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Non-functioning Adenoma (non-functioning + adenoma)

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Medical Sciences	100%

Selected Abstracts

Clinical outcomes and learning curve of a laparoscopic adrenalectomy in 103 consecutive cases at a single institute

INTERNATIONAL JOURNAL OF UROLOGY, Issue 6 2006
MASATOSHI ETO
Objective:, We examined the clinical outcomes and the learning curve for a laparoscopic adrenalectomy (LA) in 103 consecutive cases performed by three surgeons at our institute, according to the type of adrenal disorder. Patients and Methods:, One hundred and three patients with adrenal tumors, including 38 cases of primary aldosteronism, 33 cases of Cushing syndrome (including preclinical Cushing syndrome), 15 cases of pheochromocytoma, and nine cases of non-functioning adenoma were evaluated, while focusing on the approaches, intraoperative and postoperative data, and the learning curve of LA, according the type of adrenal disorder. Results:, There was no significant difference in the operation time, estimated blood loss, incidence of conversion to open surgery and blood transfusion, or postoperative recovery among the patients treated by LA for aldosteronoma, Cushing adenoma, pheochromocytoma, and non-functioning adenoma. In the cases of aldosteronoma and Cushing adenoma, the learning curve for the operation time and blood loss in each operator tended to decrease as the number of operations increased. On the other hand, in the cases treated by LA for pheochromocytoma, no trends in either the operation time or blood loss were observed. However, there has been neither any conversion to open surgery nor blood transfusion in cases treated by LA since 1998 (our 42nd case), even after the changes in the operators. Conclusions:, Our results clearly indicate that LA is becoming safer than before, probably due to improvements in the technique, education, and training of surgeons, in addition to the increased number of cases now treated by LA. [source]

Adrenal myelolipoma associated with adenoma

INTERNATIONAL JOURNAL OF UROLOGY, Issue 5 2004
FRANCESCA MANASSERO
Abstract The association of an adrenal myelolipoma with a non-functioning adenoma is very rare. Herein, we report on such a case in an asymptomatic 64-year-old woman. To the best of our knowledge, there is only one other case of non-functioning adrenocortical adenoma associated with myelolipoma in the same gland. Furthermore, only two other adenomas (mineral corticoids and corticosteroid producing tumors) associated with myelolipomas have been reported, and both myelolipomas were less than 1 cm in size. In conclusion, the 8.5 cm myelolipoma in our case is the largest compared with the three previously reported ones. [source]

Late Lyme disease masking a non-functioning adenoma of the anterior lobe of the pituitary gland

ANDROLOGIA, Issue 3 2002
M. Möhrenschlager
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]

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]

Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry

INTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2005
KOUSUKE TAKEHARA
Abstract Background: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms. Methods: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas. Isolated nuclei from frozen samples were used for fluorescence in situ hybridization (FISH) analysis, and formalin-fixed, paraffin-embedded tissues from the same materials were analyzed using flow cytometry (FCM) for DNA ploidy. Sections from paraffin blocks were stained immunohistochemically with antibodies against Ki-67 and p53. For FISH analysis, we used an ,-centromeric enumeration probe for chromosome 17. Results: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7). In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type. Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004). Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas. Only the latter two cases strongly expressed p53 protein. Conclusions: Our study characterized various biological features of benign and malignant adrenal cortical tumors. The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor. [source]