Treatment of Hirsutism with a Gonadotropin-Releasing Hormone Agonist (Nafarelin)∗

Andreyko, Janice L.; Monroe, Scott M.; Jaffe, Robert B.

doi:10.1210/jcem-63-4-854

Cited by 82 publications

(20 citation statements)

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“…As expected [25][26][27], both treatments decreased the free-testosterone levels by about 50% after 48 weeks of treatment, while DHEAS concentrations were virtually unchanged. LH and FSH were reduced by both treat ments, but to a greater extent in the goserelin + OC group.…”

Section: Discussionsupporting

confidence: 80%

An Open Randomized Comparative Study of an Oral Contraceptive Containing Ethinyl Estradiol and Cyproterone Acetate with and without the GnRH Analogue Goserelin in the Long-Term Treatment of Hirsutism

Vegetti

Testa

Maggioni

et al. 1996

Gynecol Obstet Invest

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A multicenter randomized study was carried out to compare the efficacy of combined therapy with a GnRH analog (goserelin) + an oral contraceptive (OC) containing ethinyl estradiol and cyproterone acetate and the same OC alone in the treatment of severe hirsutism. The effect of these two therapies was assessed in a subjective and an objective evaluation of hair growth. According to the subjective evaluation, judged by physician and patient, 95% of patients obtained a partial response. The objective response was assessed by measuring the mean diameter of hair from 3 different areas and 1 control area. The decrease in hair diameter compared to pretreatment was statistically significant for both treatments, mainly for the abdomen and face. The difference between the two groups did not reach statistical significance. Therefore, we assume that OC alone remains the treatment of choice for hirsutism. However, the addition of the GnRH analog to OC needs further investigation and could be justified for patients with no response to standard monotherapy.

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Section: Discussionsupporting

confidence: 80%

An Open Randomized Comparative Study of an Oral Contraceptive Containing Ethinyl Estradiol and Cyproterone Acetate with and without the GnRH Analogue Goserelin in the Long-Term Treatment of Hirsutism

Vegetti

Testa

Maggioni

et al. 1996

Gynecol Obstet Invest

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“…Though studies employing suppressive doses of GnRH agonists (25)(26)(27)(28) point to the ovary as the predominant source of androgen excess in PCOS, the time course of androgen suppression has not previously been examined. In most studies, T was not measured until 1 month after commencing therapy, by which time, mean levels had fallen by 48 -77% (25)(26)(27)(28). In the present study, T levels decreased by 20% as early as 4 h after administration of the GnRH antagonist, falling into the normal range at 8 h. In the PCOS patients treated with the GnRH antagonist for 7 days, no further inhibition of T was observed.…”

Section: Discussionmentioning

confidence: 99%

“…The degree of T suppression was similar in normal and PCOS subjects. The failure of T levels, in either normal or PCOS women, to suppress to the range of oophorectomized women observed with prolonged GnRH agonist therapy (25)(26)(27)(28) may reflect the shorter duration of antagonist administration. Alternatively, it may be that the Nal-Glu GnRH antagonist used in this study is a less potent suppressor of ovarian synthesis/secretion than its agonist counterparts.…”

Section: Discussionmentioning

confidence: 99%

“…Though previous studies using long-acting GnRH agonists have indicated a predominantly ovarian source of androgen excess in PCOS (25)(26)(27)(28), no data is available on the time course over which androgen suppression occurs. In this study, we used complete GnRH receptor blockade to examine the impact of acute and short-term decreases in LH on gonadal steroid secretion in PCOS.…”

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confidence: 99%

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Use of a Gonadotropin-Releasing Hormone Antagonist as a Physiologic Probe in Polycystic Ovary Syndrome: Assessment of Neuroendocrine and Androgen Dynamics¹

Hayes

Taylor

Hall

1998

The Journal of Clinical Endocrinology & Metabolism

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The majority of patients with polycystic ovary syndrome (PCOS) exhibit an increase in both the frequency and amplitude of LH secretion, which is thought to contribute to the hyperandrogenism associated with this disorder. The increase in LH pulse amplitude may reflect either enhanced pituitary sensitivity to GnRH and/or an increase in hypothalamic GnRH secretion. To determine whether endogenous GnRH secretion is increased in PCOS and to document the degree and time course of androgen suppression after acute LH inhibition, the Nal-Glu GnRH antagonist was administered sc at 4 doses (5, 15, 50, and 150 g/kg) to 11 women with PCOS. The response to GnRH receptor blockade was compared with data from regularly cycling women (n ϭ 50) studied in the early and late follicular, and early luteal phases. The response to more prolonged GnRH receptor blockade was determined in a subset of patients, in whom 150 g/kg of the GnRH antagonist was administered sc every 24 h for 3 days (n ϭ 7) and continued for 7 days in 3 subjects.LH levels decreased in a dose-dependent fashion after administration of the GnRH antagonist (P Ͻ 0.0001), with a maximum percent inhibition of 83 Ϯ 2%. At all except the 5 g/kg dose, mean LH levels remained significantly lower than baseline for up to 20 h post antagonist (P Ͻ 0.002). At all antagonist doses, both the degree and duration of LH suppression were similar in PCOS and normal women. The maximum percent inhibition of FSH was 39 Ϯ 2%, which was significantly less than that of LH (P Ͻ 0.001). Testosterone (T) levels fell significantly within 4 h of antagonist administration, with maximum percent inhibition of 39 Ϯ 3% occurring at 8 h. In the patients in whom 150 g/kg of the antagonist was given for 3-7 days, no further suppression of either gonadotropins or T was noted.Our conclusions were: 1) The equivalent susceptibility of LH to submaximal GnRH receptor blockade in normal and PCOS women suggests that the elevated LH levels in PCOS are not the result of an increase in the quantity of GnRH secreted. These data imply that it is the frequency of GnRH stimulation per se and/or enhanced pituitary sensitivity to endogenous GnRH that underlie the gonadotropin abnormalities in PCOS; and 2) The rapid suppression of T with increasing GnRH antagonist dose is consistent with acute regulation of T secretion by LH. (J Clin Endocrinol Metab 83: 2343-2349, 1998 W HILE polycystic ovary syndrome (PCOS) is a heterogeneous disorder for which several pathogenic mechanisms have been proposed (1-4), abnormal gonadotropin secretion is a dominant feature in a large subgroup. Such patients are characterized by increased serum levels of LH in association with normal or low levels of FSH, resulting in an elevated LH/FSH ratio (5-10).The relative contributions of the pituitary and hypothalamus to the abnormal gonadotropin secretory dynamics in PCOS have been difficult to quantify. The increase in LH pulse amplitude characteristic of PCOS (6,7,9,(11)(12)(13)(14) may represent either enhanced pituitary sensitivity or in...

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“…1], These properties of GnRH agonists have led to several clinical applications in gynecolo gy, pediatric endocrinology and andrology. GnRH agonist therapy has been used to treat hirsutism [2], polycystic ovarian disease [3], uterine fibroids [4], breast cancer [5], pre cocious puberty [6,7] and endometriosis [8,9], Clinical studies in which FSH and LH concentrations were measured during GnRH agonist therapy have shown that an acute rise in serum gonadotropin occurs within days after the administration of the drug. This initial rise is followed by a de crease of gonadotropins to baseline values (4-8 mlU/ml) and a concomitant decrease of estradiol to levels usually below 50 pg/ml.…”

Section: Introductionmentioning

confidence: 99%

Absence of Immunoreactive Luteinizing Hormone following Gonadotropin-Releasing Hormone Agonist Therapy in Women with Endometriosis

Bischof

Herrmann

1988

Gynecol Obstet Invest

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Pituitary desensitization following infusion of gonadotropin-releasing hormone (GnRH) is measurable if bioactivity instead of immunoreactivity is considered. We hypothesized that GnRH agonist therapy induces the same kind of desensitization, but that radioimmunoassays (RIA) for gonadotropins based on polyclonal antibodies cannot show this effect because they recognize inactive fragments of gondadotropins. To test this hypothesis we measured luteinizing hormone (LH) with two different assays: one RIA was based on a polyclonal rabbit anti-hLH, while the other one was an immunoradiometric assay (IRMA) based on 2 different mouse monoclonal anti-hLH. LH measurements were performed on plasma samples obtained from 13 women with laparoscopically proven endometriosis and treated with microcapsules of the GnRH agonist D-Trp6-GnRH (Ferring) once a month. The correlation between LH measurements with both assays in 36 control plasma samples and in another 13 samples obtained before treatment in women with endometriosis was excellent (r = 0.959). In contrast, in women treated with GnRH agonist, the RIA yielded values ranging from undetectable to 12 mIU/ml, whereas 60 out of 66 values were undetectable with the IRMA. We conclude that the monoclonal anti-hLH antibodies in the IRMA either recognize an epitope close to the active site and/or do not recognize the biologically inactive LH fragments which are known to be produced during GnRH agonist therapy. Thus, monoclonal-antibody-based IRMA provide a new and interesting clinical tool to follow the effects of therapies which desensitize the gonadotropic function of the pituitary.

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Treatment of Hirsutism with a Gonadotropin-Releasing Hormone Agonist (Nafarelin)∗

Cited by 82 publications

References 0 publications

An Open Randomized Comparative Study of an Oral Contraceptive Containing Ethinyl Estradiol and Cyproterone Acetate with and without the GnRH Analogue Goserelin in the Long-Term Treatment of Hirsutism

An Open Randomized Comparative Study of an Oral Contraceptive Containing Ethinyl Estradiol and Cyproterone Acetate with and without the GnRH Analogue Goserelin in the Long-Term Treatment of Hirsutism

Use of a Gonadotropin-Releasing Hormone Antagonist as a Physiologic Probe in Polycystic Ovary Syndrome: Assessment of Neuroendocrine and Androgen Dynamics¹

Absence of Immunoreactive Luteinizing Hormone following Gonadotropin-Releasing Hormone Agonist Therapy in Women with Endometriosis

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Treatment of Hirsutism with a Gonadotropin-Releasing Hormone Agonist (Nafarelin)∗

Cited by 82 publications

References 0 publications

An Open Randomized Comparative Study of an Oral Contraceptive Containing Ethinyl Estradiol and Cyproterone Acetate with and without the GnRH Analogue Goserelin in the Long-Term Treatment of Hirsutism

An Open Randomized Comparative Study of an Oral Contraceptive Containing Ethinyl Estradiol and Cyproterone Acetate with and without the GnRH Analogue Goserelin in the Long-Term Treatment of Hirsutism

Use of a Gonadotropin-Releasing Hormone Antagonist as a Physiologic Probe in Polycystic Ovary Syndrome: Assessment of Neuroendocrine and Androgen Dynamics1

Absence of Immunoreactive Luteinizing Hormone following Gonadotropin-Releasing Hormone Agonist Therapy in Women with Endometriosis

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Use of a Gonadotropin-Releasing Hormone Antagonist as a Physiologic Probe in Polycystic Ovary Syndrome: Assessment of Neuroendocrine and Androgen Dynamics¹