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

Lania, Andrea; Gangi, Emanuela; Romoli, Roberto; Losa, Marco; Travaglini, P.; Meringolo, Domenico; Ambrosi, Bruno; Faglia, G.; Beck‐Peccoz, Paolo; Spada, Anna

doi:10.1046/j.1365-2362.2002.00981.x

Cited by 11 publications

(6 citation statements)

References 31 publications

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“…As a result of the negative feedback mechanism, FSH may remain within the normal range. However, in almost half of the reviewed cases FSH levels were elevated, which supports the theory of impaired negative feedback mechanism [24]. Normal FSH concentrations are capable of inducing OHSS, probably because of enhanced FSH bioactivity [25,26].…”

Section: Clinical Presentationsupporting

confidence: 60%

Ovarian Hyperstimulation Caused by Gonadotroph Pituitary Adenoma – Review

Halupczok¹,

Kluba-Szyszka²,

Bidzińska−Speichert³

et al. 2015

Adv Clin Exp Med

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Ovarian hyperstimulation syndrome (OHSS) occurs mostly as an iatrogenic complication of assisted reproductive technology. Gonadotroph pituitary adenomas are rarely associated with OHSS. To the authors' knowledge, to date only 30 cases of spontaneous ovarian stimulation associated with gonadotroph adenomas have been reported in women and only 2 in children. The most common symptoms in such cases included menstrual disturbances, abdominal or pelvic pain, abdominal distension and increased girth. Galactorrhea, nausea and vomiting were also reported. Neurological symptoms occurred when the size of the pituitary tumor reached at least 20 mm. Transvaginal ultrasound examination usually demonstrated enlarged multicystic ovaries. MRIs of the pituitary revealed macroadenomas up to 61 mm in maximum diameter. The hormonal profiles of the reported cases showed normal or elevated FSH levels, suppressed LH levels, elevated estradiol levels and supranormal concentrations of prolactin. Transsphenoidal surgery is the therapy of choice, however other treatment modalities can be utilized in selected cases (Adv Clin Exp Med 2015, 24, 4, 695-703).

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Section: Clinical Presentationsupporting

confidence: 60%

Ovarian Hyperstimulation Caused by Gonadotroph Pituitary Adenoma – Review

Halupczok¹,

Kluba-Szyszka²,

Bidzińska−Speichert³

et al. 2015

Adv Clin Exp Med

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“…The absence of suppression may constitute the pathophysiology of these tumors (15,19). In our case, immunohistochemical examination of the tumor tissue was negative for ER-a, indicating that high serum estrogen levels may fail to exert a suppressive effect on tumor tissue due to the absence of receptors in these cells.…”

Section: Discussionmentioning

confidence: 58%

A pituitary adenoma secreting follicle-stimulating hormone with ovarian hyperstimulation: treatment using a gonadotropin-releasing hormone antagonist

Garmes

Grassiotto

Fernandes

et al. 2012

Fertility and Sterility

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“…Interestingly, one study demonstrated that estrogen-induced negative feedback of gonadotropin secretion is disrupted in patients with gonadotroph adenomas. 26 Thus, we hypothesize that normal or high expression of GSTP1 may contribute to gonadotroph adenoma development through regulation of estrogen-induced negative feedback of gonadotropin secretion. Anyway, further investigation is necessary to profile the exact role of GSTP1 in each type of pituitary adenoma.…”

Section: Discussionmentioning

confidence: 99%

Reduction of GSTP1 expression by DNA methylation correlates with clinicopathological features in pituitary adenomas

et al. 2008

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p-Class glutathione-S-transferase (GSTP1) located on chromosome 11q13 encodes a phase II metabolic enzyme that detoxifies reactive electrophilic intermediates. GSTP1 plays an important role in the protecting cells from cytotoxic and carcinogenic agents and is expressed in normal tissues at variable levels in different cell types. Altered GSTP1 activity and expression have been reported in many tumors and this is largely due to GSTP1 DNA hypermethylation. The role of GSTP1 in pituitary tumorigenesis has not been investigated. In this study, we evaluated the GSTP1 expression level and GSTP1 DNA methylation status in a series of pituitary adenomas. Using immunohistochemistry, we identified expression of GSTP1 in all of the various normal hormoneproducing adenohypophysial cell types. In pituitary adenomas, loss or reduced expression of GSTP1 was detected in 27 of 53 tumors (50.9%). Expression of GSTP1 was significantly lower in invasive adenomas than in noninvasive adenomas (Po0.05). Using methylation-specific polymerase chain reaction (MS-PCR), GSTP1 DNA promoter hypermethylation was detected in adenomas (38 of 53, 71.7%) but not in normal tissues. GSTP1 methylation was more frequent in grade II, III, and IV tumors (66.7, 85, and 83%, respectively) than in grade I tumors (33%, Po0.05). In addition, the frequency of GSTP1 methylation was higher in invasive tumors (85%) than in noninvasive tumors (59%; Po0.05). Methylation status correlated with significant downregulation of GSTP1 expression; the frequency of GSTP1 methylation was higher in tumors with reduced-GSTP1 expression (85%) than in tumors with normal or high GSTP1 expression (54%; Po0.05).These data indicate that GSTP1 inactivation through CpG hypermethylation is common in pituitary adenomas and may contribute to aggressive pituitary tumor behavior.

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

Cited by 11 publications

References 31 publications

Ovarian Hyperstimulation Caused by Gonadotroph Pituitary Adenoma – Review

Ovarian Hyperstimulation Caused by Gonadotroph Pituitary Adenoma – Review

A pituitary adenoma secreting follicle-stimulating hormone with ovarian hyperstimulation: treatment using a gonadotropin-releasing hormone antagonist

Reduction of GSTP1 expression by DNA methylation correlates with clinicopathological features in pituitary adenomas

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