The Effects of Bromocriptine, Thyrotropin-Releasing Hormone, and Gonadotropin-Releasing Hormone on Hormone Secretion by Gonadotropin-Secreting Pituitary Adenomas<i>in Vivo</i>and<i>in Vitro</i>

Lamberts, Steven W. J.; Verleun, T.; Oosterom, R.; Hofland, Leo J.; Ginkel, L. A. van; Loeber, J.G.; Vroonhoven, C. C. J. Van; Stefanko, S. Z.; Jong, Frank H. de

doi:10.1210/jcem-64-3-524

Cited by 51 publications

(27 citation statements)

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“…However, the effects of the DA agonist bromocriptine on reducing NFPA size has been disappointing, as most studies have shown only modest size reduction in a minority of treated tumors (12,14,17,21,25). Therefore, bromocriptine therapy has not been advocated on a routine basis.…”

Section: Discussionmentioning

confidence: 99%

“…Radiotherapy is the only modality shown to be effective in the prevention of residual tumor growth (7)(8)(9). The use of dopamine (DA) agonists has been previously explored as a treatment alternative for NFPA (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). Greenman and co-workers have shown that postoperative DA treatment resulted in a decrease or stabilization of tumor mass in 90% of patients in contrast to 2 and 5 years re-growth rates of 30 and 70% in untreated patients respectively (26).…”

Section: Introductionmentioning

confidence: 99%

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Dopamine agonist therapy of clinically non-functioning pituitary macroadenomas. Is there a role for 123I-epidepride dopamine D2 receptor imaging?

Herder¹,

Reijs²,

Feelders³

et al. 2006

eur j endocrinol

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Objective: Clinically non-functioning pituitary adenomas (NFPAs) can express functional dopamine D2 receptors. Therapy with dopamine (DA) agonists may result in a NFPA size reduction. However, DA agonist-sensitive and -resistant NFPAs are clinically indistinguishable. We have studied the correlation between in vivo imaging of D2 receptors using 123 I-epidepride and the radiological response of NFPA to DA in 18 patients. Methods: Patients were treated with either cabergoline (1-2 mg/week) or quinagolide (150-300 mg/day) for a mean period of 89.7 months (range, 34-187 months). Results: Pituitary uptake of 123 I-epidepride varied from slight uptake classified as grade 0 to very high classified as grade 3. Grade 0 uptake was found in four patients; grade 1 in three; grade 2 in ten, and grade 3 in one. NFPA stabilization or shrinkage with DA agonist therapy showed no significant difference between grade 0, 1, and 2 tumors (mean tumor stabilization or shrinkage: 31, 30, and 36% respectively). However, when we considered a decrease in tumor size ranging from 0 to 20% as tumor stabilization and O20% decrease in tumor size as true shrinkage, one out of four NFPAs with grade 1 uptake, two out of three with grade 1 uptake, and eight out of ten with grade 2 uptake showed tumor shrinkage. Conclusion: In conclusion, there is limited clinical usefulness of dopamine D2 receptor imaging for predicting the clinical efficacy of DA agonist in selected patients with NFPAs. DA agonist therapy in NFPAs can result in tumor stabilization and shrinkage.European Journal of Endocrinology 155 717-723

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dopamine agonist therapy of clinically non-functioning pituitary macroadenomas. Is there a role for 123I-epidepride dopamine D2 receptor imaging?

Herder¹,

Reijs²,

Feelders³

et al. 2006

eur j endocrinol

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“…Although gonadotropin secretion decreases during continuous GnRH administration in normals, patients with GnRH-responsive pituitary adenomas demonstrate a persistent agonist effect with sustained increases in gonadotropin secretion (5). GnRH-induced secretory responses have been demonstrated in static cell cultures of pituitary tumors (6)(7)(8). However, the physiological regulation of neoplastic gonadotrophs by pulsatile GnRH has not been examined in vitro, and little is known about the mechanism underlying GnRH responsiveness in neoplastic gonadotrophs.…”

Section: Introductionmentioning

confidence: 99%

Gonadotropin-releasing hormone receptor mRNA expression by human pituitary tumors in vitro.

Alexander

Klibanski²

1994

J. Clin. Invest.

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An important question in the pathogenesis and regulation of human gonadotroph adenomas is whether heterogeneous gonadotropin responses to gonadotropin-releasing hormone (GnRH) are due to dysregulation of GnRH receptor biosynthesis and/ or cell-signaling pathways. We investigated gonadotropin responsiveness to pulsatile GnRH in 13 gonadotroph adenomas. All tumors had evidence of follicle-stimulating hormone (FSH) ft and a subunit biosynthesis using reverse transcriptase/polymerase chain reaction (RTPCR) techniques. Four tumors significantly increased gonadotropin and/or free subunit secretion during pulsatile 10-8 M GnRH administration. The GnRH antagonist Antide (10-' to 108 M) blocked secretory increases in all GnRH-responsive tumors. Gonadotropin and/or free subunit secretion increased after 60 mM KCl, confirming that GnRH nonresponsiveness was not due to intracellular gonadotropin depletion. We hypothesized that GnRH nonresponsiveness in these tumors may be due to GnRH receptor (GnRHRc) biosynthetic defects. RTPCR analyses detected GnRH-Rc transcripts only in responsive tumors and normal human pituitary. This is the first demonstration of a cell-surface receptor biosynthetic defect in human pituitary tumors. We conclude (a) one third of gonadotroph tumors respond to pulsatile GnRH in vitro, (b) GnRH-Rc mRNA is detected in human gonadotroph adenomas and predicts GnRH responsiveness, and (c) GnRHRc biosynthetic defects may underlie GnRH nonresponsiveness in gonadotroph tumors. (J. Clin. Invest. 1994.93:2332-2339

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“…The correlation of FSH and TRH has been described in previous articles. In patients with pituitary adenomas, TRH showed a stimulatory effect on FSH secretion [52,53]. However, in a study using pituitary cell aggregates, it has been shown that TRH was ineffective in releasing FSH [54].…”

Section: Interaction Of Somatolactotroph and Gonadotroph Throughmentioning

confidence: 99%

Paracrine Control of Gonadotrophs by Somatolactotrophs through TRHinduced Follistatin Production

Kanasaki¹

2011

TONEUROEJ

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There is increasing evidence for the existence of local regulation of hormone secretion among pituitary cells. Hormone-producing pituitary cells may communicate with each other and with folliculostellate cells. Activin is one of the regulators of follicle stimulating hormone (FSH) secretion and gene expression, whereas follistatin negatively regulates FSH production by binding to and bioneutralizing the effects of activin. In prolactin-secreting GH3 cells, hypothalamic thyrotropin-releasing hormone (TRH) has been known to stimulate prolactin synthesis and secretion. Follistatin is produced in GH3 cells and is up-regulated by TRH in an ERK dependent manner. Prolactin mRNA levels in GH3 cells are not affected by increasing the dose of exogenous follistatin, and TRH-induced prolactin expression is not modulated in the presence of follistatin. Follistatin produced in somatolactotroph GH3 cells does not affect prolactin production in these cells. In pituitary gonadotroph cell line, L T2, activin increases FSH promoter activity and mRNA expression, and follistatin completely inhibits this activin-increased FSH gene expression. On the other hand, activin reduces the basal activity of prolactin transcription and follistatin prevents these effects. When GH3 cells and L T2 cells are co-cultured, activin-induced FSH promoter activity is completely inhibited in the presence of follistatin. In addition, FSH mRNA is not detected in L T2 cells, when co-cultured with GH3 cells. These observations using the model for somatolactotroph and gonadotroph suggest the possibility that somatolactotrophs and gonadotrophs interact with each other, and TRH might indirectly affect gonadotropin production though follistatin.

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The Effects of Bromocriptine, Thyrotropin-Releasing Hormone, and Gonadotropin-Releasing Hormone on Hormone Secretion by Gonadotropin-Secreting Pituitary Adenomasin Vivoandin Vitro

Cited by 51 publications

References 0 publications

Dopamine agonist therapy of clinically non-functioning pituitary macroadenomas. Is there a role for 123I-epidepride dopamine D2 receptor imaging?

Dopamine agonist therapy of clinically non-functioning pituitary macroadenomas. Is there a role for 123I-epidepride dopamine D2 receptor imaging?

Gonadotropin-releasing hormone receptor mRNA expression by human pituitary tumors in vitro.

Paracrine Control of Gonadotrophs by Somatolactotrophs through TRHinduced Follistatin Production

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