Androgen suppressive effect of GnRH agonist in ovarian hyperthecosis and virilizing turnours*

Pascale, Marco Maria; Pugeat, Michel; Roberts, Melissa L.; Rousset, H; Déchaud, H.; Dutrieux-Berger, N; Tourniaire, J

doi:10.1111/j.1365-2265.1994.tb01820.x

Cited by 109 publications

(31 citation statements)

References 26 publications

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“…On the other hand, DHEAS may be decreased in the case of sulphatase enzyme defect and in adrenocortical cancer. In ovarian tumours, raised testosterone may be LH-dependent and in some cases can be suppressed by treatment with gonadotrophin-releasing hormone (GNRH) agonist, oestrogen-progestogen or cyproterone acetate (CPA) (70). However, it should be noted that hyperthecosis and ovarian androgen-secreting tumours are both LH-dependent and therefore should be further explored by complementary imaging (71).…”

Section: Laboratory and Biomarkersmentioning

confidence: 99%

The polycystic ovary syndrome: a position statement from the European Society of Endocrinology

Conway¹,

Dewailly²,

Diamanti-Kandarakis³

et al. 2014

European Journal of Endocrinology

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567

492

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Polycystic ovary syndrome (PCOS) is the most common ovarian disorder associated with androgen excess in women, which justifies the growing interest of endocrinologists. Great efforts have been made in the last 2 decades to define the syndrome. The presence of three different definitions for the diagnosis of PCOS reflects the phenotypic heterogeneity of the syndrome. Major criteria are required for the diagnosis, which in turn identifies different phenotypes according to the combination of different criteria. In addition, the relevant impact of metabolic issues, specifically insulin resistance and obesity, on the pathogenesis of PCOS, and the susceptibility to develop earlier than expected glucose intolerance states, including type 2 diabetes, has supported the notion that these aspects should be considered when defining the PCOS phenotype and planning potential therapeutic strategies in an affected subject. This paper offers a critical endocrine and European perspective on the debate on the definition of PCOS and summarises all major aspects related to aetiological factors, including early life events, potentially involved in the development of the disorder. Diagnostic tools of PCOS are also discussed, with emphasis on the laboratory evaluation of androgens and other potential biomarkers of ovarian and metabolic dysfunctions. We have also paid specific attention to the role of obesity, sleep disorders and neuropsychological aspects of PCOS and on the relevant pathogenetic aspects of cardiovascular risk factors. In addition, we have discussed how to target treatment choices based according to the phenotype and individual patient's needs. Finally, we have suggested potential areas of translational and clinical research for the future with specific emphasis on hormonal and metabolic aspects of PCOS.

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Section: Laboratory and Biomarkersmentioning

confidence: 99%

The polycystic ovary syndrome: a position statement from the European Society of Endocrinology

Conway¹,

Dewailly²,

Diamanti-Kandarakis³

et al. 2014

European Journal of Endocrinology

Self Cite

567

492

View full text Add to dashboard Cite

show abstract

“…The performance of a 2-to 5-day low-dose dexamethasone suppression test has been suggested, but this approach has not been studied for hyperandrogenism in postmenopausal women (20). Finally, there are small and contradictory results concerning the discriminatory effect of gonadotropin suppression in the evaluation of postmenopausal hyperandrogenism (12,21). Immunohistochemical analysis is not directly involved in discriminating tumor lesions from nontumor pathology but has already been used to elucidate the mechanism of an ovarian tumoral hyperandrogenism (22).…”

Section: Introductionmentioning

confidence: 99%

Impact of clinical, hormonal, radiological, and immunohistochemical studies on the diagnosis of postmenopausal hyperandrogenism

Sarfati

Bachelot

Coussieu

et al. 2011

European Journal of Endocrinology

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Objective: Evaluation of postmenopausal women with suspicion of androgen-secreting tumor. Design and patients: We retrospectively studied 22 postmenopausal women referred to our center for suspicion of androgen-secreting tumor. All patients had clinical, biological, and morphological evaluation. In absence of adrenal tumors, ovarian surgery was most often proposed and immunohistochemistry (IHC) studies were performed. Results: Ovarian tumors were detected by ultrasound and/or magnetic resonance imaging in eight patients. Two adrenal androgen-secreting tumors were diagnosed by an adrenal computed tomography (CT) scan. The clinical presentation of the women with or without tumors was similar. Nevertheless, women with tumor exhibited significantly higher testosterone levels and lower basal FSH and LH levels than the other women (2.6G2.7 vs 0.9G0.9 ng/ml, P!0.05; 26.5G22.9 vs 66.5G 26.0 IU/l, P!0.01; and 12.0G8.6 vs 24.1G8.9 IU/l, P!0.05 respectively). Based on a likelihood ratio test, patients with a tumor had 8.4 and 10.8 times higher risk of having a testosterone level R1.4 ng/ml or an FSH level %35 IU/l. Finally, IHC analysis with an anti-P450c17a antibody allowed the identification of an elevated number of ovarian androgen-producing cells in five patients in whom no tumor was found. Conclusions: Androgen-secreting tumors are clinically difficult to discriminate from other causes of postmenopausal hyperandrogenism. Testosterone and FSH were the two discriminative markers in a multivariate analysis. Ovarian and adrenal tumors were detected by imaging studies. However, ovarian non-tumoral causes of hyperandrogenism may be difficult to detect with conventional histology.

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“…Gonadotropin has been known to suppress androgen secretion by ovarian virilizing tumor. Pascal et al13 suggested that various ovarian androgen-secreting tumors, as well as hyperthecosis, were not autonomous but apparently depended upon continuous gonadotropin stimulation. Imai et al14 also noted a direct suppressive effect of GnRHa on ovarian steroidogenesis.…”

Section: Discussionmentioning

confidence: 99%

A Case of Ovarian Steroid Cell Tumor, Not Otherwise Specified, Treated with Surgery and Gonadotropin Releasing Hormone Agonist

Chung

Lee

2014

J Menopausal Med

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Steroid cell tumors account for less than 0.1% of all ovarian tumors. There are three steroid cell tumor subtypes: steroid cell tumor not otherwise specified (NOS), stromal luteoma and Leydig cell tumor. Steroid cell tumor, NOS, is the most common type and has malignant potential. This report describes a case of an ovarian steroid cell tumor, NOS. A 35-year-old woman visited hospital with the complaint of metrorrhagia. Physical examination revealed increased pubic hair. Transvaginal ultrasound indentified a 4.9 × 3.4 cm, well-circumscribed and solid left ovarian tumor. After laparoscopic left oophorectomy, the tumor was revealed as an ovarian steroid cell tumor, NOS. During the laparoscopic surgery, tumor ruptured. Complete surgical staging was performed and no evidence of metastasis was found. Gonadotropin releasing hormone agonist was administered monthly for 6 months. The patient has had no evidence of recurrence for 43 months.

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Androgen suppressive effect of GnRH agonist in ovarian hyperthecosis and virilizing turnours*

Cited by 109 publications

References 26 publications

The polycystic ovary syndrome: a position statement from the European Society of Endocrinology

The polycystic ovary syndrome: a position statement from the European Society of Endocrinology

Impact of clinical, hormonal, radiological, and immunohistochemical studies on the diagnosis of postmenopausal hyperandrogenism

A Case of Ovarian Steroid Cell Tumor, Not Otherwise Specified, Treated with Surgery and Gonadotropin Releasing Hormone Agonist

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