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Pituitary Adenomas (pituitary + adenoma)

Distribution by Scientific Domains

Medical Sciences	93%

Distribution within Medical Sciences

General & Internal Medicine	12%
Pathology	9%

Kinds of Pituitary Adenomas

human pituitary adenoma

Selected Abstracts

Cross-Sectional Imaging Characteristics of Pituitary Adenomas, Invasive Adenomas and Adenocarcinomas in Dogs: 33 Cases (1988,2006)

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010
Rachel E. Pollard
Background: Pituitary tumors in dogs can be adenomas, invasive adenomas, or adenocarcinomas. In people, invasive adenomas and pituitary adenocarcinomas carry a worse prognosis than adenomas. Hypothesis/Objective: To identify differentiating features on cross-sectional imaging in dogs with pituitary adenomas, invasive adenomas, and adenocarcinomas. Animals: Thirty-three dogs that had computed tomography (CT) or magnetic resonance imaging (MRI) performed and a necropsy diagnosis of pituitary adenoma (n= 20), invasive adenoma (n= 11), or adenocarcinoma (n= 2). Methods: Medical records were retrospectively reviewed for signalment, history, and diagnosis. CT and MR images were reviewed for characteristics of pituitary tumors. Results: Mean (± standard deviation) age for dogs with pituitary adenomas (10.6 ± 2.9 years) was greater than that of those with invasive adenomas (8.3 ± 2.7 years, P= .04). Eighteen out of 20 (90%) dogs with adenomas had contrast-enhancing masses. Thirteen out of 20 (65%) had homogeneous enhancement. Mean adenoma height was 1.2 ± 0.7 cm. Eight out of 20 (40%) adenomas were round and 8/20 (40%) compressed surrounding brain. Eleven out of 11 dogs (100%) with invasive adenomas had contrast-enhancing masses. Seven out of 11 (64%) masses were homogeneous. Mean invasive adenoma height was 1.8 ± 0.7 cm, which was significantly greater than adenomas (P= .03). Mass shape varied from round to oval to irregular. Six out of 11 (55%) masses compressed surrounding brain. Clinical and imaging features were variable for 2 dogs with adenocarcinomas. Conclusions and Clinical Relevance: Invasive adenoma should be suspected if a dog with a pituitary tumor is <7.7 years of age and has a mass >1.9 cm in vertical height. Adenocarcinomas are uncommon and metastatic lesions were not seen with imaging. [source]

Clinical and radiological features of patients with macroprolactinaemia

CLINICAL ENDOCRINOLOGY, Issue 3 2003
Mark W. J. Strachan
Summary objectives Macroprolactin is a complex of prolactin (PRL) and IgG and may account for a significant proportion of cases of ,idiopathic hyperprolactinaemia'. In this study, we sought to determine the prevalence and clinical features of macroprolactinaemia in patients diagnosed with hyperprolactinaemia in our region, with a view to determining how patients with macroprolactinaemia should be investigated and managed. patients and methods An Immuno-1 automated immunoassay system with polyethylene glycol (PEG) precipitation was used to identify macroprolactin, with a recovery of , 50% taken as indicating significant macroprolactinaemia. Macroprolactin was found in 58 (21%) of 273 patients with a total PRL > 700 mU/l. The clinical records of 51 (44 female) were available for retrospective review. results The mean (range) age of patients was 39·5 (18,82) years. The median (range) concentrations for the various forms of PRL were: total PRL 1130 mU/l (728,5116), monomeric PRL 240 mU/l (50,656) and macroprolactin 895 mU/l (381,4854). Classical symptoms of hyperprolactinaemia were present in 39% of patients, although in many there were other possible explanations for their symptomatology. Pituitary adenomas were identified in six out of 36 people who underwent neuroimaging. Five of these patients had a microadenoma and one had a 10-mm macroadenoma (although, in this patient macroprolactin was identified after the discovery of the tumour). There was no relationship between macroprolactin concentrations and the presence of hyperprolactinaemic symptoms or neuroimaging abnormalities. conclusions Macroprolactinaemia is a common occurrence in patients with hyperprolactinaemia, but associated symptomatology may not necessarily be linked. The neuroimaging abnormalities were also probably incidental findings and it is questionable whether neuroimaging is necessary when significant macroprolactinaemia is identified and the concentration of monomeric PRL is not elevated (using the Immuno-1 assay system, following PEG precipitation). [source]

A sensitive mutation-specific screening technique for GNAS1 mutations in cases of fibrous dysplasia: the first report of a codon 227 mutation in bone

HISTOPATHOLOGY, Issue 6 2007
B D Idowu
Aims:, To report on the mutation-specific restriction enzyme digest (MSRED) method using paraffin-embedded tissue as a means of detecting GNAS1 mutations in fibrous dysplasia (FD), and to determine if any of the reported GNAS1 mutations in endocrine neoplasms, not previously documented in FD, can be found in FD. Methods and results:, Sixty-seven cases of extragnathic FD were analysed as two groups, 1997,2002 and 2003,06, chosen because tissue fixation and decalcification methods were more accurately recorded in the latter. MSRED revealed that between 2003 and 2006, 93% of 28 ,in house' extragnathic cases harboured a GNAS1 mutation, compared with 75% of 32 cases before 2003. Fixation times of no more than 48 h and decalcification in ethylenediamine tetraacetic acid gave the best results. Of the 56 mutations detected (five gnathic, 51 extragnathic), 32 (57%) were R201H, 21 (38%) were R201C and three (5%) were Q227L. Two Q227L extragnathic cases had unusual clinical/radiological findings. No mutations were detected in osteofibrous dysplasia. Conclusion:, Detection of GNAS1 mutations by MSRED is a valuable adjunct to the histopathological diagnosis of FD. This is the first report of a Q227L mutation in FD, although it has been previously documented in pituitary adenoma. [source]

Thyroid hormone resistance: the role of mutational analysis

INTERNAL MEDICINE JOURNAL, Issue 11 2006
C. M. Florkowski
Abstract The finding of increased thyroxine (T4) and tri-iodothyronine (T3) levels in a patient with normal or increased thyroid-stimulating hormone is unexpected and presents a differential diagnosis between a thyroid-stimulating hormone-secreting pituitary adenoma, generalized resistance to thyroid hormone (RTH) and laboratory artefact. Without careful clinical and biochemical evaluation, errors may occur in patient diagnosis and treatment. In the case of RTH, mutation of the thyroid hormone receptor beta gene results in generalized tissue resistance to thyroid hormone. As the pituitary gland shares in this tissue resistance, euthyroidism with a normal thyroid-stimulating hormone is usually maintained by increased thyroid hormones. To date, we have identified eight pedigrees in New Zealand with mutations in the thyroid hormone receptor beta gene, including two novel mutations. Mutational analysis of the thyroid hormone receptor beta gene allows definitive diagnosis of RTH, potentially avoiding the need for protracted and expensive pituitary function testing and imaging. Mutational analysis also enables family screening and may help to avoid potential misdiagnosis and inappropriate treatment. [source]

Cross-Sectional Imaging Characteristics of Pituitary Adenomas, Invasive Adenomas and Adenocarcinomas in Dogs: 33 Cases (1988,2006)

Cardiac failure and multiple organ dysfunction syndrome in a patient with endocrine adenomatosis

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2002
M. W. Dünser
In this case report, we present the successful therapy of severe cardiac failure in pituitary adrenal insufficiency. A previously healthy 56-year-old-man in pituitary coma due to an atypical variant of multiple endocrine adenomatosis (pituitary adenoma and pheochromocytoma) suffered from cardiac failure resistant to catecholamine and standard hydrocortisone therapy. After two bolus injections of dexamethasone (2 × 24 mg) mean arterial pressure and cardiac function dramatically improved, probably due to restoration of permissive effects on catecholamine action and reversal of pathophysiological mechanisms of cardiac failure. We conclude that in patients with severe cardiovascular failure in pituitary coma the administration of potent glucocorticoids may be more effective in reversing cardiovascular failure than standard dosages of hydrocortisone. [source]

A growth hormone-secreting adenoma with incomplete nerve bundle formation

NEUROPATHOLOGY, Issue 3 2008
Hidetoshi Ikeda
We present a unique case of an adenoma secreting growth hormone (GH), showing incomplete nerve bundle formation without ganglion cells. A 47-year-old man presenting with acromegaly was revealed to have high serum GH and IGF-1 levels. The concentrations of the other adenohypophysial hormones were within the normal range. Histology revealed an unusual pituitary adenoma containing many nerve bundle-like structures. Adenoma cells with ovoid or round hyperchromatic nuclei and eosinophilic cytoplasms lacked the typical features of ganglion cells. The nerve bundles consisted of slender elongated cells. These fibers were arranged into groups in a roughly parallel fashion. By immunohistochemistry, many adenoma cells were positive for GH, prolactin, thyrotropin beta, synaptophysin and chromogranin. Fibrous bodies revealed by keratin immunostaining were found only in adenoma cells. Scattered star-shaped adenoma cells showed the same immunoreactivity as folliculo-satellite cells. Adenoma cells, but not the bundle-like structures, were also positive for Pit-1. Immunostaining for neurofilament protein, GFAP, vimentin, and S-100 protein revealed variable amounts of fibrils within the bundle-like structures. Scattered immunoreactivity for myelin basic protein and synaptophysin was also found in the bundle area. Our case is the first GH-secreting pituitary adenoma showing incomplete nerve bundle differentiation and lacking mature ganglion cells. [source]

Multiple endocrine neoplasia type 1-associated cystic pancreatic endocrine neoplasia and multifocal cholesterol granulomas

PATHOLOGY INTERNATIONAL, Issue 4 2010
Noriko Kimura
A novel combination of tumors was found in a 68 year-old female with Multiple Endocrine Neoplasia type-1 (MEN 1) that included a cystic pancreatic endocrine neoplasm (CPEN), a pituitary adenoma, and multifocal cholesterol granulomas (MCGs) in the breast, pleura, and the extremities. The pancreatic tumor displayed a single central locule surrounded by a thin rim of neoplastic parenchyma. The tumor showed heterogeneity in the architecture that included glandular, trabecular and solid patterns. The tumor cells of the pancreas were immunohistochemically positive for both endocrine and pancreatic acinar markers including chromogranin A, synaptophysin, glucagon, lipase, and reg protein. Electron microscopy revealed that there were numerous smaller dense-cored neurosecretory granules, larger zymogen-like granules and microvilli on the apical side of the tumor cells. The pancreatic tumor was diagnosed as CPEN with acinar cell features. Analysis of the DNA extracted from the tissues revealed that there is a MEN1 germline mutation in exon 10 codon 527, and somatic mutation in exon 2 codon 32 in the pancreatic tumor, and one base pair deletion in exon 2 codon 79 in the pituitary adenoma. Here, we report the case and discuss possible pathogenesis of CPEN and MCGs in a patient with MEN 1. [source]

Intracranial tumor surgery in patients >70 years of age: is clinical practice worthwhile or futile?

ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2009
S. G. Rogne
Objectives,,, To study survival and functional outcome after intracranial tumor surgery in elderly patients. Materials and methods,,, This is a retrospective study of 289 consecutive patients of age ,70 years, who underwent primary surgery (resection or biopsy) in the time period 2003,2007 for an intracranial tumor (87 astrocytomas, 79 meningiomas, 62 brain metastases, 33 pituitary adenomas and 28 other tumors). Results,,, The surgical mortality was 2.8%. Overall survival at 6 months, 1, 2 and 5 years was 73%, 57%, 46% and 38% respectively. Histology, pre-operative Eastern Cooperative Oncology Group (ECOG) performance score and resection, as opposed to biopsy, were significantly associated with survival. Gender, age and American Association of Anaesthetists (ASA) score were not significantly related to survival. One-year survival after surgery for astrocytoma, meningioma, brain metastases and pituitary adenoma were 24%, 94%, 31% and 96% respectively. More than 85% of the patients who were alive 6 months after surgery had a stable or improved ECOG score compared with their pre-operative score. Conclusions,,, Surgery for intracranial tumors in selected elderly patients is worthwhile, not futile. Age alone should not be used as a selection criterion for treatment. [source]

The role of optical coherence tomography in the detection of pituitary adenoma

ACTA OPHTHALMOLOGICA, Issue 7 2009
Charlotta Johansson
Abstract. Purpose:, To analyse retinal nerve fibre layer (RNFL) thickness in eyes with compression of the optic chiasm by a pituitary adenoma. RNFL thickness was analysed with optical coherence tomography (OCT) and compared to visual field measurements using high-pass resolution perimetry (HRP). Methods:, Sixteen eyes from eight patients with pituitary adenoma were studied. All had bitemporal visual field depression caused by compression of the optic chiasm. Patients were submitted to an ophthalmic examination more than 14 months after surgery (seven patients had undergone trans-sphenoidal and one trans-cranial adenomectomy). The examination included HRP, fundus photography and measurement of the peripapillar RNFL thickness using OCT. Results:, In spite of temporal visual field depression, not all eyes showed reduced RNFL thickness by OCT. This was also true for some eyes in which RNFL was judged to be reduced on fundus photographs. Contrary to our expectations, RNFL thickness in the nasal quadrant was normal in nine of the 16 eyes. Corresponding figures for the superior, inferior and temporal quadrants were eight, six and five, respectively. The overall RNFL thickness, as measured by OCT, did not correlate well with neural capacity, which is an index of remaining retino-cortical neural channels in HRP. Conclusion:, RNFL thickness as measured with OCT was reduced in most, but not all, eyes with temporal field depression caused by chiasmal compression. The pattern of RNFL loss did not correlate well with the visual field defect. Sensitivity of RNFL thickness measurement in OCT was low. The method has limited value in the diagnosis of pituitary tumour compression. [source]

Functional magnetic resonance imaging corresponds to Humphrey perimetry in a patient with pituitary adenoma

ACTA OPHTHALMOLOGICA, Issue 2 2006
Kirsten Nielsen
No abstract is available for this article. [source]

Screening of Cushing's syndrome in adult patients with newly diagnosed diabetes mellitus

CLINICAL ENDOCRINOLOGY, Issue 2 2007
Giuseppe Reimondo
Summary Objective Recent studies have shown that a relatively high number of diabetic patients may have unsuspected Cushing's syndrome (CS). The aim of the present study was to screen for CS in adult patients with newly diagnosed diabetes mellitus who were not selected for clinical characteristics, such as poor control and obesity, which may increase the pre-test probability of CS. Design, patients and measurement We prospectively evaluated 100 consecutive diabetic patients at diagnosis from 2003 to 2004. No patient had clear Cushingoid features. Screening was performed by using the overnight 1-mg dexamethasone suppression test (DST) after complete recovery from acute concomitant illnesses and attainment of satisfactory glycaemic control. The threshold of adequate suppression after DST was set at 110 nmol/l. Results Five patients failed to suppress cortisol after DST and underwent a repeated DST and a confirmatory standard 2-day, 2-mg DST after 3,6 months from the baseline evaluation. In one woman, a definitive diagnosis of CS was made by a surgically proven pituitary adenoma, and glycaemic control improved after cure of CS. Conclusions The results of the present study support the view that unknown CS is not rare among patients with diabetes mellitus. This is the first demonstration that screening for CS may be feasible at the clinical onset of diabetes in an unselected cohort of patients. Therefore, early diagnosis and treatment of CS may provide the opportunity to improve the prognosis of diabetes. [source]

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

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2002
A. Lania
Abstract Background Several in vitro studies suggest that gonadotropin-secreting pituitary adenomas (Gn-omas) and non functioning pituitary adenomas (NFPA) originate from gonadotroph cells. Patients with Gn-oma and NFPA frequently show abnormal gonadotropin response to TRH. The aim of the study was to investigate whether the estrogen-induced negative feedback is operating in either patients with Gn-oma or NFPA. Materials and methods Serum gonadotropin levels were evaluated at 24 h after ethinylestradiol administration (1 mg per os; EE2 test) in seven patients with a diagnosis of Gn-oma, based on the presence of high follicle-stimulating hormone (FSH) and/or lutenising hormone (LH) levels with normal or high levels of sex steroids, in 22 patients with NFPA with normal or low levels of gonadotropin and sex steroids, and 30 sex- and age-matched healthy subjects. A normal response to EE2 test was arbitrarily defined as a serum LH and FSH decrease of at least 40 and 30% below basal levels. Results Among patients with Gn-oma, only one had a normal FSH inhibition and another, a normal LH inhibition. Among the 22 patients with NFPA, the EE2 test caused a normal FSH or LH reduction in 10 and 15, respectively, while a normal reduction of both FSH and LH was observed in nine. Conclusions The study demonstrates that estrogen-induced negative feedback of gonadotropin secretion is disrupted in almost all patients with Gn-oma and in half of those with NFPA. This defective feedback is reminiscent of the resistance to thyroid hormones and glucocorticoids observed in patients with thyroid-stimulating hormone- (TSH-) and adrenocorticotropic hormone- (ACTH-)secreting adenomas, respectively. [source]

Genome-wide amplification and allelotyping of sporadic pituitary adenomas identify novel regions of genetic loss

GENES, CHROMOSOMES AND CANCER, Issue 3 2003
D. J. Simpson
Through the use of a candidate gene approach, several previous studies have identified loss of heterozygosity (LOH) at putative tumor-suppressor gene (TSG) loci in sporadic pituitary tumors. This study reports a genome-wide allelotyping by use of 122 microsatellite markers in a large cohort of tumors, consisting of somatotrophinomas and non-functioning adenomas. Samples were first subject to prior whole genome amplification by primer extension pre-amplification (PEP) to circumvent limitations imposed by insufficient DNA for whole-genome analysis with this number of microsatellite markers. The overall mean frequency of loss in invasive tumors was significantly higher than that in their non-invasive counterparts (7 vs. 3% somatotrophinomas; 6 vs. 3% non-functioning adenomas, respectively). Analysis of the mean frequency of LOH, across all markers to individual chromosomal arms, identified 13 chromosomal arms in somatotrophinomas and 10 in non-functioning tumors, with LOH greater than the 99% upper confidence interval calculated for the rate of overall random allelic loss. In the majority of cases, these losses were more frequent in invasive tumors than in their non-invasive counterparts, suggesting these to be markers of tumor progression. Other regions showed similar frequencies of LOH in both invasive and non-invasive tumors, implying these to be early changes in pituitary tumorigenesis. This genome-wide study also revealed chromosomal regions where losses were frequently associated with an individual marker, for example, chromosome arm 1q (LOH > 30%). In some cases, these losses were subtype-specific and were found at a higher frequency in invasive tumors than in their non-invasive counterparts. Identification of these regions of loss provides the first preliminary evidence for the location of novel putative TSGs involved in pituitary tumorigenesis that are, in some cases, subtype-specific. This investigation provides an unbiased estimate of global aberrations in sporadic pituitary tumors as assessed by LOH analysis. The identification of multiple "hotspots" throughout the genome may be a reflection of an unstable chromatin structure that is susceptible to a deletion or epigenetic-mediated gene-silencing events. © 2003 Wiley-Liss, Inc. [source]

Pituitary Transcription Factors: From Congenital Deficiencies to Gene Therapy

JOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2006
M. H. Quentien
Despite the existence of interspecies phenotypic variability, animal models have yielded valuable insights into human pituitary diseases. Studies on Snell and Jackson mice known to have growth hormone, prolactin and thyroid-stimulating hormone deficiencies involving the hypoplastic pituitary gland have led to identifying alterations of the pituitary specific POU homeodomain Pit-1 transcription factor gene. The human phenotype associated with rare mutations in this gene was found to be similar to that of these mice mutants. Terminal differentiation of lactotroph cells and direct regulation of the prolactin gene both require interactions between Pit-1 and cell type specific partners, including panpituitary transcriptional regulators such as Pitx1 and Pitx2. Synergistic activation of the prolactin promoter by Pitx factors and Pit-1 is involved not only in basal condition, but also in responsiveness to forskolin, thyrotrophin-releasing-hormone and epidermal growth factor. In corticotroph cells, Pitx1 interacts with Tpit. Tpit mutations have turned out to be the main molecular cause of neonatal isolated adrenocorticotrophin deficiency. This finding supports the idea that Tpit plays an essential role in the differentiation of the pro-opiomelanocortin pituitary lineage. The effects of Pit-1 are not restricted to hormone gene regulation because this factor also contributes to cell division and protects the cell from programmed cell death. Lentiviral vectors expressing a Pit-1 dominant negative mutant induced time- and dose-dependent cell death in somatotroph and lactotroph adenomas in vitro. Gene transfer by lentiviral vectors should provide a promising step towards developing an efficient specific therapeutic approach by which a gene therapy programme for treating human pituitary adenomas could be based. [source]

Cross-Sectional Imaging Characteristics of Pituitary Adenomas, Invasive Adenomas and Adenocarcinomas in Dogs: 33 Cases (1988,2006)

Comparative proteomics analysis of human pituitary adenomas: Current status and future perspectives

MASS SPECTROMETRY REVIEWS, Issue 6 2005
Xianquan Zhan
Abstract This article will review the published research on the elucidation of the mechanisms of pituitary adenoma formation. Mass spectrometry (MS) plays a key role in those studies. Comparative proteomics has been used with the long-term goal to locate, detect, and characterize the differentially expressed proteins (DEPs) in human pituitary adenomas; to identify tumor-related and -specific biomarkers; and to clarify the basic molecular mechanisms of pituitary adenoma formation. The methodology used for comparative proteomics, the current status of human pituitary proteomics studies, and future perspectives are reviewed. The methodologies that are used in comparative proteomics studies of human pituitary adenomas are readily exportable to other different areas of cancer research. © 2004 Wiley Periodicals, Inc., Mass Spec Rev 24:783,813, 2005 [source]

Intracranial tumor surgery in patients >70 years of age: is clinical practice worthwhile or futile?

Dynamics of visual improvement following chiasmal decompression.

ACTA OPHTHALMOLOGICA, Issue 5 2002
Quantitative pre-, postoperative observations
ABSTRACT. Purpose:, To study early visual restoration following surgical removal of pituitary adenomas compressing the optic chiasm. Methods:, Eleven patients were examined with high-pass resolution perimetry (HRP) before and after trans-sphenoidal adenomectomy. Visual fields were examined on the second postoperative day. The result was interpreted in terms of the estimated fraction of functioning retino-cortical connections. Results:, In the upper and lower temporal visual field quadrants, the mean increases in the fraction of functioning neural channels were 19% (p <,0.001) and 17% (p =,0.001), respectively, on day 2 after surgery. These increased to 35% on day 12. The nasal hemifield showed no change on day 2, but functioning neural channels had increased by 15% on day 5 (p =,0.017). Mean visual acuity improved from 0.6 preoperatively to 1.0 on day 2 (p =,0.030) but did not change significantly thereafter. Conclusion:, All visual field sectors and visual acuity improved after surgery. Improvement starting in the temporal hemifield was already evident on the second postoperative day. [source]

Outcome of fractionated stereotactic radiotherapy in patients with pituitary adenomas resistant to conventional treatments: a 5·25-year follow-up study

CLINICAL ENDOCRINOLOGY, Issue 1 2010
Camilla Schalin-Jäntti
Summary Objective, To investigate the long-term outcome of fractionated stereotactic radiotherapy (FSRT) [45 Gy (range 45,54) in 25 fractions] in patients with pituitary adenomas characterized by tumour progression or hormonally active disease despite surgery and/or medical therapy. Design, This was an observational follow-up study of 5·25 years (median; range 1·7,10·4). Patients and measurements, Pituitary tumour volume, visual acuity/fields, hypersecretion, hypopituitarism, cerebrovascular disease, second brain tumours and mortality were examined at regular intervals after FSRT in 30 patients with pituitary adenomas (20 nonfunctioning macroadenomas, 10 functioning). Prior to FSRT, 83% had been operated 1,3 times, 47% had visual field deficits/impaired vision and 50% pituitary dysfunction. Progressive disease, stable disease, partial and complete tumour response were defined by MRI. Results, Tumour growth control was 100%. At the end of follow-up, 30% had stable disease, 60% partial and 10% complete tumour response. Visual function was preserved and 36% of patients with prior field deficits improved. GH decreased from 4·2 (range, 2·3,6·5) to 1·1 (range, 0·5,1·5) ,g/l (P < 0·001) in patients with acromegaly, and medical therapy could be reduced. In large prolactinomas, partial response or complete tumour response was achieved. FSRT was well tolerated. Pituitary function remained normal in 27%, 33% of patients had stable dysfunction, 17% deteriorated further and 23% developed new dysfunction. There were no cerebrovascular events, second brain tumours or FSRT-related deaths. Conclusion, According to this long-term follow-up study, FSRT is an efficient and safe adjuvant therapy for pituitary adenomas refractory to conventional treatments. [source]

Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas

CLINICAL ENDOCRINOLOGY, Issue 5 2010
Hwa Young Cho
Summary Objective, The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs). Our goal was to compare the clinical characteristics and natural history between patients with SCAs and non-SCAs. Design/patients, We reviewed the medical records of all patients who underwent transsphenoidal surgery for NFPAs from January 1990 to October 2007 at the Seoul National University Hospital. Measurements, We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients. Results, In total, 28 patients with SCAs and 134 patients with non-SCAs were analysed. The mean age at the time of diagnosis was 44 years (range, 13,67 years) in the SCA group and 50 years (18,79 years) in the non-SCA group (P = 0·026), with respective follow-up periods of 5·2 (range, 1·0,16·0 years) and 4·2 years (0·5,16·1 years) (P = 0·255). Overall recurrence rates of SCAs and non-SCAs were 25·0% and 26·9% respectively (P = 0·839). More than two recurrences (P = 0·001) and recurrence after more than 5 years (P = 0·040) were associated with SCAs. Multiple recurrences of SCAs were confined to younger patients. Conclusion, The overall recurrence rate was similar between SCAs and non-SCAs. However, young patients with SCAs had a higher frequency of multiple and late recurrences, which showed more aggressive tumour behaviour. Therefore, we suggest that patients with SCAs, especially patients diagnosed at a young age, require careful long-term monitoring. [source]

Perioperative plasma active and total ghrelin levels are reduced in acromegaly when compared with in nonfunctioning pituitary tumours even after normalization of serum GH

CLINICAL ENDOCRINOLOGY, Issue 1 2007
Takakazu Kawamata
Summary Objective, Ghrelin is a novel gastric peptide known to stimulate GH secretion, but the relationship between ghrelin and the GH-insulin-like growth factor (IGF)-1 axis in GH excess or deficiency is poorly understood. This study investigated dysregulation of ghrelin secretion in acromegaly and its short-term postoperative recovery. Methods, A prospective study was conducted on eight patients who underwent complete transsphenoidal resection of GH-producing pituitary adenomas (acromegaly group) and 22 for endocrinologically nonfunctioning pituitary tumours (control group). Active and total plasma ghrelin levels were measured serially before and after surgery. Results, Preoperative active and total plasma ghrelin concentrations (mean ± SD; fmol/ml) were significantly reduced in acromegalic patients when compared with those in the controls (9·6 ± 4·3 and 157·4 ± 65·6 vs. 21·8 ± 13·0 and 267·1 ± 111·4; P = 0·023 and P = 0·021, respectively). Both levels were still significantly suppressed on postoperative Day 7 in the acromegaly group when compared with those in the control group (11·7 ± 4·3 and 197·8 ± 68·9 vs. 22·5 ± 12·6 and 302·7 ± 100·0; P = 0·038 and P = 0·018, respectively). The ratios of active to total ghrelin were not significantly different between the two groups before and after operation. In acromegalic patients, active and total ghrelin levels remained significantly suppressed even after normalization of serum GH levels. Conclusions, The putative negative feedback mechanism of GH on ghrelin secretion may in part account for the low ghrelin levels observed in acromegalic patients, and the mechanism may persist even after normalization of serum GH. [source]

Radiosurgery for pituitary adenomas

CLINICAL ENDOCRINOLOGY, Issue 5 2004
M. Brada
First page of article [source]

GH-secreting pituitary adenomas infrequently contain inactivating mutations of PRKAR1A and LOH of 17q23,24

CLINICAL ENDOCRINOLOGY, Issue 4 2003
Hiroyuki Yamasaki
Summary objective The molecular events leading to the development of GH-secreting pituitary tumours remain largely unknown. Gs, (GNAS1) mutations are found in 27,43% of sporadic GH-secreting adenomas in the Caucasian population, but the frequency of GNAS1 mutations in Japanese and Korean acromegalic patients was reported to be lower, 4,9% and 16%, respectively. Other genes responsible for the tumourigenesis of GH-secreting pituitary adenomas have not been detected yet. PRKAR1A, which codes for the RI, regulatory subunit of cyclic AMP-dependent protein kinase A (PKA) on 17q23,24, was recently reported to contain inactivating mutations in some Carney complex families, which involved GH-secreting adenomas in about 10%. We re-evaluated the frequency of GNAS1 mutations and investigated PRKAR1A on the hypothesis that it might play a role in the tumourigenesis of GH-secreting adenomas. design We analysed exons 8 and 9 of GNAS1 and all exons and the exon,intron boundaries of PRKAR1A with the PCR and by direct sequencing using genomic DNA extracted from 32 GH-secreting pituitary adenomas (30 GH-secreting adenomas, two GH and PRL-secreting adenomas) and 28 corresponding peripheral blood samples, and performed loss of heterozygosity (LOH) analysis of 17q23,24 with four microsatellite markers and intragenic markers of PRKAR1A. results Seventeen of 32 (53·1%) tumours showed somatic-activating mutations of GNAS1: 16 (53·3%) of 30 GH-secreting adenomas and one of two GH and PRL-secreting adenomas. Neither inactivating somatic mutations of PRKAR1A nor LOH of 17q23,24 were detected in any of the tumours examined. conclusion We reconfirm the important role of activating mutations of GNAS1 in GH-secreting adenomas, and conclude that PRKAR1A does not play a significant role in the tumourigenesis. [source]

Does normalization of prolactin levels result in weight loss in patients with prolactin secreting pituitary adenomas?

CLINICAL ENDOCRINOLOGY, Issue 4 2002
R. Yermus
No abstract is available for this article. [source]

The release of leptin and its effect on hormone release from human pituitary adenomas

CLINICAL ENDOCRINOLOGY, Issue 6 2001
Márta Korbonits
BACKGROUND Leptin is the protein product of the obese gene, known to play an important role in body energy balance. The leptin receptor exists in numerous isoforms, the long isoform being the major form involved in signal transduction. Leptin expression has recently been demonstrated in the human pituitary, both in normal tissue and in pituitary adenomas. The long isoform of the leptin receptor has also been shown to be present in pituitary adenomas; however, contrasting results have been obtained regarding its expression in the normal human pituitary. AIM The aim of this study was (i) to investigate the presence and pattern of distribution of leptin mRNA and the long isoform of its receptor mRNA in the normal pituitary and in different types of pituitary adenomas with RT-PCR; (ii) to study leptin secretion from human pituitary tumours in culture and (iii) to assess in vitro pituitary hormone release following stimulation with human leptin. RESULTS Leptin receptor long isoform expression was detected in 2/4 GH-secreting adenomas, 12/17 non-functioning adenomas, 5/9 ACTH-secreting adenomas, 1/2 prolactinomas, 2/2 FSH-secreting adenomas and 5/5 normal pituitaries. The receptor long isoform did not segregate with any particular tumour type, and varying levels of expression were detected between the tissues studied. Leptin mRNA was detected at a low level of expression in 2/7 GH-secreting adenomas, 9/14 non-functioning adenomas, 2/3 ACTH-secreting adenomas, 1/3 prolactinomas and 1/3 FSH-secreting adenomas. We were unable to detect leptin mRNA in any of the five normal pituitaries removed at autopsy; however, immunostaining of a non-tumorous pituitary adjacent to an adenoma removed at transsphenoidal surgery showed scattered leptin positive cells. Culture of pituitary adenomas showed that 16/47 released leptin into the incubation media. Leptin release did not correlate with tumour type or with any of the other pituitary hormones released. In vitro leptin stimulation of pituitary tumours caused stimulation of FSH and ,-subunit secretion from a non-functioning adenoma and TSH secretion from a somatotroph adenoma. CONCLUSION We conclude that not only is leptin stored within the pituitary, but it may also be released from pituitary cells and modulate other pituitary hormone secretion. Pituitary leptin may therefore be a novel paracrine regulator of pituitary function. [source]