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Pituitary Tumours (pituitary + tumour)
Selected AbstractsIntracytoplasmic sperm injection as a complement to gonadotrophin treatment in infertile men with hypogonadotrophic hypogonadismINTERNATIONAL JOURNAL OF ANDROLOGY, Issue 4 2005BRANKO ZORN Summary In this study we sought to determine whether intracytoplasmic sperm injection (ICSI) could improve the efficacy of treatment with gonadotrophins in gonadotrophin-deficient men in terms of pregnancy. A series of six adult men (aged 26,47 years) with hypogonadotrophic hypogonadism (HH) is reported: four men with prepubertal isolated idiopathic HH (IIHH) and two adult-onset HH, as part of hypopituitarism secondary to surgical treatment of a pituitary tumour. All were azoospermic. To restore spermatogenesis, all received hormonal treatment with intramuscular human menopausal gonadotrophins (HMG) and human chorionic gonadotrophin (HCG) for 2 to 23 months. High basal serum inhibin B was predictive of rapid and complete recovery of spermatogenesis. In the two adult-onset HH, a natural pregnancy was achieved within 3 months. The four men with IIHH underwent ICSI because of poor sperm quality. ICSI using fresh or frozen-thawed ejaculated spermatozoa was performed after 6,23 months of gonadotrophin treatment. ICSI provided good clinical results in terms of fertilization and embryo quality, and resulted in three pregnancies that ended in three term deliveries. In men with oligozoospermia related to prepubertal IIHH, ICSI shortens the hormonal treatment and enhances the chances of pregnancy. [source] Suspected pituitary apoplexy in a German shorthaired pointerJOURNAL OF SMALL ANIMAL PRACTICE, Issue 11 2003S. N. Long Pituitary apoplexy is a syndrome which has been described in humans caused by acute haemorrhage or infarction within a pituitary tumour or a non-tumorous pituitary gland. This report describes the authors'observations of a dog in which vomiting, visual disturbances, seizures, altered consciousness and diencephalic dysfunction occurred in association with haemorrhage originating from a pituitary macroadenoma. The clinical signs were thought to be consistent with disruption of the hypothalamus and brainstem, together with raised intracranial pressure due to intraventricular haemorrhage. These signs, and the pathological findings, bear a striking resemblance to those associated with the syndrome of pituitary apoplexy, seen in humans. [source] Radiation-induced brain disorders in patients with pituitary tumoursJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 3 2004A Bhansali Summary Radiation-induced brain disorders (RIBD) are uncommon and they are grave sequelae of conventional radiotherapy. In the present report, we describe the clinical spectrum of RIBD in 11 patients who received post-surgery conventional megavoltage irradiation for residual pituitary tumours. Of these 11 patients (nine men, two women), seven had been treated for non-functioning pituitary tumours and four for somatotropinomas. At the time of irradiation the age of these patients ranged from 30 to 59 years (mean, 39.4 ± 8.3; median, 36) with a follow-up period of 6,96 months (mean, 18.3 ± 26.4; median, 11). The dose of radiation ranged from 45 to 90 Gy (mean, 51.3 ± 13.4; median, 45), which was given in 15,30 fractions (mean, 18.6 ± 5.0; median, 15) with 2.8 ± 0.3 Gy (median, 3) per fraction. The biological effective dose calculated for late complications in these patients ranged from 78.7 to 180 Gy (mean, 99.1 ± 27.5; median, 90). The lag time between tumour irradiation and the onset of symptoms ranged from 6 to 168 months (mean, 46.3 ± 57.0; median, 57). The clinical spectrum of RIBD included new-onset visual abnormalities in five, cerebral radionecrosis in the form of altered sensorium in four, generalized seizures in four, cognitive dysfunction in five, dementia in three and motor deficits in two patients. Magnetic resonance imaging (MRI)/CT of the brain was suggestive of radionecrosis in eight, cerebral oedema in three, cerebral atrophy in two and second neoplasia in one patient. Associated hormone deficiencies at presentation were hypogonadism in eight, hypoadrenalism in six, hypothyroidism in four and diabetes insipidus in one patient. Autopsy in two patients showed primitive neuroectodermal tumour (PNET) and brainstem radionecrosis in one, and a cystic lesion in the left frontal lobe following radionecrosis in the other. We conclude that RIBD have distinctive but varying clinical and radiological presentations. Diabetes insipidus and PNET as a second neoplastic disorder in adults following pituitary irradiation have not been reported previously. [source] Attribution of tumour lethality and estimation of the time to onset of occult tumours in the absence of cause-of-death InformationJOURNAL OF THE ROYAL STATISTICAL SOCIETY: SERIES C (APPLIED STATISTICS), Issue 2 2000H. Ahn A new statistical approach is developed for estimating the carcinogenic potential of drugs and other chemical substances used by humans. Improved statistical methods are developed for rodent tumorigenicity assays that have interval sacrifices but not cause-of-death data. For such experiments, this paper proposes a nonparametric maximum likelihood estimation method for estimating the distributions of the time to onset of and the time to death from the tumour. The log-likelihood function is optimized using a constrained direct search procedure. Using the maximum likelihood estimators, the number of fatal tumours in an experiment can be imputed. By applying the procedure proposed to a real data set, the effect of calorie restriction is investigated. In this study, we found that calorie restriction delays the tumour onset time significantly for pituitary tumours. The present method can result in substantial economic savings by relieving the need for a case-by-case assignment of the cause of death or context of observation by pathologists. The ultimate goal of the method proposed is to use the imputed number of fatal tumours to modify Peto's International Agency for Research on Cancer test for application to tumorigenicity assays that lack cause-of-death data. [source] How reliably can autoimmune hypophysitis be diagnosed without pituitary biopsyCLINICAL ENDOCRINOLOGY, Issue 1 2010Trevor A. Howlett Summary Autoimmune hypophysitis is a rare chronic inflammatory condition of the pituitary gland which typically presents with hypopituitarism and a pituitary mass. Cases involving anterior pituitary alone (65%) are six times more common in women, typically presenting during pregnancy or postpartum (57%). Anterior and posterior pituitary involvement (25%) are twice as common in women, and neurohypophysis alone (10%) occurs equally in both sexes. It has a prevalence of around 5 per million, an annual incidence of 1 in 7 to 9 million and in our experience represents the known or suspected cause of 0·5% of cases of hypopituitarism, <1% of pituitary masses and 2% of nonfunctioning macro lesions presenting to an endocrine clinic. However, ,missed' cases of autoimmune hypophysitis may be the aetiology of some other unexplained cases of hypopituitarism. Clinically, headache and visual disturbance are common. Anterior hypopituitarism shows a characteristic but atypical pattern of deficiency of ACTH followed by TSH, gonadotrophins and prolactin deficiency or hyperprolactinaemia. Eighteen percent of cases have evidence of another autoimmune condition. On magnetic resonance imaging (MRI), autoimmune hypophysitis is typically symmetrical and homogeneous with thickened but undisplaced stalk in contrast to typical findings with pituitary tumours. Ultimately, the histological diagnosis of autoimmune hypophysitis can only be confirmed by surgery but a presumptive diagnosis can often be made on the basis of a combination of context and clinical features, and pituitary biopsy is not always clinically necessary for effective clinical management of the patient. [source] Immunohistochemical localization of somatostatin receptor subtypes in benign and malignant adrenal tumoursCLINICAL ENDOCRINOLOGY, Issue 6 2008Nicole Unger Summary Background, Somatostatin mediates its action through five receptor subtypes (sst1,5) that are widely distributed in various endocrine tissues and tumours. Because of the inhibitory effects of somatostatin, long-acting analogues have been synthesized. In contrast to their well-established use in neuroendocrine and pituitary tumours, little is known about their potential use in adrenal tumours. Objective, We examined somatostatin receptor protein expression in adrenal tumours of various aetiologies. Immunostaining was performed with specific polyclonal antibodies for sst1,5. Design, Seven benign and eight malignant pheochromocytomas (PHEOs), eight aldosterone-secreting adenomas (APAs), nine cortisol-secreting adenomas (CPAs), seven nonfunctioning adrenal tumours (NFAs) and 25 adrenal carcinomas (CAs) as well as eight normal adrenal glands were investigated. Measurements, Staining pattern, distribution and subcellular localization of the somatostatin receptor subtypes were evaluated. Results, In the majority of normal cortices the expression of sst1,5 was limited to the reticular zone. The medulla was predominantly positive for sst3. Most cortical adenomas were positive for all five subtypes. However, in the majority of these tumours, less than 30% of cells were positively stained. A high expression of sst4 was found in CPAs but only very few cortical carcinomas exhibited sst immunostaining. All benign PHEOs were positive for sst3. The majority presented with more than 60% of tumour cells stained. By contrast, only six out of eight malignant PHEOs were positive for sst3. Conclusions, Somatostatin receptor subtypes are expressed in PHEOs as well as in tumours of the adrenal cortex with tumour-specific distribution patterns. This may offer new diagnostic and therapeutic possibilities. [source] Surgical debulking of pituitary macroadenomas causing acromegaly improves control by lanreotideCLINICAL ENDOCRINOLOGY, Issue 6 2008N. Karavitaki Summary Background, Macroadenomas causing acromegaly are cured surgically in only around 50% of patients. Primary medical treatment with somatostatin analogues has been suggested to be a means of treating patients with a potentially poor surgical outcome. Previous retrospective studies have also suggested that surgical debulking of pituitary tumours causing acromegaly improves control by somatostatin analogues. No prospective study using lanreotide has been carried out thus far to assess whether this is the case. Objective, We carried out a prospective study to assess whether surgical debulking of pituitary macroadenomas causing acromegaly improved the subsequent control of acromegaly by the somatostatin analogue lanreotide. Patients and methods, We treated 26 consecutive patients [10 males and 16 females , median age 53·5 years (range 22,70)] with macroadenoma causing acromegaly unselected for somatostatin response for 16 weeks with lanreotide, maximizing GH and IGF-I suppression, if necessary, by incremental dosing. Surgical resection was carried out and the patients were re-assessed off medical treatment at 16 weeks following surgery. Those with nadir GH > 2 mU/l in the oral glucose tolerance test (OGTT) and a mean GH in the GH day curve (GHDC) > 5 mU/l were subsequently restarted on lanreotide and the responses were assessed at the same time points as during the preoperative lanreotide treatment. Results, GH values fell on lanreotide treatment and prior to surgery they were considered ,safe' (mean GH in GHDC < 5 mU/l) in eight patients (30·7%). After surgery, they were ,safe' in 18 patients (69·2%). The figures for normal IGF-I were 11 (42·3%) before surgery and 23 (88·5%) after surgery. After surgery, six patients had nadir GH > 2 mU/l in the OGTT and ,unsafe' GH levels (mean GH in GHDC > 5 mU/l); on re-exposure to lanreotide, GH levels fell in all patients and at the end of 16 weeks postsurgery, they were ,safe' in three of them (50%) (P < 0·05). Pituitary tumour volume was also assessed prospectively, preoperatively on lanreotide and showed a mean fall of 33·1%. Eighty-three percent of patients had > 20% shrinkage. Conclusions, In this first prospective study using lanreotide, surgical debulking of pituitary tumours causing acromegaly improved subsequent postoperative control by the somatostatin analogue lanreotide. Surgery should, therefore, be considered in patients with macroadenoma causing acromegaly, even if there is little prospect of surgical cure. Lanreotide causes significant pituitary tumour shrinkage in the majority of patients. [source] Age-related penetrance of endocrine tumours in multiple endocrine neoplasia type 1 (MEN1): a multicentre study of 258 gene carriersCLINICAL ENDOCRINOLOGY, Issue 4 2007Andreas Machens Summary Objective, In multiple endocrine neoplasia type 1 (MEN1), age-related tumour penetrance according to the type of MEN1 germline mutation has not been investigated in-depth. This study was conducted to examine whether carriers of out-of-frame/truncating and in-frame MEN1 mutations differ in age-related tumour penetrance. Design, A multicentre study with biochemical, hormonal and radiological screening for MEN1-associated tumours. Patients, A total of 258 MEN1 carriers from six major German tertiary referral centres averaging 43 years of age at last follow-up. Measurements, Main outcome measure was time to first diagnosis of MEN1-associated tumours. Results, Independent of the year of birth and observation period, time to first tumour diagnosis did not vary much by the type of MEN1 germline mutation or endocrine organ system, and perhaps not even by the type of endocrine tumour when the amount of time was considered by which the diagnosis probably has been advanced through the manifestation of hormonal symptoms. Parathyroid hyperplasia and adenomas developed almost twice as often as enteropancreatic and pituitary tumours (77%vs. 49,32%), and more than five to sevenfold as often as adrenal cortical tumours and carcinoids (77%vs. 15,10%), reaching penetrance rates of up to 90%, 60%, 40%, 26% and 17%, respectively. The heterogeneity of tumour penetrance was marked, ranging from 9 years to 25 years for the earliest, and from 68 years to 77 years for the latest tumour manifestation. Conclusions, Because of our inability of predicting tumour penetrance and malignant transformation individually, life-long follow-up of MEN1 carriers is warranted to prevent tumour morbidity. [source] Perioperative plasma active and total ghrelin levels are reduced in acromegaly when compared with in nonfunctioning pituitary tumours even after normalization of serum GHCLINICAL ENDOCRINOLOGY, Issue 1 2007Takakazu 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] GH-secreting pituitary adenomas infrequently contain inactivating mutations of PRKAR1A and LOH of 17q23,24CLINICAL ENDOCRINOLOGY, Issue 4 2003Hiroyuki 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] The release of leptin and its effect on hormone release from human pituitary adenomasCLINICAL ENDOCRINOLOGY, Issue 6 2001Márta 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] | ||||||||||