Inhibition by Somatostatin of LH-RH-Induced LH Release in Normal Menstruating Women

Chiodera, P.; Volpi, R.; d’Amato, L.; M, Fatone; Cigarini, C.; Favà, Alexandre; Caiazza, A.; Rossi, G. L.; Coiro, V.

doi:10.1159/000298884

Cited by 18 publications

(12 citation statements)

References 5 publications

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“…Although somatostatin analogues might affect LH secretion in premenopausal patients (Chiodera et al, 1986), in our postmenopausal patients no significant effects on plasma E2 levels were observed. This finding confirms the results of the study of Manni et al (1989) who also found no effect of combined octreotide/bromocriptine treatment on plasma LH, FSH and E2 levels.…”

Section: Anti-tumour Effectscontrasting

confidence: 69%

Feasibility, endocrine and anti-tumour effects of a triple endocrine therapy with tamoxifen, a somatostatin analogue and an antiprolactin in post-menopausal metastatic breast cancer: a randomized study with long-term follow-up

Bontenbal

Foekens²,

Lamberts³

et al. 1998

Br J Cancer

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Summary Suppression of the secretion of prolactin, growth hormone and insulin-like growth factor 1 (IGF-1) might be important in the growth regulation and treatment of breast cancer. Because oestrogens may counteract the anti-tumour effects of such treatment, the combination of an anti-oestrogen (tamoxifen), a somatostatin analogue (octreotide) and a potent anti-prolactin (CV 205-502) might be attractive. In this respect, we performed a first exploratory long-term study on the feasibility of combined treatment and possible clear differences in endocrine and anti-tumour effects during such combined treatment vs standard treatment with tamoxifen alone. Twenty-two post-menopausal patients with metastatic breast cancer (ER and/or PR positive or unknown) were randomized to receive either 40 mg of tamoxifen per day or the combination of 40 mg of tamoxifen plus 75 ig of CV 205-502 orally plus 3 x 0.2 mg of octreotide s.c. as first-line endocrine therapy. An objective response was found in 36% of the patients treated with tamoxifen alone and in 55% of the patients treated with combination therapy. Median time to progression was 33 weeks for patients treated with tamoxifen and 84 weeks for patients treated with combination therapy, but the numbers are too small for hard conclusions. There was no difference in overall post-relapse survival between the two treatment arms. With respect to the endocrine parameters, there was a significant decrease of plasma IGF-1 levels in both treatment arms, whereas during combined treatment plasma growth hormone tended to decrease and plasma prolactin levels were strongly suppressed; in some patients insulin and transforming growth factor a (TGF-a) decreased during the triple therapy. Although there was no significant difference in mean decrease of plasma IGF-1 levels between the two treatment arms, combined treatment resulted in a more uniform suppression of IGF-1. Therefore, the addition of a somatostatin analogue and an anti-prolactin may potentially enhance the efficacy of anti-oestrogens in the treatment of breast cancer owing to favourable endocrine and possible direct anti-tumour effects. Large phase IlIl trials using depot formulations (to increase the feasibility) of somatostatin analogues are warranted to demonstrate the potential extra beneficial anti-tumour effects of such combination therapy.

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Section: Anti-tumour Effectscontrasting

confidence: 69%

Feasibility, endocrine and anti-tumour effects of a triple endocrine therapy with tamoxifen, a somatostatin analogue and an antiprolactin in post-menopausal metastatic breast cancer: a randomized study with long-term follow-up

Bontenbal

Foekens²,

Lamberts³

et al. 1998

Br J Cancer

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“…Somatostatin is a 14-amino acid endogenous hypothalamic peptide with a short half-life that, besides blunting the LH response to gonadotropin-releasing hormone (GnRH) (110) and decreasing growth hormone (GH) pituitary secretion (111), inhibits pancreatic insulin release (112). Somatostatin analogs should therefore be potential drugs for the treatment of PCOS.…”

Section: New Potential Drug: Somatostatin Analogsmentioning

confidence: 99%

Insulin-sensitizing agents in polycystic ovary syndrome

Pasquali

Gambineri

2006

eur j endocrinol

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Insulin-sensitizing agents have been recently proposed as the therapy of choice for polycystic ovary syndrome (PCOS), since insulin resistance and associated hyperinsulinemia are recognized as important pathogenetic factors of the syndrome. Moreover, since almost all obese PCOS women and more than half of those of normal weight are insulin resistant, and therefore present some degree of hyperinsulinemia, the use of insulin sensitizers should be suggested in most patients with PCOS. Insulin sensitizer treatment has been associated with a reduction in serum androgen levels and gonadotropins, and with an improvement in serum lipids and in prothrombotic factor plasminogenactivator inhibitor type 1, whatever the insulin sensitizer used. This therapy has also been associated with a decrease in hirsutism and acne, and with a regulation of menses and an improvement of ovulation and fertility. Notable improvements in all these parameters have also been described after a change in lifestyle approach, particularly in the presence of obesity. Lifestyle interventions should therefore be combined with insulin sensitizers in PCOS when obesity is present.

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“…In our study, PCOS women had much lower SS levels than the control, a significantly negative correlation be tween basal LH and SS existed in group 1. It was found that SS could induce a significant decrease in LH ampli tude by directly or indirectly lowering the sensitivity of gonadotrophs to gonadotropin-releasing hormone [2], An SS analogue, octreotide, was reported to suppress LH and ovarian androgen secretion in PCOS and to result in a more 'appropriate' hormonal milieu [6], These observa tions support that insufficient endogenous SS may be responsible for elevated LH levels in PCOS women, espe cially of group 1. Furthermore, a reduced Ei level not only causes a reduced negative feedback on LH release by the pituitary, but also results in an impaired opioid-mediated inhibitory control on GnRH by the hypothalamus [7], Increased gonadotropin secretion by opioid antagonism was expected in normal women but not found in PCOS women.…”

Section: Discussionmentioning

confidence: 99%

Responses of Somatostatin, Beta-Endorphin and Dynorphin A to a Glucose Load in Two Groups of Women with Polycystic Ovarian Syndrome

Wang

1996

Horm Res

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To investigate the relationship between elevated LH, hyperinsulinemia and neuropeptides in polycystic ovarian syndrome (PCOS), we measured the endogenous levels of insulin, somatostatin (SS), β-endorphin (β-EP) and dynorphin A (Dyn A) before and after a glucose load in three groups: group 1 (LH/ FSH ≥ 3, n = 30); group 2 (LH/FSH < 3, n = 25), and controls (n = 15). In the basal state, significantly negative correlations were found between LH and SS (r = -0.51, p < 0.05) in group 1 and between LH and β-EP (r = -0.49, p < 0.05) in group 2. After a glucose load, PCOS women had greater β-EP and Dyn A responses in group 1 and impaired SS response in group 2 as compared with the control. The data suggest endogenously lower SS, higher β-EP and Dyn A may contribute to the elevation of LH and insulin secretions in PCOS.

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Inhibition by Somatostatin of LH-RH-Induced LH Release in Normal Menstruating Women

Cited by 18 publications

References 5 publications

Feasibility, endocrine and anti-tumour effects of a triple endocrine therapy with tamoxifen, a somatostatin analogue and an antiprolactin in post-menopausal metastatic breast cancer: a randomized study with long-term follow-up

Feasibility, endocrine and anti-tumour effects of a triple endocrine therapy with tamoxifen, a somatostatin analogue and an antiprolactin in post-menopausal metastatic breast cancer: a randomized study with long-term follow-up

Insulin-sensitizing agents in polycystic ovary syndrome

Responses of Somatostatin, Beta-Endorphin and Dynorphin A to a Glucose Load in Two Groups of Women with Polycystic Ovarian Syndrome

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