pre-and postoperative hor¬ monal investigations and morphological studies by electron microscope double-label immunotechnique on the excised tumour are reported.Case report A boy aged 7 years and 4 months was referred to our hospital for precocious puberty and the presence of a large intra-and suprasellar lesion at CT scan. On physical examination, his height was 115 cm (10th percentile) and his weight 26 kg (75th percentile). Neither gynecomastia nor galactorrhea was present. Isosexual advanced pu¬ berty was revealed by the presence of testes of 4-5 ml volume, penis of 9.5 cm length and pubic and axillary hairs; the Tanner stage was P2 G3. X-ray examination showed a bone age of 9 years. Visual field perimetries demonst...

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Section: Discussionmentioning

confidence: 90%

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: Hormonal and immunocytochemical studies.

Ambrosi

Bassetti²,

Ferrario³

et al. 1990

Acta Endocrinologica

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“…GnRH-A may also influence pituitary prolactin release directly. This has been shown by observations on spontaneous menstrual cycles, during which prolactin and gonadotropin levels increased spon taneously, and by observed increases in prolactin levels following exogenous GnRH stimulation [18,19], Other studies have also shown a link between GnRH-Ainduced pituitary desensitization and reduction in pro lactin levels [20][21][22], Since prolactin is thought to impair ovarian function [23], this effect of GnRH-A treatment might actually be beneficial for follicular maturation.…”

Section: Discussionmentioning

confidence: 89%

Induction of Pharmacological Hypogonadotropism Using Gonadotropin-Releasing Hormone Agonists in Patients Undergoing Controlled Ovarian Stimulation

Lindner

Braendle

Lichtenberg

et al. 1990

Gynecol Obstet Invest

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Pharmacological hypogonadotropism was induced in 167 women using the gonadotropin-releasing hormone agonists (GnRH-A) buserelin acetate or triptorelin acetate. 84 patients (group 1) began treatment using 1.2 mg/ day buserelin acetate intranasally during the follicular phase (days 1–3); 41 patients (group II) began the same treatment, supported by 10 mg medroxyprogesterone acetate for 10 days, during the early luteal phase; 42 patients (group 3) received triptorelin acetate as an intramuscular depot injection, supported by 10 mg medroxyprogesterone acetate for 10 days, during the early luteal phase. Serum luteinizing hormone, follicle-stimulating hormone, oestradiol (E₂), prolactin, and testosterone levels were monitored. Pituitary function was assessed by (1) measurement of endogenous luteinizing hormone fluctuation; (2) response to luteinizing hormone releasing hormone administration, and (3) response to oestradiol benzoate (E₂ test). Complete pituitary desensitization was only assumed, if all three tests were negative. The LH-RH test and the E₂ test were shown to be the most reliable indicator of pituitary function. E₂ administration led to further reduction of gonadotropin secretion after pituitary desensitization. The desensitization time was 41.1 ± 11.7 days in group 1 and was significantly reduced to 20.7 ± 10.5 days in group 2 (p < 0.01); a further, non-significant shortening to 15.1 ± 3.0 days was observed in group 3. Changes in endocrine parameters demonstrated hypogonadotropic hypo-oestrogenism after initial pituitary stimulation.

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“…The subsequent progressive rise of FSH levels, already seen by other authors (24), may suggest the occurrence of additional peripheral events, such as the decrease of inhibin production by GnRH analogs, similarly to what is observed in vitro with the native hormone (2 5), or the increased effect of activin (24). As to the marked suppression of PRL concentrations observed during treatment with the agonist, although this immediately reflects the decrease of sex hormones, a direct inhibitory effect of the LHRH agonist on PRL synthesis and secretion also has been proposed (26)(27)(28).…”

Section: Discussionmentioning

confidence: 93%

Long-term endocrine effects of administration of either a non-steroidal antiandrogen or a luteinizing hormone-releasing hormone agonist in men with prostate cancer

DeCensi¹,

Torrisi

Fontana

et al. 1993

Acta Endocrinologica

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The claimed ability of non-steroidal antiandrogens to preserve libido and sexual potency is sought as a potential improvement in the palliative management of prostate cancer. A critical issue for the clinical use of these compounds is, however, the reported evidence in the rat of an excessive increase in testosterone concentrations as a consequence of the androgen negative feedback interruption. On the other hand, the recovery of testicular function after long-term inhibition by luteinizing hormone-releasing hormone (LHRH) analogs is also an important concern in view of the proposed use of these compounds for the treatment of several non-malignant conditions. We addressed these issues by studying the long-term endocrine effects induced by the administration of either the non-steroidal antiandrogen nilutamide or the depot preparation of d-Trp6-LHRH in men with prostate cancer. Treatment with the antiandrogen induced a marked increase in gonadotropin levels, LH concentrations rising from a mean (sem) of 17.5±1.6 to a maximum of 56.6±6.9 kU/l (p<0.001), while mean testosterone and 17β estradiol-concentrations rose only by about 50% and 70% over pretreatment values, testosterone levels reaching a plateau after 1 month of treatment. In the subjects treated with the LHRH agonist, 6 months after discontinuation of long-term administration the mean (±sem) LH had risen to 36.9±6.8 IU/l while mean testosterone levels were still as low as 1.7±0.7 and rose only to a maximum of 4.2±1 nmol/l after high-dose human chorionic gonadotropin loadings. We conclude that in elderly men with prostate cancer: (i) stimulation of the entire axis by non-steroidal antiandrogens induces only a mild testosterone increase, the testis being the site of the reduced response; (ii) prolonged inhibition of the pituitary-gonadal axis induced by LHRH agonists may not be reversible at the testicular level.

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d-Trp⁶-Luteinizing Hormone-Releasing Hormone Inhibits Sulpiride-Induced Hyperprolactinemia in Normal Men

Cited by 10 publications

References 14 publications

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: Hormonal and immunocytochemical studies.

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: Hormonal and immunocytochemical studies.

Induction of Pharmacological Hypogonadotropism Using Gonadotropin-Releasing Hormone Agonists in Patients Undergoing Controlled Ovarian Stimulation

Long-term endocrine effects of administration of either a non-steroidal antiandrogen or a luteinizing hormone-releasing hormone agonist in men with prostate cancer

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d-Trp6-Luteinizing Hormone-Releasing Hormone Inhibits Sulpiride-Induced Hyperprolactinemia in Normal Men

Cited by 10 publications

References 14 publications

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: Hormonal and immunocytochemical studies.

Precocious puberty in a boy with a PRL-, LH- and FSH-secreting pituitary tumour: Hormonal and immunocytochemical studies.

Induction of Pharmacological Hypogonadotropism Using Gonadotropin-Releasing Hormone Agonists in Patients Undergoing Controlled Ovarian Stimulation

Long-term endocrine effects of administration of either a non-steroidal antiandrogen or a luteinizing hormone-releasing hormone agonist in men with prostate cancer

Contact Info

Product

Resources

About

d-Trp⁶-Luteinizing Hormone-Releasing Hormone Inhibits Sulpiride-Induced Hyperprolactinemia in Normal Men