関: adrenal cortical adenoma

WordNet

of or derived from the cortex of the adrenal glands
a benign epithelial tumor of glandular origin

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/07/03 21:59:17」(JST)

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A adrenocortical adenoma (or adrenal cortical adenoma) is a benign tumor of the adrenal cortex.

It can present with Cushing's syndrome or primary aldosteronism.^[1]

Is a well circumscribed, yellow tumour in the adrenal cortex, which is usually 2-5 cm in diameter. The color of the tumour, as with adrenal cortex as a whole, is due to the stored lipid (mainly cholesterol), from which the cortical hormones are synthesized. These tumors are frequent incidental findings at post mortem examination, and appear to have produced no significant metabolic disorder; only a very small percentage lead to Cushing's syndrome. Nevertheless, these apparently non-functioning adenomas are most often encountered in elder obese people. There is some debate that they may really represent nodules in diffuse nodular cortical hyperplasia. Very occasionally, a true adrenal cortical adenoma is associated with the clinical manifestations of Conn's syndrome, and can be shown to be excreting mineralocorticoids.

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^ "Definition: adrenocortical adenoma from Online Medical Dictionary".

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1. 副腎皮質腫瘍の臨床症状および評価 clinical presentation and evaluation of adrenocortical tumors
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5. 副腎皮質癌の治療 treatment of adrenocortical carcinoma

English Journal

Glutamate receptors and the regulation of steroidogenesis in the human adrenal gland: the metabotropic pathway.

Felizola SJ, Nakamura Y, Satoh F, Morimoto R, Kikuchi K, Nakamura T, Hozawa A, Wang L, Onodera Y, Ise K, McNamara KM, Midorikawa S, Suzuki S, Sasano H.Author information Department of Pathology, Tohoku University Graduate School of Medicine, Sendai, Japan.AbstractBACKGROUND: l-glutamate is a major excitatory neurotransmitter in the mammalian brain. Glutamate receptors have been reported in the rat adrenal cortex and in human aldosterone-producing adenomas (APA). However, details regarding the expression levels and functions of these receptors in human adrenocortical tissues remain unknown.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2014 Jan 25;382(1):170-7. doi: 10.1016/j.mce.2013.09.025. Epub 2013 Sep 27.
BACKGROUND: l-glutamate is a major excitatory neurotransmitter in the mammalian brain. Glutamate receptors have been reported in the rat adrenal cortex and in human aldosterone-producing adenomas (APA). However, details regarding the expression levels and functions of these receptors in human adreno
PMID 24080311

Long-term follow-up in adrenal incidentalomas: an Italian Multicenter Study.

Morelli V, Reimondo G, Giordano R, Della Casa S, Policola C, Palmieri S, Salcuni AS, Dolci A, Mendola M, Arosio M, Ambrosi B, Scillitani A, Ghigo E, Beck-Peccoz P, Terzolo M, Chiodini I.Author information Department of Clinical Sciences and Community Health, University of Milan, Milan.AbstractContext. The long-term consequences of subclinical hypercortisolism (SH) in patients with adrenal incidentalomas (AI) are unknown. Setting-Patients. In this retrospective multicentric study, 206 AI patients with a ≥5 yrs follow-up (median, range: 72.3, 60-186 months) were enrolled. Intervention-Main Outcome Measure. The adrenocortical function, adenoma size, metabolic changes and incident cardiovascular events (CVE) were assessed. We diagnosed SH in 11.6% of patients, in the presence of cortisol after 1mg-dexamethasone suppression test (1mg-DST) >5 μg/dL (138 nmol/L) or ≥2 out of: low ACTH, increased urinary free cortisol and 1mg-DST >3 μg/dL (83 nmol/L). Results. At baseline, age, CVE and type-2 diabetes (T2DM) prevalence were higher in patients with than in patients without SH (62.2±11yrs vs 58.5±10yrs; 20.5% vs 6%; 33.3% vs 16.8%, respectively, P<0.05). SH and T2DM were associated with prevalent CVE (OR 3.1, 95%CI 1.1-9.0 and OR 2.0, 95%CI 1.2-3.3, respectively) regardless of age. At the end of the follow-up, SH was diagnosed in 15 patients without SH at baseline. An adenoma size >2.4 cm was associated with the risk of developing SH (SN 73.3%, SP 60.5%, P=0.014). Weight, glycemic, lipidic and blood pressure control worsened in 26%, 25%, 13% and 34% of patients, respectively. A new CVE occurred in 22 patients. SH was associated with the worsening of ≥2 metabolic parameters (OR 3.32, 95%CI 1.6-6.9) and with incident CVE (OR 2.7, 95%CI 1.0-7.1) regardless of age and follow-up. Conclusion. SH is associated with the risk of incident CVE. Beside the clinical follow-up, in patients with an AI >2.4 cm also a long-term biochemical follow-up is required, for the risk of SH development.
The Journal of clinical endocrinology and metabolism.J Clin Endocrinol Metab.2014 Jan 1:jc20133527. [Epub ahead of print]
Context. The long-term consequences of subclinical hypercortisolism (SH) in patients with adrenal incidentalomas (AI) are unknown. Setting-Patients. In this retrospective multicentric study, 206 AI patients with a ≥5 yrs follow-up (median, range: 72.3, 60-186 months) were enrolled. Intervention-Ma
PMID 24423350

LowER EXPRESSION OF THE TWIK-RELATED ACID-SENSITIVE K+ CHANNEL 2 (TASK-2) GENE IS A HALLMARK OF ALDOSTERONE PRODUCING ADENOMA CAUSING HUMAN PRIMARY ALDOSTERONISM.

Lenzini L, Caroccia B, Campos AG, Fassina A, Belloni AS, Seccia TM, Kuppusamy M, Ferraro S, Skander G, Bader M, Rainey WE, Rossi GP.Author information Internal Medicine 4 &AbstractContext. The molecular mechanisms of primary aldosteronism, a common cause of human hypertension, are unknown, but alterations of K+ channels can play a key role. Objective. To investigate: i) the expression of the Twik-related Acid-Sensitive K+ channels (TASK) in Aldosterone Producing Adenomas (APAs); ii) the role of TASK-2 in aldosterone synthesis; iii) the determinants of TASK-2 blunted expression in APA. Design. We analyzed the transcriptome and the microRNA profiles of 32 consecutive APA and investigated the protein expression and localization of TASK-2 in APA and adrenocortical cell lines (H295R and HAC15) using immunoblotting and confocal microscopy. The functional effect of TASK-2 blunted activity caused by a dominant negative mutation on steroidogenic enzymes and aldosterone production was also assessed. TASK-2 regulation by selected microRNA was studied by a luciferase assay. Results. TASK-2 was consistently less expressed at the transcript and protein level in APAs than in the normal human adrenal cortex. H295R cells transfection with a TASK-2 dominant negative mutant construct significantly increased the aldosterone production by 153% and the gene expression of Aldosterone synthase (CYP11B2, gene expression fold change 3.1 vs control, p<0.05) and of the Steroidogenic acute regulatory protein (STAR) (gene expression fold change 1.8 vs control, p <0.05). Two microRNAs - hsa-miR-23 and hsa-miR-34- were found to decrease TASK-2 expression by binding to the 3' UTR of the TASK-2 gene. Conclusions. The TASK-2 channel lower expression represents a hallmark of APA and is associated to a higher expression of hsa-miR-23 and hsa-miR-34. The ensuing blunted TASK-2 activity increased the production of aldosterone in vitro and the expression of STAR and CYP11B2. Hence, the lower expression of TASK-2 channel in APA cells can explain high aldosterone secretion in human primary aldosteronism in spite of the suppression of angiotensin II, the hypertension and the hypokalemia.
The Journal of clinical endocrinology and metabolism.J Clin Endocrinol Metab.2013 Dec 20:jc20132900. [Epub ahead of print]
Context. The molecular mechanisms of primary aldosteronism, a common cause of human hypertension, are unknown, but alterations of K+ channels can play a key role. Objective. To investigate: i) the expression of the Twik-related Acid-Sensitive K+ channels (TASK) in Aldosterone Producing Adenomas (APA
PMID 24285684

Japanese Journal

原発性アルドステロン症に併発したサブクリニカルクッシング症候群が症候性に移行した1例

稲垣裕介,植村元秀,中田渡 [他],中井康友,高山仁志,辻村晃,野々村祝夫,北村哲宏,大月道夫
泌尿器科紀要 = Acta urologica Japonica 59(11), 719-722, 2013-11
… The histopathological examination revealed an adrenocortical adenoma. …
NAID 120005350254

4. 副腎の外科(<特集>内分泌外科の現状と将来)

今井常夫
日本外科学会雑誌 113(6), 496-501, 2012-11-01
NAID 110009554102

An unusual presentation of Carney complex with diffuse primary pigmented nodular adrenocortical disease on one adrenal gland and a nonpigmented adrenocortical adenoma and focal primary pigmented nodular adrenocortical disease on the other