trelstar has been researched along with Adenoma* in 10 studies
10 other study(ies) available for trelstar and Adenoma
Article | Year |
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Pituitary adenoma and apoplexy during GnRH agonist treatment for IVF - case report.
Topics: Adenoma; Adult; Emergency Treatment; Female; Fertilization in Vitro; Gonadotropin-Releasing Hormone; Humans; Neurosurgical Procedures; Pituitary Apoplexy; Pituitary Gland; Pituitary Neoplasms; Triptorelin Pamoate | 2020 |
Pituitary apoplexy induced by triptorelin in patient with prostate cancer.
Topics: Adenocarcinoma; Adenoma; Aged; Antineoplastic Agents, Hormonal; Diplopia; Headache; Humans; Hypophysectomy; Magnetic Resonance Imaging; Male; Neoplasms, Multiple Primary; Neoplasms, Unknown Primary; Pituitary Apoplexy; Pituitary Neoplasms; Prostatic Neoplasms; Triptorelin Pamoate | 2015 |
[Virilization of a post-menopausal woman. Diagnostic and therapeutic considerations].
Virilizing tumors are rare disorders that commonly develop in the adrenal cortex or the ovaries. Because these tumors are usually millimetric, androgen-secreting ovarian tumors can be particularly difficult to identify through commonly available imaging techniques and can thus pose a diagnostic challenge. We present the case of a 71-year-old woman who presented with severe clinical hyperandrogenism and biochemical traits suggestive of an ovarian source but who was diagnosed with a 10-cm adrenal mass. Topics: Adenoma; Adrenal Gland Neoplasms; Adrenalectomy; Aged; Androgens; Carcinoma, Transitional Cell; Cyproterone Acetate; Dexamethasone; Diagnosis, Differential; False Negative Reactions; Female; Gonadotropin-Releasing Hormone; Gonadotropins, Pituitary; Humans; Incidental Findings; Neoplasms, Second Primary; Ovarian Diseases; Postmenopause; Triptorelin Pamoate; Urinary Bladder Neoplasms; Virilism | 2009 |
Pituitary apoplexy caused by GnRH-agonist treatment revealing gonadotroph adenoma.
Topics: Adenoma; Aged; Contrast Media; Cyproterone Acetate; Gadolinium; Gadolinium DTPA; Humans; Magnetic Resonance Imaging; Male; Organometallic Compounds; Pentetic Acid; Pituitary Apoplexy; Pituitary Neoplasms; Prostatic Neoplasms; Triptorelin Pamoate | 1995 |
Ovarian suppression with triptorelin and adrenal stimulation with adrenocorticotropin in functional hyperadrogenism: role of adrenal and ovarian cytochrome P450c17 alpha.
To validate combined ovarian suppression with triptorelin and adrenal stimulation with ACTH in the diagnosis of female hyperandrogenism and to provide new insights into the adrenal-ovarian relationship present in this disorder.. Comparison of sexual steroids and basal and ACTH-stimulated steroid levels before and after ovarian suppression induced by triptorelin.. Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain.. Thirty-nine nonselected women with hyperandrogenism.. Serum levels of T, 17-hydroxyprogesterone (17-OHP), 17-hydroxy-pregnenolone, DHEA and DHEAS, androstenedione (delta 4-A), 11-deoxycortisol, and cortisol.. Elevated T independent of ovarian suppression pointed to an adrenal disorder in six patients (one with an androgen-producing adenoma, two with late-onset 21-hydroxylase deficiency, three with functional adrenal hyperandrogenism). Nineteen patients had functional ovarian hyperandrogenism as elevated T normalized after ovarian suppression and were subdivided into ovDHEAS+ (n = 7) and ovDHEAS = (n = 12) subgroups depending on the presence of DHEAS hypersecretion. Finally, 14 patients had idiopathic hirsutism according to normal T before and after ovarian suppression. Comparisons of initial hormonal values between groups and with reference values obtained from normal women (n = 11) disclosed in functional adrenal hyperandrogenism an elevation of T and basal and stimulated DHEAS, delta 4-A, and 17-OHP with respect to normal women. These abnormalities were also present in ovDHEAS+ except for basal delta 4-A, which was normal, whereas only T and stimulated 17-OHP were elevated in ovDHEAS =. In the idiopathic group all steroids were normal with the exception of a mild elevation in stimulated DHEAS.. These results show a continuum of abnormalities in hyperandrogenic women, suggesting an enhanced cytochrome P450c17 alpha activity in the adrenal and the ovary as the shared mechanism between functional adrenal hyperandrogenism and functional ovarian hyperandrogenism. Topics: Adenoma; Adolescent; Adrenal Gland Neoplasms; Adrenal Glands; Adrenocorticotropic Hormone; Adult; Female; Humans; Hyperandrogenism; Ovary; Polycystic Ovary Syndrome; Steroid 17-alpha-Hydroxylase; Testosterone; Triptorelin Pamoate; Ultrasonography | 1994 |
Gonadotropin and alpha-subunit responses to chronic gonadotropin-releasing hormone analog administration in patients with glycoprotein hormone-secreting pituitary tumors.
Pituitary tumors secreting intact glycoprotein hormones (LH, FSH, and TSH) and/or alpha-subunit are being increasingly recognized. Because chronic administration of GnRH analogs decreases gonadotropin secretion in normal subjects, we investigated gonadotropin and alpha-subunit responses to chronic GnRH analog administration in five men with glycoprotein hormone-secreting pituitary tumors. Two patients (patients A and B) received the GnRH agonist analog (D-Trp6-Pro9-NEt-LHRH) for 4 weeks as a daily sc dose (8 micrograms/kg.day). In both, secretion of LH and/or alpha-subunit increased markedly. Subsequently, three patients received a higher analog dose (32 micrograms/kg.day) for a longer duration (8 weeks). One patient with a LH- and FSH-secreting tumor (patient C) had a highly significant (P less than 0.001) fall in serum LH and FSH concentrations; however, alpha-subunit secretion increased. During a subsequent study, when this patient received a lower dose (8 micrograms/kg.day) for 8 weeks, gonadotropin suppression also occurred. In two additional patients who received this dose (32 micrograms/kg.day), it had a persistent agonist effect on FSH beta (patient D) and alpha-subunit secretion (patient E). A marked increase in alpha-subunit secretion occurred in all five patients, regardless of whether basal serum alpha-subunit concentrations were elevated. These patients received the GnRH analog at doses 2-8 times greater than those that suppress gonadotropin secretion in normal men. Serum LH and FSH concentrations decreased in only one patient with a gonadotropin-secreting adenoma. The serum LH and FSH responses to acute GnRH stimulation did not predict the gonadotropin responses to chronic GnRH analog administration. Thus, gonadotropin and alpha-subunit production by most pituitary adenomas is augmented during chronic GnRH analog administration, consistent with defective GnRH desensitization in the adenomatous tissue. Despite the heterogeneous gonadotropin responses to the GnRH analog in these patients, serum alpha-subunit levels increased in all patients, indicating dissociation in the secretion of intact gonadotropins and alpha-subunit. Topics: Adenoma; Adrenocorticotropic Hormone; Adult; Aged; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Growth Hormone; Humans; Luteinizing Hormone; Male; Middle Aged; Pituitary Hormones, Anterior; Pituitary Neoplasms; Prolactin; Testosterone; Thyrotropin; Triptorelin Pamoate | 1989 |
Gonadotropin-releasing hormone agonists are unsuccessful in reducing tumoral gonadotropin secretion in two patients with gonadotropin-secreting pituitary adenomas.
Whether GnRH agonist treatment leads to reduced gonadotropin secretion and tumor volume in patients with gonadotropin-secreting pituitary adenomas is controversial. We studied the effect of GnRH analog treatment in two such patients, one with a recurrent FSH- and LH-secreting pituitary adenoma (patient 1) and one with a recurrent FSH- and alpha-subunit-secreting pituitary adenoma (patient 2). Patient 1 was treated with 200 micrograms Buserelin daily for 65 days, and patient 2 received three injections of 3 mg [D-Trp6]-LHRH formulated in microcapsules at 21-day intervals. In both patients, plasma FSH, LH (RIA), and alpha-subunit concentrations increased initially and remained above the pretreatment values throughout the treatment period. Plasma LH, measured by immunoradiometric assay, remained well above the detection limit. Plasma bioactive LH and testosterone became undetectable in patient 2, but did not change in patient 1. In neither patient did pituitary tumor size (determined by computed tomographic scan) change during treatment. We conclude that 1) the overall effect of GnRH analogs in patients with gonadotroph cell adenomas is stimulation of gonadotropin release by the tumor, although LH release varies according to how plasma LH is measured, possibly related to the origin of the hormone (normal or tumor gonadotroph cells), and 2) GnRH analog treatment does not reduce tumor size. Topics: Adenoma; Adult; Buserelin; Drug Evaluation; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Gonadotropins, Pituitary; Humans; Luteinizing Hormone; Male; Middle Aged; Neoplasm Recurrence, Local; Pituitary Neoplasms; Stimulation, Chemical; Testosterone; Time Factors; Triptorelin Pamoate | 1988 |
Luteinizing hormone-secreting pituitary tumor: biosynthetic characterization and clinical studies.
Although gonadotropin-secreting pituitary adenomas are increasingly recognized, tumors secreting only LH are rare. Since gonadotropin production by pituitary adenomas may reflect imbalanced glycoprotein biosynthesis, we studied tumor LH and subunit biosynthesis and secretion in a patient with a LH- and alpha-subunit-producing pituitary tumor. Northern blot analysis of RNA from the tumor revealed the presence of mRNAs encoding both alpha- and beta-subunits of LH with a marked excess of the mRNA encoding LH beta. Analysis of tumor extracts by gel filtration chromatography confirmed an excess of free LH beta relative to free alpha-subunit. Clinical studies demonstrated that the secretion of LH and alpha-subunit by the tumor increased in response to the acute administration of LHRH (100 micrograms, iv) and decreased during a 4-h dopamine infusion (4 micrograms/kg X min). During a 4-week course of LHRH analog (D-Trp6-Pro9-NEt-LHRH) administration, given as a daily sc dose (8 micrograms/kg X day), serum LH and alpha-subunit concentrations increased 7- and 3-fold, respectively, consistent with a chronic agonist effect. Chronic administration of bromocriptine resulted in reduction of serum LH and alpha-subunit levels to normal. Topics: Adenoma; Bromocriptine; Combined Modality Therapy; Dopamine; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Male; Middle Aged; Pituitary Neoplasms; Prolactin; RNA, Messenger; RNA, Neoplasm; Testosterone; Triptorelin Pamoate | 1987 |
Gonadotropin-secreting pituitary adenoma with concomitant hypersecretion of testosterone and elevated sperm count. Treatment with LRH agonist.
Hypersecretion of both FSH and LH was demonstrated in a man with pituitary macroadenoma, who also presented elevated levels of blood testosterone and an increased sperm count. The patient underwent transsphenoidal surgery followed immediately by cranial irradiation. Immunocytochemical analysis of the tumour revealed the presence of FSH, LH, TSH and the alpha-subunit. Gel chromatography of the serum on Sephadex G-100 revealed immunoactive FSH, LH and the alpha-subunit which coeluted with the labelled standards of corresponding hormones. Blood levels of both gonadotropins and testosterone remained persistently elevated up to one year following surgical decompression of the tumour and radiotherapy. It was decided to treat this patient with sc administration of 100 micrograms D-Trp6-LRH biweekly. After 20 weeks, LRH-analogue treatment resulted in the reduction of serum FSH and LH levels and a diminishing in tumour size as assessed by computed tomography scan of the pituitary. This report shows that in a patient with clinically and biochemically documented gonadotropin-secreting adenoma, inducing a state of persistent gonadal hyperfunction, pituitary surgery and cranial irradiation failed to normalize the biochemical abnormality; however, therapy with D-Trp6-LRH agonist induced clinical, biochemical and radiologic improvement. Topics: Adenoma; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Male; Middle Aged; Pituitary Gland; Pituitary Neoplasms; Radionuclide Imaging; Sperm Count; Testosterone; Triptorelin Pamoate | 1986 |
The luteinizing hormone-releasing hormone (LHRH) agonist [D-Trp6-Pro9-NEt]LHRH increased rather than lowered LH and alpha-subunit levels in a patient with an LH-secreting pituitary tumor.
Episodic secretion of LH, and the responses of serum LH, alpha-subunit, and testosterone concentrations to the acute administration of LHRH and the chronic administration of the LHRH agonist analog [D-Trp6-Pro9-NEt]LHRH (D-Trp6-Pro9) were evaluated in a 33-yr-old man previously reported to have an LH-secreting pituitary tumor unaccompanied by FSH hypersecretion. Basal serum LH and alpha-subunit concentrations were elevated [57 +/- 0.7 (SEM) mIU/ml (range, 45-71) and 26 ng/ml, respectively]. Frequent sampling revealed six LH secretory spikes over a 24-h period with increments above basal levels varying from 23-40% and interspike intervals ranging from 1.5-5 h. The concentrations of LH or alpha-subunit after iv administration of 150 micrograms LHRH did not increase above these intrinsic LH secretory increments (delta LH: 23%; delta alpha-subunit: 21%). The low basal serum FSH concentrations (3.5 mIU/ml) and elevated basal serum testosterone levels (1480 ng/dl) were unchanged after LHRH. Administration of clomiphene citrate produced no increase in serum LH, FSH, or testosterone concentrations. An attempt was made to decrease LH secretion in this patient using D-Trp6-Pro9. Administration of 200 micrograms daily sc of this LHRH analog for 21 days was associated with increases in serum LH and alpha-subunit concentrations. Mean serum LH and alpha-subunit levels for the 21 days of analog administration were 110 +/- 5.4 (SEM) mIU/ml (range, 70-170) and 64 +/- 3 (SEM) ng/ml (range, 32-84), respectively. During the 9-day period after discontinuance of the LHRH analog, levels of both serum LH and alpha-subunit declined precipitously and mean serum LH and alpha-subunit levels were 58 +/- 7 (SEM) mIU/ml (range, 18-90) and 22 +/- 3 (SEM) ng/ml (range, 12-44), respectively. We conclude that this patient's pituitary tumor has diminished responsiveness to acute LHRH administration and that the effect of chronic D-Trp6-Pro9 is stimulatory rather than inhibitory, as occurs after chronic administration of this analog to normal subjects. The blunted responsiveness to LHRH administration and the lack of response to clomiphene citrate suggest tumor autonomy. The presence of modest paradoxical responsiveness of serum LH and alpha-subunit concentrations during the course of daily D-Trp6-Pro9 administration suggests that central regulatory mechanisms, if present, are abnormal. Topics: Adenoma; Adult; Clomiphene; Follicle Stimulating Hormone; Glycoprotein Hormones, alpha Subunit; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Male; Peptide Fragments; Pituitary Hormones, Anterior; Pituitary Neoplasms; Testosterone; Triptorelin Pamoate | 1984 |