糖質コルチコイド抑制性高アルドステロン症
WordNet
- a steroid hormone that is produced by the adrenal cortex of animals; affects functioning of gonads and has anti-inflammatory activity
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English Journal
- Aldosterone- and cortisol-co-secreting adrenal tumors: the lost subtype of primary aldosteronism.
- Späth M, Korovkin S, Antke C, Anlauf M, Willenberg HS.Author information Department of Endocrinology, Diabetes and Rheumatology Clinic of Nuclear Medicine Institute of Pathology, University Hospital Duesseldorf, Moorenstrasse 5, D-40225 Duesseldorf, Germany.AbstractCurrent guidelines suggest proving angiotensin-independent aldosterone secretion in patients with primary aldosteronism (PA). It is further recommended to demonstrate unilateral disease because of its consequence for therapy. A general screening for excess secretion of other hormones is not recommended. However, clinically relevant autonomous aldosterone production rarely originates in adrenal tumors, compromised of zona glomerulosa cells only. This article reviews published data on aldosterone- and cortisol-co-secreting tumors and shows that pre-operative diagnosis of such a lesion is beneficial for patients. Overt or subclinical glucocorticoid hypersecretion may interfere with diagnostic studies, e.g. adrenal venous sampling, screening of familial forms of PA on the basis of serum 18-hydroxy-cortisol (18-OH-F) determination, and provoke glucocorticoid deficiency after surgical removal of the tumor. In addition, knowledge from histological and molecular studies in patients with aldosterone- and cortisol-co-secreting tumors challenges some concepts of the development of adrenal autonomy. The presence of an aldosterone- and cortisol-co-secreting adrenocortical tumor should be considered if a patient has i) PA and an adenoma that is larger than 2.5 cm, ii) cortisol that is non-suppressible with overnight low-dose dexamethasone, or iii) grossly elevated serum levels of hybrid steroids, such as 18-OH-F.
- European journal of endocrinology / European Federation of Endocrine Societies.Eur J Endocrinol.2011 Apr;164(4):447-55. doi: 10.1530/EJE-10-1070. Epub 2011 Jan 26.
- Current guidelines suggest proving angiotensin-independent aldosterone secretion in patients with primary aldosteronism (PA). It is further recommended to demonstrate unilateral disease because of its consequence for therapy. A general screening for excess secretion of other hormones is not recommen
- PMID 21270113
- Association of adrenal medullar and cortical nodular hyperplasia: a report of two cases with clinical and morpho-functional considerations.
- Valdés G, Roessler E, Salazar I, Rosenberg H, Fardella C, Martínez P, Velasco A, Velasco S, Orellana P.Author information Departamentos de Nefrología, Anatomía Patológica, Endocrinología, Urología, y Radiología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile. gvaldes@med.puc.clAbstractArterial hypertension of adrenal etiology is mainly attributed to primary hyperaldosteronism. However, subtle expressions of hyperadrenergic or glucocorticoid excess can also generate arterial hypertension. The present report describes two hypertensive patients cataloged as resistant essential hypertensives, in whom adrenal masses were found incidentally, who highlight the need to recognize these tenuous clinical or laboratory presentations. Case 1 was a 50-yr-old female with hyperadrenergic hypertension associated to a left adrenal node, normal cortisol and aldosterone:renin ratio, marginally increased urinary normetanephrine, and a positive 131I MIBG radioisotope scan. Adrenalectomy normalized blood pressure and urinary metanephrines. Pathology showed a hyperplastic adrenal medulla associated to a multinodular cortical hyperplasia. Case 2 was a 62- yr-old female with progressive hypertension, a slight Cushing phenotype, non-suppressible hypercortisolism, normal urinary metanephrines, and bilateral adrenal nodes. Bilateral adrenalectomy and subsequent replacement normalized blood pressure and phenotypic stigmata. Pathology demonstrated bilateral cortical multinodular hyperplasia and medullary hyperplasia. The clinical study in both patients was negative for MEN. The apparently rare association of cortical and medullary lesions presented by both patients is probably overlooked in routine pathology exams, but should be meticulously searched since the crosstalk between the adrenal cortex and medulla may prompt dual abnormalities.
- Endocrine.Endocrine.2006 Dec;30(3):389-96.
- Arterial hypertension of adrenal etiology is mainly attributed to primary hyperaldosteronism. However, subtle expressions of hyperadrenergic or glucocorticoid excess can also generate arterial hypertension. The present report describes two hypertensive patients cataloged as resistant essential hyper
- PMID 17526953
- The utility of three different methods for measuring urinary 18-hydroxycortisol in the differential diagnosis of suspected primary hyperaldosteronism.
- Reynolds RM, Shakerdi LA, Sandhu K, Wallace AM, Wood PJ, Walker BR.Author information Endocrinology Unit, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, UK. r.reynolds@ed.ac.ukAbstractOBJECTIVE: Urine 18-hydroxycortisol (18-OHF) measurements are claimed to discriminate between primary hyperaldosteronism due to Conn's syndrome/adrenal adenoma or idiopathic bilateral adrenal hyperplasia (BAH), and also to identify cases of glucocorticoid-suppressible hyperaldosteronism (GSH). We have evaluated three urine 18-OHF methods using a panel of urine samples from patients with hypertension.
- European journal of endocrinology / European Federation of Endocrine Societies.Eur J Endocrinol.2005 Jun;152(6):903-7.
- OBJECTIVE: Urine 18-hydroxycortisol (18-OHF) measurements are claimed to discriminate between primary hyperaldosteronism due to Conn's syndrome/adrenal adenoma or idiopathic bilateral adrenal hyperplasia (BAH), and also to identify cases of glucocorticoid-suppressible hyperaldosteronism (GSH). We ha
- PMID 15941931
Japanese Journal
- 特発性アルドステロン症と糖質コルチコイド奏効性アルドステロン症
- Glucocorticoid-responsive hyperaldosteronism自験例の21年にわたる検討成績とその病態:本邦17α-hydroxylase欠損症報告例との対比
- Normotensive Glucocorticoid-Suppressible Hyperaldosteronism in Adult.
Related Links
- View This Abstract Online Glucocorticoid-suppressible hyperaldosteronism: effects of crossover site and parental origin of chimaeric gene on phenotypic expression. Clin Sci (Lond). 1995; 88(5):563-70 (ISSN: 0143-5221) Jamieson A ...
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★リンクテーブル★
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- 英
- glucocorticoid suppressible hyperaldosteronism, GSH
- 同
- デキサメタゾン抑制性高アルドステロン症 dexamethasone suppressible hyperaldosteronism DSH
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- 関
- repressible
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糖質コルチコイド
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高アルドステロン症