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1. Chiou TT, Chiang PH, Fuh M, Liu RT, Lee WC, Lee WC, Ng HY, Tsai YC, Chuang FR, Huang CC, Lee CT: Factors determining cardiovascular and renal outcomes after adrenalectomy in patients with aldosterone-producing adrenal adenoma. Tohoku J Exp Med; 2009 May;218(1):17-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Factors determining cardiovascular and renal outcomes after adrenalectomy in patients with aldosterone-producing adrenal adenoma.
  • Primary aldosteronism is an important cause of secondary hypertension, because it is potentially curable, especially in case of unilateral aldosterone-producing adrenal adenoma (APA).
  • Adrenalectomy successfully normalized or improved hypertension, hypokalemia, and aldosterone excess.
  • Pre-operative systolic blood pressure (BP), diastolic BP, and post-operative plasma aldosterone concentrations were the only variables significantly different between the hypertensive and normotensive patients.
  • In conclusion, pre-operative BP and post-operative plasma aldosterone are important in predicting post-adrenalectomy hypertension, and a lower pre-operative plasma renin predicts the improvement in renal function after adrenalectomy.
  • [MeSH-major] Adrenal Cortex Neoplasms. Adrenalectomy. Adrenocortical Adenoma. Aldosterone / blood. Cardiovascular System / metabolism. Hypertension. Kidney

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  • (PMID = 19398869.001).
  • [ISSN] 1349-3329
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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2. Sakamoto N, Tojo K, Saito T, Fujimoto K, Isaka T, Tajima N, Ikeda K, Yamada H, Furuta N, Sasano H: Coexistence of aldosterone-producing adrenocortical adenoma and pheochromocytoma in an ipsilateral adrenal gland. Endocr J; 2009;56(2):213-9
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  • [Title] Coexistence of aldosterone-producing adrenocortical adenoma and pheochromocytoma in an ipsilateral adrenal gland.
  • A 40-year-old female, diagnosed as essential hypertension, demonstrated a 2 cm mass in left adrenal gland by computed tomography without abnormal endocrinological findings. (131)I-adosterol and (123)I-metaiodobenzylguanidine (MIBG) scintigraphy at 39 years of age showed no abnormal accumulation.
  • Follow up (131)I-adosterol scintigraphy performed one year later showed apparently abnormal uptake and slightly elevated uptake in left adrenal gland.
  • Endocrinological date revealed suppressed plasma renin activity, and elevated plasma aldosterone concentration, and noradrenalin levels.
  • Furthermore, selective adrenal venous sampling with intravenous ACTH infusion indicated aldosterone-producing adrenocortical adenoma (APA) in left adrenal gland.
  • During operation of adrenal tumor, blood pressure elevated markedly and complication of pheochromocytoma (PC) was suspected.
  • Immunohistochemical findings after left adrenolectomy revealed that the adrenal mass was compatible with APA and PC.
  • Herein, we present an extremely rare case of the simultaneous occurrence of both APA and PC in an ipsilateral adrenal gland.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenocortical Adenoma / pathology. Pheochromocytoma / pathology
  • [MeSH-minor] Adrenal Cortex Neoplasms / pathology. Adrenal Glands / pathology. Adult. Aldosterone / blood. Female. Humans. Hypokalemia / complications. Incidental Findings. Neoplasms, Multiple Primary. Tomography, X-Ray Computed

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  • (PMID = 19023159.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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3. Rossi GP, Belfiore A, Bernini G, Desideri G, Fabris B, Ferri C, Giacchetti G, Letizia C, Maccario M, Mallamaci F, Mannelli M, Palumbo G, Rizzoni D, Rossi E, Agabiti-Rosei E, Pessina AC, Mantero F, Primary Aldosteronism Prevalence in Italy Study Investigators: Comparison of the captopril and the saline infusion test for excluding aldosterone-producing adenoma. Hypertension; 2007 Aug;50(2):424-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of the captopril and the saline infusion test for excluding aldosterone-producing adenoma.
  • We performed a prospective head-to-head comparison of the accuracy of the captopril test (CAPT) and the saline infusion test (SAL) for confirming primary aldosteronism due to an aldosterone-producing adenoma (APA) in patients with different sodium intake.
  • They were composed of the patients with a high aldosterone/renin ratio baseline and 1 every 4 patients without such criterion.
  • The accuracy of post-CAPT or post-SAL plasma aldosterone values for diagnosing APA was estimated with the area under the receiver operator characteristics curves.
  • The area under the receiver operator characteristics curve of plasma aldosterone for both tests was higher (P<0.0001) than that under the diagonal, but the between-test difference was borderline significant (P=0.054).
  • The optimal aldosterone cutoff value for identifying APA was 13.9 and 6.75 ng/dL for the CAPT and SAL, respectively.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Captopril. Hyperaldosteronism / diagnosis. Sodium Chloride

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  • (PMID = 17592070.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 451W47IQ8X / Sodium Chloride; 9G64RSX1XD / Captopril
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4. Mete O, Asa SL: Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions. Endocr Pathol; 2009;20(3):182-5
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  • [Title] Aldosterone-producing adrenal cortical adenoma with oncocytic change and cytoplasmic eosinophilic globular inclusions.
  • We report an interesting morphological alteration in the adrenal of a 72-year-old woman suffering from severe hypertension due to primary hyperaldosteronism.
  • The laparoscopic left adrenalectomy specimen revealed an adrenal cortical adenoma composed of varying proportions of oncocytic and clear cells, predominantly showing central oncocytic change.
  • Oncocytes also exhibited numerous eosinophilic intracytoplasmic globular inclusions, which are not commonly observed in aldosterone-producing adrenal cortical adenomas.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Aldosterone / secretion. Inclusion Bodies / pathology

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  • (PMID = 19462261.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 4964P6T9RB / Aldosterone
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5. Guthoff M, Schnauder G, Kirchhoff K, Kurth R, Horger M, Müssig K: [Normokalaemic primary aldosteronism due to an aldosterone-producing adrenal adenoma--Case 06/2009]. Dtsch Med Wochenschr; 2009 Jul;134(31-32):1582
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  • [Title] [Normokalaemic primary aldosteronism due to an aldosterone-producing adrenal adenoma--Case 06/2009].
  • Plasma renin activity was reduced and both the plasma aldosterone concentration and the aldosterone to renin ratio were elevated.
  • A saline infusion test showed no suppression of the plasma aldosterone concentration, nor did an orthostatic testing show an increase.
  • MRI revealed an adenoma of the right adrenal gland.
  • DIAGNOSIS, TREATMENT AND COURSE: The results were consistent with primary aldosteronism due to an aldosterone-producing adenoma of the adrenal gland.
  • The histological findings confirmed an adenoma of the adrenal gland.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / diagnosis. Hyperaldosteronism / etiology
  • [MeSH-minor] Adrenalectomy / methods. Adult. Aldosterone / blood. Aldosterone / secretion. Diagnosis, Differential. Humans. Hypertension / etiology. Laparoscopy. Magnetic Resonance Imaging. Male. Renin / blood

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  • (PMID = 19629922.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin
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6. Karagiannis A, Tziomalos K, Kakafika AI, Athyros VG, Harsoulis F, Mikhailidis DP: Medical treatment as an alternative to adrenalectomy in patients with aldosterone-producing adenomas. Endocr Relat Cancer; 2008 Sep;15(3):693-700
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  • [Title] Medical treatment as an alternative to adrenalectomy in patients with aldosterone-producing adenomas.
  • Primary aldosteronism (PA) and, in particular, its two commonest subtypes (i.e. idiopathic hyperaldosteronism (IHA) and aldosterone-producing adenoma (APA)) have been recognized as the most common cause of secondary hypertension.
  • While 'conservative' medical treatment with aldosterone receptor antagonists is the therapeutic approach of choice in controlling blood pressure in patients with PA due to IHA, the more invasive (laparoscopic) adrenalectomy seems to be the most suitable therapy for patients with APA.
  • In this review, we focus on the medical approach for the management of APA in cases where surgical excision of the adrenal is not possible.
  • [MeSH-major] Adrenal Cortex Neoplasms / drug therapy. Adrenocortical Adenoma / drug therapy. Mineralocorticoid Receptor Antagonists / therapeutic use
  • [MeSH-minor] Adrenalectomy. Aldosterone / secretion. Humans. Hyperaldosteronism / drug therapy. Hyperaldosteronism / etiology

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  • (PMID = 18586836.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 4964P6T9RB / Aldosterone
  • [Number-of-references] 84
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7. Nogueira EF, Gerry D, Mantero F, Mariniello B, Rainey WE: The role of TASK1 in aldosterone production and its expression in normal adrenal and aldosterone-producing adenomas. Clin Endocrinol (Oxf); 2010 Jul;73(1):22-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of TASK1 in aldosterone production and its expression in normal adrenal and aldosterone-producing adenomas.
  • OBJECTIVES: Aldosterone production in the adrenal glomerulosa is mainly regulated by angiotensin II and K+.
  • Adrenal glomerulosa cells are uniquely sensitive to extracellular K+.
  • Genetic deletion of subunits of K+-selective leak-channels (KCNK), TASK1 and/or TASK3, in mice generates animals with hyperaldosteronism and histological changes in the adrenal cortex.
  • Herein, we studied the expression of TASK1 in human adrenocortical cells, as well as its role in aldosterone production in H295R cells.
  • DESIGN: TASK1 expression was investigated by comparative microarray analysis of aldosterone-producing adenomas (APA) and normal adrenals (NAs).
  • Knockdown of TASK1 (with siRNA) induced the expression of steroidogenic acute regulatory (StAR) protein and aldosterone synthase (CYP11B2), and also stimulated pregnenolone and aldosterone production.
  • CONCLUSIONS: Our study reveals the predominant expression of TASK1 over other KCNK family genes in the human adrenal cortex.
  • Herein, we also described the role of TASK1 in the regulation of human aldosterone production through regulation of intracellular Ca2+ and CaMK signalling pathways.

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  • (PMID = 19878209.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK043140; United States / NIDDK NIH HHS / DK / R01 DK043140-16S1; United States / NIDDK NIH HHS / DK / DK43140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / KCNK1 protein, human; 0 / Kcnk1 protein, mouse; 0 / Nerve Tissue Proteins; 0 / Potassium Channels, Tandem Pore Domain; 0 / RNA, Small Interfering; 0 / potassium channel subfamily K member 3; 4964P6T9RB / Aldosterone; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
  • [Other-IDs] NLM/ NIHMS156002; NLM/ PMC4158746
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8. Cartier D, Jégou S, Parmentier F, Lihrmann I, Louiset E, Kuhn JM, Bastard C, Plouin PF, Godin M, Vaudry H, Lefebvre H: Expression profile of serotonin4 (5-HT4) receptors in adrenocortical aldosterone-producing adenomas. Eur J Endocrinol; 2005 Dec;153(6):939-47

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profile of serotonin4 (5-HT4) receptors in adrenocortical aldosterone-producing adenomas.
  • OBJECTIVE: We aimed to investigate the expression profile of serotonin4 (5-HT4) receptors in adrenocortical aldosterone-producing adenoma (APA) tissues in comparison with normal adrenal cortex.
  • DESIGN AND METHODS: Total 5-HT4 receptor mRNAs were quantified by real-time quantitative polymerase chain reaction (PCR) assay, and the mRNAs encoding the 5-HT4 receptor isoforms were characterized by reverse transcription (RT)-PCR in seven normal adrenal cortices and 11 APA tissues.
  • The distribution of 5-HT4 receptor mRNAs was investigated by in situ hybridization in both normal adrenal and APA tissues, and the presence of 5-HT in APA tissues was studied by immunohistochemistry.
  • In situ hybridization studies showed that 5-HT4 receptor mRNAs were expressed in both zona glomerulosa and zona fasciculata/reticularis of the normal cortex and in groups of APA steroidogenic cells disseminated in the tumor tissues.
  • They also demonstrate the presence of 5-HT in both mast cells and tumor steroidogenic cells, providing evidence for a possible autocrine/paracrine activation of aldosterone secretion within adenoma tissues.

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  • (PMID = 16322401.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 158165-40-3 / Receptors, Serotonin, 5-HT4; 4964P6T9RB / Aldosterone
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9. Rossi GP, Sticchi D, Giuliani L, Bernante P, Zavattiero S, Pessina AC, Nussdorfer GG: Adiponectin receptor expression in the human adrenal cortex and aldosterone-producing adenomas. Int J Mol Med; 2006 Jun;17(6):975-80
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  • [Title] Adiponectin receptor expression in the human adrenal cortex and aldosterone-producing adenomas.
  • The adrenal gland, by secreting glucorticoid and mineralocorticoid hormones, intervenes in cardiovascular and glucose metabolism regulation and is surrounded by adipose tissue.
  • Hence, we investigated the hypothesis that adiponectin receptor types 1 and 2 (adipo-R1 and adipo-R2) are expressed in the human adrenal gland and in adrenocortical zona glomerulosa cell-derived aldosterone-producing adenoma (APA) tissue.
  • We used real-time reverse transcription-polymerase chain reaction to demonstrate the mRNA of adipo-R1 and adipo-R2 in 10 histologically normal human adrenal cortexes that were obtained from patients with renal cancer undergoing nephrectomy with ipsilateral adrenalectomy and in 10 APAs.
  • Results consistently showed the expression of specific mRNAs of adiponectin receptors in all histologically normal human adrenal cortexes and APAs.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Aldosterone / biosynthesis. Receptors, Cell Surface / genetics

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  • (PMID = 16685404.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / ADIPOR1 protein, human; 0 / ADIPOR2 protein, human; 0 / RNA, Messenger; 0 / Receptors, Adiponectin; 0 / Receptors, Cell Surface; 4964P6T9RB / Aldosterone
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10. Karagüzel G, Bahat E, Imamoğlu M, Ahmetoğlu A, Yildiz K, Okten A: An unusual case of an aldosterone-producing adrenocortical adenoma presenting with rhabdomyolysis. J Pediatr Endocrinol Metab; 2009 Nov;22(11):1087-90
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  • [Title] An unusual case of an aldosterone-producing adrenocortical adenoma presenting with rhabdomyolysis.
  • Here, we report a case of primary hyperaldosteronism due to unilateral aldosterone-producing adenoma in a 14 year-old girl who developed rhabdomyolysis following hypokalemia.
  • To our knowledge, this is the first case of adrenocortical adenoma presenting with rhabdomyolysis in a child.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Aldosterone / metabolism. Rhabdomyolysis / metabolism
  • [MeSH-minor] Adolescent. Adrenal Glands / radiography. Adrenalectomy. Combined Modality Therapy. Female. Humans. Hypokalemia / complications. Hypokalemia / metabolism. Hypokalemia / pathology. Mineralocorticoid Receptor Antagonists / therapeutic use. Spironolactone / therapeutic use. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 20101896.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 27O7W4T232 / Spironolactone; 4964P6T9RB / Aldosterone
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11. Shigematsu K, Kawai K, Irie J, Sakai H, Nakashima O, Iguchi A, Shimamatsu J, Shimamatsu K, Kusaba Y, Takahara O: Analysis of unilateral adrenal hyperplasia with primary aldosteronism from the aspect of messenger ribonucleic acid expression for steroidogenic enzymes: a comparative study with adrenal cortices adhering to aldosterone-producing adenoma. Endocrinology; 2006 Feb;147(2):999-1006
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of unilateral adrenal hyperplasia with primary aldosteronism from the aspect of messenger ribonucleic acid expression for steroidogenic enzymes: a comparative study with adrenal cortices adhering to aldosterone-producing adenoma.
  • Unilateral adrenal hyperplasia with primary aldosteronism is very rare and shows similar endocrine features to aldosterone-producing adenoma and bilateral adrenal hyperplasia.
  • In this study, the mRNA expression of steroidogenic enzymes in unilateral adrenal hyperplasia was examined by in situ hybridization.
  • We found subcapsular micronodules composed of spironolactone body-containing cells, which showed intense expression for 3beta-hydroxysteroid dehydrogenase, 11beta-hydroxylase, 18-hydroxylase, and 21-hydroxylase but not 17alpha-hydroxylase, indicating aldosterone production.
  • Additionally, it was noted that a nodule with active aldosterone production was closely adjacent to one showing intense 17alpha-hydroxylase expression.
  • In the adrenal cortices adhering to aldosterone-producing adenoma, the majority of hyperplastic zona glomerulosa and hyperplastic nodules demonstrated a decreased steroidogenic activity.
  • However, minute nodules indicative of active aldosterone production were found at high frequency.
  • These results suggest that the subcapsular micronodules observed might be the root of aldosterone-producing adenoma.
  • Furthermore, we emphasize the need for long-term follow-up after unilateral adrenalectomy or enucleation of the adenoma because of the possibility that buds with autonomous aldosterone production may still be present in the contralateral or remaining adrenal tissue.
  • [MeSH-major] Adenoma / enzymology. Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / enzymology. Hyperaldosteronism / enzymology. RNA, Messenger / metabolism. Steroid Hydroxylases / genetics

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  • (PMID = 16282357.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.14.- / Steroid Hydroxylases; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.99.10 / Steroid 21-Hydroxylase
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12. Satoh F, Abe T, Tanemoto M, Nakamura M, Abe M, Uruno A, Morimoto R, Sato A, Takase K, Ishidoya S, Arai Y, Suzuki T, Sasano H, Ishibashi T, Ito S: Localization of aldosterone-producing adrenocortical adenomas: significance of adrenal venous sampling. Hypertens Res; 2007 Nov;30(11):1083-95
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  • [Title] Localization of aldosterone-producing adrenocortical adenomas: significance of adrenal venous sampling.
  • Accurate localization of aldosterone-producing adenoma (APA) is essential for the treatment of primary aldosteronism (PA).
  • In order to confirm the clinical usefulness of adrenal venous sampling (AVS), we retrospectively studied 87 cases of PA in whom AVS was conducted.
  • We collected right and left adrenal venous effluents simultaneously before and after adrenocorticotropic hormone (ACTH) stimulation for measurements of aldosterone concentration (A) and cortisol concentration (C).
  • Based on AVS results, we judged 66 cases as having unilateral aldosterone hypersecretion and the remaining 21 cases as having no apparent laterality.
  • Of the above 66 subjects, 61 underwent laparoscopic removal of the adrenal gland through a retroperitoneal approach.
  • The presence of APA was histopathologically confirmed, and blood pressure decreased significantly with normalization of plasma aldosterone concentration (PAC) in all cases.
  • [MeSH-major] Adenoma / diagnosis. Adrenal Cortex Neoplasms / diagnosis. Aldosterone / blood. Blood Specimen Collection / methods. Hydrocortisone / blood

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  • [CommentIn] Hypertens Res. 2007 Nov;30(11):1009-10 [18250546.001]
  • (PMID = 18250558.001).
  • [ISSN] 0916-9636
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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13. Wu VC, Chueh SC, Chang HW, Lin WC, Liu KL, Li HY, Lin YH, Wu KD, Hsieh BS: Bilateral aldosterone-producing adenomas: differentiation from bilateral adrenal hyperplasia. QJM; 2008 Jan;101(1):13-22
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  • [Title] Bilateral aldosterone-producing adenomas: differentiation from bilateral adrenal hyperplasia.
  • Most such patients have either idiopathic bilateral adrenal hyperplasia (BAH) or unilateral aldosterone-producing adenoma (APA).
  • RESULTS: Patients with bilateral APA had similar blood pressure, arterial blood gas analysis, spot urinary potassium to creatinine ratio and clinical symptoms to those with BAH, but lower serum potassium levels (p = 0.027), lower plasma renin activity (p = 0.037), and higher plasma aldosterone concentrations (p = 0.029).
  • Aldosterone-renin ratio (ARR) after administration of 50 mg captopril was higher in bilateral APA than in BAH patients (p = 0.023), but not different between unilateral APA and BAH (p = 0.218).
  • A cut-off of ARR >100 ng/dl per ng/ml/h and plasma aldosterone >20 ng/dl after captopril significantly differentiated bilateral APA from BAH.
  • The clinical presentations of bilateral functional adenoma are not different from BAH, but patients with low serum potassium and ARR >100 after captopril should be carefully evaluated for bilateral adenoma.
  • [MeSH-major] Adenoma / metabolism. Adrenal Cortex Neoplasms / metabolism. Adrenal Glands / pathology. Aldosterone / biosynthesis

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  • (PMID = 18203722.001).
  • [ISSN] 1460-2725
  • [Journal-full-title] QJM : monthly journal of the Association of Physicians
  • [ISO-abbreviation] QJM
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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14. Chang HW, Chu TS, Huang HY, Chueh SC, Wu VC, Chen YM, Hsieh BS, Wu KD: Down-regulation of D2 dopamine receptor and increased protein kinase Cmu phosphorylation in aldosterone-producing adenoma play roles in aldosterone overproduction. J Clin Endocrinol Metab; 2007 May;92(5):1863-70
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  • [Title] Down-regulation of D2 dopamine receptor and increased protein kinase Cmu phosphorylation in aldosterone-producing adenoma play roles in aldosterone overproduction.
  • CONTEXT: The mechanism associated with the overproduction of aldosterone by aldosterone-producing adenomas (APA) is unknown.
  • OBJECTIVE: The objective of the study was to explore the role of the D2 dopamine receptor (D2R) on aldosterone synthesis and secretion and clarify the clinical importance of this role on aldosterone overproduction in APA.
  • RESULTS: D2R expression in APA was examined in 24 patients and was much less than that in the nontumorous adrenal cortex.
  • D2R mRNA levels in APA were inversely correlated with CYP11B2 mRNA levels and the patient's plasma aldosterone concentration.
  • Angiotensin II (AII)-stimulated aldosterone secretion and CYP11B2 mRNA expression in human adenocarcinoma cells (H295R) was attenuated by the D2 agonist, bromocriptine (BMC).
  • PKCmu-specific short-hairpin RNA significantly decreased AII-induced CYP11B2 mRNA expression and aldosterone secretion.
  • Despite similar total PKCmu levels in APA and the nontumorous adrenal cortex, expression of phosphorylated PKCmu in APA was much higher.
  • CONCLUSION: This is the first study to demonstrate that the D2R modulated aldosterone secretion and synthesis through a specific attenuation of PKCmu activity, as well as the intracellular calcium level.
  • Down-regulation of the D2R in APA, in turn, increased PKCmu activity and led to overproduction of aldosterone in affected patients.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Aldosterone / biosynthesis. Protein Kinase C / physiology. Receptors, Dopamine D2 / physiology

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  • (PMID = 17299068.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 11128-99-7 / Angiotensin II; 137750-34-6 / Receptors, Dopamine D4; 4964P6T9RB / Aldosterone; 85166-31-0 / Inositol 1,4,5-Trisphosphate; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 2.7.10.- / protein kinase D; EC 2.7.11.13 / Protein Kinase C; SY7Q814VUP / Calcium
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15. Shigematsu K, Nishida N, Sakai H, Igawa T, Suzuki S, Kawai K, Takahara O: Primary aldosteronism with aldosterone-producing adenoma consisting of pure zona glomerulosa-type cells in a pregnant woman. Endocr Pathol; 2009;20(1):66-72
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  • [Title] Primary aldosteronism with aldosterone-producing adenoma consisting of pure zona glomerulosa-type cells in a pregnant woman.
  • Aldosterone-producing adenoma (APA) consisting of pure zona glomerulosa (ZG)-type cells is extremely rare, and primary aldosteronism complicated by pregnancy is also rare.
  • Elevated plasma aldosterone concentration and hypokalemia were observed, and an magnetic resonance imaging scan demonstrated a right adrenal mass.
  • Pathologically, the adrenal mass was diagnosed as APA, and in addition to the cytological features, in situ hybridization and real-time polymerase chain reaction proved that all the component cells were ZG-type cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Hyperaldosteronism / etiology. Pregnancy Complications / pathology. Zona Glomerulosa / pathology
  • [MeSH-minor] Adrenalectomy. Adult. Aldosterone / blood. Estrogen Receptor beta / biosynthesis. Female. Humans. Hypertension / etiology. Hypokalemia / etiology. Immunohistochemistry. In Situ Hybridization. Pregnancy. RNA, Messenger / analysis. Receptor, Melanocortin, Type 2 / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19199080.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor beta; 0 / RNA, Messenger; 0 / Receptor, Melanocortin, Type 2; 4964P6T9RB / Aldosterone
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16. TAIPAI Study Group, Wu VC, Chueh SC, Chang HW, Lin LY, Liu KL, Lin YH, Ho YL, Lin WC, Wang SM, Huang KH, Hung KY, Kao TW, Lin SL, Yen RF, Chen YM, Hsieh BS, Wu KD: Association of kidney function with residual hypertension after treatment of aldosterone-producing adenoma. Am J Kidney Dis; 2009 Oct;54(4):665-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of kidney function with residual hypertension after treatment of aldosterone-producing adenoma.
  • BACKGROUND: Autonomous secretion of aldosterone in patients with primary aldosteronism increases glomerular filtration rate and causes kidney damage.
  • 150 patients (61 men; overall mean age, 47.2 +/- 11.6 years) with a diagnosis of aldosterone-producing adenoma had undergone unilateral adrenalectomy at National Taiwan University Hospital from July 1999 to January 2007.
  • CONCLUSIONS: Two-thirds of patients with aldosterone-producing adenoma were cured of hypertension by means of unilateral adrenalectomy.
  • [MeSH-major] Adenoma / physiopathology. Adrenal Cortex Neoplasms / physiopathology. Adrenalectomy. Aldosterone / blood. Glomerular Filtration Rate. Hypertension / physiopathology. Kidney / physiopathology

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  • [CommentIn] Am J Kidney Dis. 2009 Oct;54(4):594-7 [19781452.001]
  • (PMID = 19628318.001).
  • [ISSN] 1523-6838
  • [Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation
  • [ISO-abbreviation] Am. J. Kidney Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; AYI8EX34EU / Creatinine
  • [Investigator] Wu VC; Lin YH; Ho YL; Chang HW; Lin LY; Hu FC; Liu KL; Wang SM; Huang KH; Chang FC; Chen YM; Kuo CC; Chueh SC; Lu CC; Chang FC; Liao SC; Yen RF; Lin WC; Hsieh BS; Wu KD; Hsien FF
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17. Takeda Y, Usukura M, Yoneda T, Oda N, Ito Y, Mabuchi H: The expression of messenger RNA for ADP-ribosyl cyclase in aldosterone-producing adenomas. Clin Endocrinol (Oxf); 2005 Apr;62(4):504-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of messenger RNA for ADP-ribosyl cyclase in aldosterone-producing adenomas.
  • To determine whether the cADPR system plays a signalling role in angiotensin II (Ang II)-induced aldosterone synthesis in the human adrenal gland, we investigated the effects of Ang II on ADP-ribosyl cyclase activity in human adrenal cortical tissue.
  • In addition, the expression of ADP-ribosyl cyclase messenger RNA was evaluated in aldosterone-producing adenomas (APAs) and compared with normal adrenal tissue and nonfunctioning adenomas.
  • The effect of 8-bromo-cADPR on Ang II-induced aldosterone production from adrenal tissue was estimated.
  • The expression of ADP-ribosyl cyclase, CYP11B2 and AT(1)R mRNA was measured in APAs, nonfunctioning adenomas, adjacent adrenal tissue and normal adrenal tissue.
  • Treatment with 8-bromo-cADPR (50 micromol/l) reduced Ang II-induced aldosterone secretion.
  • The expression of ADP-ribosyl cyclase, CYP11B2 and AT(1)R mRNA was increased in APAs compared with that of nonfunctioning adenomas, adjacent adrenal tissue or normal adrenal tissue.
  • CONCLUSIONS: These results demonstrated the existence of a signalling pathway from the Ang II receptor to ADP-ribosyl cyclase in the human adrenal gland and suggest that the cADP-ribose signalling system might play an important role in the pathogenesis of APAs.
  • [MeSH-major] ADP-ribosyl Cyclase / genetics. Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Angiotensins / pharmacology. Cyclic ADP-Ribose / analogs & derivatives. RNA, Messenger / analysis

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  • (PMID = 15807884.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 8-bromo-cyclic-ADP-ribose; 0 / Angiotensins; 0 / Imidazoles; 0 / Pyridines; 0 / RNA, Messenger; 0 / Receptor, Angiotensin, Type 1; 119340-53-3 / Cyclic ADP-Ribose; 130663-39-7 / PD 123319; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 3.2.2.5 / ADP-ribosyl Cyclase; JMS50MPO89 / Losartan
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18. Saner-Amigh K, Mayhew BA, Mantero F, Schiavi F, White PC, Rao CV, Rainey WE: Elevated expression of luteinizing hormone receptor in aldosterone-producing adenomas. J Clin Endocrinol Metab; 2006 Mar;91(3):1136-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated expression of luteinizing hormone receptor in aldosterone-producing adenomas.
  • CONTEXT: The mechanisms driving steroid production in aldosterone-producing adenomas (APAs) are poorly defined.
  • However, previous studies have shown that steroid production in some cortisol-producing adenomas is regulated by aberrant expression of G protein-coupled receptors.
  • Aberrant adrenal expression of LH receptors has been shown to cause Cushing's syndrome, but the role of LH receptors in Conn's disease (hyperaldosteronism) has not been studied.
  • OBJECTIVE: The objective of the study was to determine whether APAs express elevated LH receptor, compared with normal adrenal (NA).
  • Aldosterone synthase transcription was studied in H295R adrenocortical cells transfected with an LH receptor expression construct and reporter constructs prepared from CYP11B2 5'-flanking DNA.
  • MAIN OUTCOME MEASURE: Regulation of CYP11B2 gene expression by aberrant LH receptor expression in aldosterone-producing adrenal adenoma was measured.
  • CONCLUSION: LH receptor expression is elevated in many APAs, which makes LH a potential cause of the excessive production of aldosterone in a subset of these adrenal tumors.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Aldosterone / metabolism. Receptors, LH / genetics
  • [MeSH-minor] Adrenal Glands / embryology. Adrenal Glands / physiology. Corpus Luteum / physiology. DNA Primers. Female. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Ovarian Follicle / physiology. Plasmids. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Cells, Cultured

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  • (PMID = 16332935.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK43140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, LH; 4964P6T9RB / Aldosterone
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19. Lenzini L, Seccia TM, Aldighieri E, Belloni AS, Bernante P, Giuliani L, Nussdorfer GG, Pessina AC, Rossi GP: Heterogeneity of aldosterone-producing adenomas revealed by a whole transcriptome analysis. Hypertension; 2007 Dec;50(6):1106-13

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heterogeneity of aldosterone-producing adenomas revealed by a whole transcriptome analysis.
  • Aldosterone-producing adenomas (APAs) are a common cause of arterial hypertension, but the underlying molecular mechanisms are unknown, although a transcriptional modulation of aldosterone synthase (CYP11B2) has been suggested.
  • Aldosterone synthesis involves 2 main rate-limiting steps: cholesterol transport into mitochondria and CYP11B2 gene transcription.
  • Evidence supports a role of Ca(2+)/calmodulin-dependent protein kinases (CAMKs) in the regulation of angiotensin II- and potassium-stimulated aldosterone production.
  • Thus, aldosterone overproduction in APAs involves complex alterations of aldosterone synthesis regulation rather than simply increased aldosterone synthase gene expression.
  • [MeSH-major] Adenoma / metabolism. Adrenal Cortex Neoplasms / metabolism. Aldosterone / biosynthesis. Gene Expression Profiling

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  • (PMID = 17938379.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 2.7.11.17 / CAMK1 protein, human; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 1; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2
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20. Dundr P, Povýsil C, Zelinka T, Tvrdík D, Ciprová V, Novák K: Adrenocortical adenoma with rhabdoid features. Pathol Res Pract; 2006;202(3):177-81
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  • [Title] Adrenocortical adenoma with rhabdoid features.
  • We report a case of an aldosterone producing adrenocortical adenoma with rhabdoid features in a 16-year-old girl.
  • Rhabdoid features have been described in many tumors of variable histogenesis; however, to the best of our knowledge, the presence of rhabdoid phenotype has never been described in either adrenocortical adenoma or carcinoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / pathology. Adrenocortical Adenoma / pathology. Rhabdoid Tumor / metabolism
  • [MeSH-minor] Adolescent. Adrenalectomy. Aldosterone / metabolism. Biomarkers, Tumor / analysis. Female. Follow-Up Studies. Humans. Treatment Outcome

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  • (PMID = 16448785.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 4964P6T9RB / Aldosterone
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21. Caroccia B, Fassina A, Seccia TM, Recarti C, Petrelli L, Belloni AS, Pelizzo MR, Rossi GP: Isolation of human adrenocortical aldosterone-producing cells by a novel immunomagnetic beads method. Endocrinology; 2010 Mar;151(3):1375-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolation of human adrenocortical aldosterone-producing cells by a novel immunomagnetic beads method.
  • We detected intense CD56 immunostaining in the zona glomerulosa (ZG) and medulla of the normal human adrenal gland and therefore identified CD56, the neural cell adhesion molecule, as a membrane antigen specific for the ZG, aldosterone-producing adenoma (APA), and chromaffin cells.
  • Morphology, gene expression studies, and aldosterone measurement confirmed that CD56 positive (+) cells were ZG and APA cells.
  • Expression levels of the CD56 and the aldosterone synthase (CYP11B2) gene were markedly higher in CD56+ cells than CD56- cells (+1600 and +2100% increase, respectively).
  • Moreover, aldosterone secretion was higher (+1380%) from CD56+ cells than from CD56- cells.
  • Hence, this novel methodology allows isolation of a pure population of ZG and APA cells exhibiting multiple characteristics of the aldosterone-producing cells.
  • [MeSH-major] Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / metabolism. Aldosterone / secretion. Antigens, CD56 / metabolism. Immunomagnetic Separation. Zona Glomerulosa / cytology

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  • (PMID = 20097714.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 4964P6T9RB / Aldosterone
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22. Ye P, Mariniello B, Mantero F, Shibata H, Rainey WE: G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism. J Endocrinol; 2007 Oct;195(1):39-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism.
  • The source of aldosterone in 30-40% of patients with primary hyperaldosteronism (PA) is unilateral aldosterone-producing adenoma (APA).
  • The mechanisms causing elevated aldosterone production in APA are unknown.
  • RNA samples from normal adrenals (n = 5), APAs (n = 10), and cortisol-producing adenomas (CPAs; n = 13) were used on 15 genomic expression arrays, each of which included 223 GPCR transcripts presented in at least 1 out of 15 of the independent microarrays.
  • Four GPCR transcripts exhibited a statistically significant increase that was greater than threefold when compared with normal adrenals, suggesting a general increase in expression when compared with normal adrenal glands.
  • [MeSH-major] Adrenal Cortex Neoplasms / secretion. Adrenocortical Adenoma / secretion. Aldosterone / secretion. Hyperaldosteronism / etiology. Receptors, G-Protein-Coupled / genetics

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  • (PMID = 17911395.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK43140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled; 4964P6T9RB / Aldosterone
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23. Boulkroun S, Samson-Couterie B, Dzib JF, Lefebvre H, Louiset E, Amar L, Plouin PF, Lalli E, Jeunemaitre X, Benecke A, Meatchi T, Zennaro MC: Adrenal cortex remodeling and functional zona glomerulosa hyperplasia in primary aldosteronism. Hypertension; 2010 Nov;56(5):885-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adrenal cortex remodeling and functional zona glomerulosa hyperplasia in primary aldosteronism.
  • Primary aldosteronism is the most common form of secondary hypertension with hypokalemia and suppressed renin-angiotensin system caused by autonomous aldosterone production.
  • Our aim was to compare zona glomerulosa (ZG) structure and function between control adrenals and the peritumoral tissue from patients operated on for aldosterone-producing adenoma.
  • ZG morphology and CYP11B1, CYP11B2, and disabled 2 expression were studied in 15 control adrenals and 25 adrenals with aldosterone-producing adenoma.
  • In control adrenals, ZG was discontinuous, and CYP11B2 expression was focal or partly continuous and localized to 3 structures, foci, megafoci, and aldosterone-producing cell clusters.
  • CYP11B2 expression was restricted to a limited number of ZG cells expressing Dab2 but not CYP11B1; aldosterone-producing cell clusters were composed of cells with an intermediate phenotype expressing CYP11B2 but not disabled 2 or CYP11B1.
  • In peritumoral tissue, large remodeling of the adrenal cortex was observed with increased nodulation and decreased vascularization that were not correlated with CYP11B2 expression.
  • In all of the adrenals from patients with aldosterone-producing adenoma, CYP11B2 expression was present in foci, megafoci, and aldosterone-producing cell clusters.
  • Transcriptome profiling indicates a close relationship between peritumoral and control adrenal cortex.
  • In conclusion, adrenal cortex remodeling, reduced vascularization, and ZG hyperplasia are major features of adrenals with aldosterone-producing adenoma.
  • Transcriptional phenotyping is not in favor of this being an intermediate step toward the formation of aldosterone-producing adenoma.
  • [MeSH-major] Adenoma / pathology. Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Hyperaldosteronism / pathology. Zona Glomerulosa / pathology
  • [MeSH-minor] Adult. Aldosterone / biosynthesis. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Female. Humans. Hyperplasia / pathology. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Steroid 11-beta-Hydroxylase / genetics. Steroid 11-beta-Hydroxylase / metabolism

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  • (PMID = 20937967.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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24. Lumachi F, Ermani M, Basso SM, Armanini D, Iacobone M, Favia G: Long-term results of adrenalectomy in patients with aldosterone-producing adenomas: multivariate analysis of factors affecting unresolved hypertension and review of the literature. Am Surg; 2005 Oct;71(10):864-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of adrenalectomy in patients with aldosterone-producing adenomas: multivariate analysis of factors affecting unresolved hypertension and review of the literature.
  • We reviewed retrospectively charts from 98 patients (range, 19-70 years old) with aldosterone-producing adenomas who underwent unilateral adrenalectomy.
  • In conclusion, in patients with an aldosterone-producing adenoma undergoing surgery, the combination of age and duration of hypertension gave the best predictive power of a linear classification function and represented the main independent risk factors affecting hypertension cure rate.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery
  • [MeSH-minor] Adult. Aged. Aldosterone / biosynthesis. Female. Humans. Hypertension / etiology. Hypertension / surgery. Logistic Models. Male. Middle Aged. Multivariate Analysis. Retrospective Studies. Risk Factors

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  • (PMID = 16468537.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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25. Williams TA, Monticone S, Morello F, Liew CC, Mengozzi G, Pilon C, Asioli S, Sapino A, Veglio F, Mulatero P: Teratocarcinoma-derived growth factor-1 is upregulated in aldosterone-producing adenomas and increases aldosterone secretion and inhibits apoptosis in vitro. Hypertension; 2010 Jun;55(6):1468-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Teratocarcinoma-derived growth factor-1 is upregulated in aldosterone-producing adenomas and increases aldosterone secretion and inhibits apoptosis in vitro.
  • Aldosterone-producing adenomas (APA) are a frequent cause of secondary hypertension characterized by autonomous hypersecretion of aldosterone.
  • However, the molecular mechanisms involved in adrenal tumorigenesis and deregulated aldosterone secretion are currently unknown.
  • Furthermore, TDGF-1 mediated a 3.8+/-0.4-fold increase in aldosterone secretion (n=4) that was specifically blocked by the phosphatidylinositol 3-kinase inhibitors wortmannin (50 nmol/L) and LY294002 (20 micromol/L).
  • Taken together, our data suggest that TDGF-1, which is significantly upregulated in APA and mediates aldosterone hypersecretion and deregulated growth in adrenocortical cells in vitro, may represent a key player in the development and pathophysiology of primary aldosteronism.
  • [MeSH-major] Adenoma / secretion. Adrenal Cortex Neoplasms / secretion. Aldosterone / secretion. Apoptosis / physiology. Biomarkers, Tumor / metabolism. Caspase 3 / metabolism. Epidermal Growth Factor / metabolism. Membrane Glycoproteins / metabolism. Neoplasm Proteins / metabolism

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  • [CommentIn] Hypertension. 2010 Jun;55(6):1306-7 [20385966.001]
  • (PMID = 20385969.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / TDGF1 protein, human; 4964P6T9RB / Aldosterone; 62229-50-9 / Epidermal Growth Factor; EC 3.4.22.- / Caspase 3
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26. Wang B, Zhang G, Ouyang J, Deng X, Shi T, Ma X, Li H, Ju Z, Wang C, Wu Z, Liu S, Zhang X: Association of DNA polymorphisms within the CYP11B2/CYP11B1 locus and postoperative hypertension risk in the patients with aldosterone-producing adenomas. Urology; 2010 Oct;76(4):1018.e1-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of DNA polymorphisms within the CYP11B2/CYP11B1 locus and postoperative hypertension risk in the patients with aldosterone-producing adenomas.
  • The aim of this study was to investigate the association of DNA polymorphisms within steroid synthesis genes (CYP11B2, CYP11B1) and the postoperative resolution of hypertension in Chinese patients undergoing adrenalectomy for aldosterone-producing adenomas (APA).
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Aldosterone / secretion. Cytochrome P-450 CYP11B2 / genetics. Hyperaldosteronism / genetics. Hypertension / genetics. Polymorphism, Single Nucleotide. Postoperative Complications / etiology. Steroid 11-beta-Hydroxylase / genetics

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20708777.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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27. Onoda N, Ishikawa T, Nishio K, Tahara H, Inaba M, Wakasa K, Sumi T, Yamazaki T, Shigematsu K, Hirakawa K: Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case. Endocr J; 2009;56(3):495-502
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  • [Title] Cushing's syndrome by left adrenocortical adenoma synchronously associated with primary aldosteronism by right adrenocortical adenoma: report of a case.
  • Bilateral adrenal masses with clinical symptoms of CS and PA were found in a 43-year-old woman.
  • Venous sampling demonstrated excess secretion of cortisol, and aldosterone from right, and left tumor, respectively.
  • The right adrenal tumor (3 cm) was yellow in color with abundant lipofuscin granules, and was composed of both eosinophilic compact cells and clear cells.
  • Left adrenal tumor (2.4 cm) was golden-yellow in color, and composed of clear cells only.
  • Expression of HSD3B2 and CYP11B mRNAs were observed in the tumor compatible with the aldosterone synthesis.
  • Furthermore, minute nodules were found at the surface of normal-appearing cortex on both sides of the adrenal glands, and the expression of HSD3B2 and CYP11B mRNAs was clearly demonstrated within the nodules, indicating aldosterone synthesis.
  • We diagnosed that the present case had 1) cortisol-producing right adrenocortical adenoma, 2) aldosterone producing left adrenocortical adenoma, and 3) cortical minute nodules with aldosterone production in both adrenal glands compatible with idiopathic adrenal hyperplasia.
  • We reviewed the cases reported, and discussed the significance of the minute nodules in the adrenal cortex, often found in association with the adrenocortical adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology

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  • (PMID = 19270420.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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28. Born-Frontsberg E, Reincke M, Beuschlein F, Quinkler M, Participants of German Conn's Registry: Tumor size of Conn's adenoma and comorbidities. Horm Metab Res; 2009 Oct;41(10):785-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor size of Conn's adenoma and comorbidities.
  • The aim of the study was to evaluate differences regarding comorbidities depending on tumor size in patients with aldosterone producing adenoma (APA).
  • Thirty-one patients (17 men, 14 women) had an adenoma size <20 mm, and 29 patients (10 men, 19 women) had an adenoma size>/=20 mm.
  • There was no difference in age, preoperative potassium, aldosterone, or creatinine levels, preoperative systolic and diastolic blood pressure, or duration of hypertension between the two groups.
  • Subgroup analysis (n=22) of follow-up data on post-operative systolic and diastolic blood pressure showed no significant difference between these subgroups with regard to potassium, aldosterone or creatinine levels, blood pressure, duration of hypertension, or comorbidities.
  • However, adenoma size was not correlated with cardio- and cerebrovascular comorbidities, and does not seem to be a prognostic factor for blood pressure outcome.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cardiovascular Diseases / complications. Cerebrovascular Disorders / complications. Hyperaldosteronism / complications

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 19548184.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
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29. Plamondon I, Agharazii M, Douville P, Lebel M: Morning plasma aldosterone predicts the subtype of primary aldosteronism independent of sodium intake. Clin Exp Hypertens; 2007 Feb;29(2):127-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morning plasma aldosterone predicts the subtype of primary aldosteronism independent of sodium intake.
  • The objective of the present study was to assess the potential predictive value of supine morning plasma aldosterone concentration, a component of the postural stimulation test (PST), in distinguishing aldosterone-producing adenoma (APA) from idiopathic adrenal hyperplasia (IAH) in a series of 61 patients with confirmed primary aldosteronism (PAL).
  • Morning plasma aldosterone values were significantly higher in patients with APA compared to those with IAH (p < 0.01) on both diets.
  • Using the receiver-operating characteristic (ROC) curve analysis, it was observed that the cutoff values in the highest (>900 pmol/L or 32 ng/dl) and lowest (<300 pmol/L or 11 ng/dl) range of the morning plasma aldosterone measurements were predictive of the subtype diagnosis in about 50% of PAL cases (31 of 61 patients).
  • Moreover, one of its components, the supine morning plasma aldosterone, can be used as an indicator for the subtype diagnosis in about half of PAL patients.
  • [MeSH-major] Aldosterone / blood. Circadian Rhythm. Hyperaldosteronism / blood. Sodium, Dietary / administration & dosage
  • [MeSH-minor] Adrenal Cortex Neoplasms / blood. Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Adenoma / blood. Adrenocortical Adenoma / diagnosis. Adult. Aged. Biomarkers / blood. Diagnosis, Differential. Female. Humans. Male. Middle Aged. ROC Curve. Reproducibility of Results. Retrospective Studies. Sensitivity and Specificity. Supine Position

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  • (PMID = 17364612.001).
  • [ISSN] 1064-1963
  • [Journal-full-title] Clinical and experimental hypertension (New York, N.Y. : 1993)
  • [ISO-abbreviation] Clin. Exp. Hypertens.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Sodium, Dietary; 4964P6T9RB / Aldosterone
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30. Giacchetti G, Ronconi V, Rilli S, Guerrieri M, Turchi F, Boscaro M: Small tumor size as favorable prognostic factor after adrenalectomy in Conn's adenoma. Eur J Endocrinol; 2009 Apr;160(4):639-46

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small tumor size as favorable prognostic factor after adrenalectomy in Conn's adenoma.
  • OBJECTIVE: Primary aldosteronism (PA) due to aldosterone-producing adenoma (APA) is the most common curable form of secondary hypertension.
  • METHODS: Renin-angiotensin-aldosterone system (upright and postsaline infusion test), serum and urinary electrolytes, office and ambulatory blood pressure monitoring were evaluated at baseline and after a follow-up of 2.7+/-2.2 years.
  • Drug history and adenoma size at morphological evaluation were also collected.
  • RESULTS: Multiple regression analysis showed that, before surgery, patients with a small adenoma (diameter <20 mm) displayed higher postsaline aldosterone values (P=0.0001), and lower serum potassium levels (P=0.020), than patients with adenoma >20 mm.
  • Recovered patients had a shorter duration of hypertension (P=0.038), and a smaller adenoma size (P=0.035).

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  • (PMID = 19131503.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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31. Tamura Y, Adachi J, Chiba Y, Mori S, Takeda K, Kasuya Y, Murayama T, Sawabe M, Sasano H, Araki A, Ito H, Horiuchi T: Primary aldosteronism due to unilateral adrenal microadenoma in an elderly patient: efficacy of selective adrenal venous sampling. Intern Med; 2008;47(1):37-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary aldosteronism due to unilateral adrenal microadenoma in an elderly patient: efficacy of selective adrenal venous sampling.
  • Computed tomography imaging appeared normal for a long duration with a left-sided nodule appearing far later; adrenal scintigraphy was first normal, and the second test showed right-sided uptake.
  • However, a repeat selective adrenal venous sampling (SAVS) indicated a left-sided lateralization of the hypersecretion of aldosterone.
  • The histopathological findings demonstrated the aldosterone-producing microadenoma with secondary micronodules.
  • [MeSH-major] Adrenal Cortex Neoplasms / blood. Adrenal Glands / blood supply. Adrenocortical Adenoma / blood. Aldosterone / blood. Hyperaldosteronism / blood

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  • (PMID = 18176003.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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32. Giuliani L, Lenzini L, Antonello M, Aldighieri E, Belloni AS, Fassina A, Gomez-Sanchez C, Rossi GP: Expression and functional role of urotensin-II and its receptor in the adrenal cortex and medulla: novel insights for the pathophysiology of primary aldosteronism. J Clin Endocrinol Metab; 2009 Feb;94(2):684-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and functional role of urotensin-II and its receptor in the adrenal cortex and medulla: novel insights for the pathophysiology of primary aldosteronism.
  • DESIGN: The expression of urotensin II and urotensin II receptor was measured by real time RT-PCR in aldosterone-producing adenoma (n = 22) and pheochromocytoma (n = 10), using histologically normal adrenocortical (n = 6) and normal adrenomedullary (n = 5) tissue as control.
  • RESULTS: Urotensin II was more expressed in pheochromocytoma than in aldosterone-producing adenoma tissue; the opposite was seen for the urotensin II receptor expression.
  • Urotensin II receptor activation in vivo in rats enhanced (by 182 +/- 9%; P < 0.007) the adrenocortical expression of immunoreactive aldosterone synthase.
  • CONCLUSIONS: Urotensin II is a putative mediator of the effects of the adrenal medulla and pheochromocytoma on the adrenocortical zona glomerulosa.
  • [MeSH-major] Adrenal Cortex / metabolism. Adrenal Medulla / metabolism. Hyperaldosteronism / etiology. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / physiology. Urotensins / genetics. Urotensins / physiology
  • [MeSH-minor] Adenoma / complications. Adenoma / genetics. Adenoma / metabolism. Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / genetics. Adrenal Gland Neoplasms / metabolism. Adult. Animals. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Pheochromocytoma / complications. Pheochromocytoma / genetics. Pheochromocytoma / metabolism. Rats. Rats, Sprague-Dawley

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  • (PMID = 19001524.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, G-Protein-Coupled; 0 / UTS2R protein, human; 0 / Urotensins; 9047-55-6 / urotensin II; EC 1.14.15.4 / Cytochrome P-450 CYP11B2
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33. Shigematsu K, Nakagaki T, Yamaguchi N, Kawai K, Sakai H, Takahara O: Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas. Eur J Endocrinol; 2008 Jun;158(6):867-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas.
  • DESIGN AND METHODS: We have recently demonstrated that the adrenal cortices attached to aldosterone-producing adenoma (APA) contained microscopic subcapsular micronodules suggestive of active aldosterone production.
  • In this study, we used in situ hybridization to investigate the mRNA expression of steroidogenic enzymes in the adrenal cortices attached to cortisol-producing adenoma (CPA) and clinically silent adenoma (non-functioning adenoma; NFA), in addition to APA.
  • Most of the cortical nodules in zona fasciculata to zona reticularis showed a suppressed steroidogenesis in the cortices attached to adenoma, but some expressed intensely all necessary steroidogenic enzyme mRNAs for cortisol synthesis.
  • CONCLUSIONS: It is thus necessary to keep in mind, on the occasion of subtotal adrenalectomy, that lesions with the potential to later develop into functional adrenocortical nodules may be present in other parts of the ipsilateral or contralateral adrenal cortices.

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  • (PMID = 18505908.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / SPATA7 protein, human; EC 1.14.15.6 / Cholesterol Side-Chain Cleavage Enzyme; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.2 / alcohol sulfotransferase
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34. Iihara M, Obara T: [Diagnosis and surgical treatment of adrenal tumors]. Nihon Geka Gakkai Zasshi; 2005 Aug;106(8):479-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Diagnosis and surgical treatment of adrenal tumors].
  • Adrenal surgery is necessary for the management of functioning adrenal tumors, such as aldosterone-producing adenoma, cortisol-producing adenoma, and pheochromocytoma.
  • The role of adrenal imaging in primary hyperaldosteronism is to separate the surgically resectable unilateral aldosteronoma from bilateral hyperplasia.
  • Once the clinical diagnosis of primary hyperaldosteronism is confirmed, adrenal computed tomography (CT) with 3-mm sections should be the first imaging study.
  • If the results of CT and NP-59 scintigraphy are equivocal, adrenal venous sampling is necessary.
  • Cortisol-producing adrenocortical adenomas are seen as adrenal masses 2.5 cm or larger in diameter in CT scanning.
  • When an adrenal mass measures more than 5 cm in diameter, a functioning adrenal carcinoma should be considered.
  • In the past decade, laparoscopic adrenalectomy has replaced open adrenalectomy as a standard operative procedure for benign adrenal tumors.
  • Adrenal-sparing laparoscopic surgery has recently become a feasible option in patients with hereditary bilateral pheochromocytomas.
  • [MeSH-major] Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / surgery
  • [MeSH-minor] Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / surgery. Adrenal Medulla. Humans

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  • (PMID = 16119111.001).
  • [ISSN] 0301-4894
  • [Journal-full-title] Nihon Geka Gakkai zasshi
  • [ISO-abbreviation] Nihon Geka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 17
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35. Lampron A, Bourdeau I, Oble S, Godbout A, Schürch W, Arjane P, Hamet P, Lacroix A: Regulation of aldosterone secretion by several aberrant receptors including for glucose-dependent insulinotropic peptide in a patient with an aldosteronoma. J Clin Endocrinol Metab; 2009 Mar;94(3):750-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of aldosterone secretion by several aberrant receptors including for glucose-dependent insulinotropic peptide in a patient with an aldosteronoma.
  • CONTEXT: Primary adrenal Cushing's syndrome can result from the aberrant adrenal expression of several hormone receptors; this mechanism has not been explored in detail in aldosterone-producing tumors.
  • OBJECTIVE: The objective of the study was to evaluate a 56-yr-old male patient with an aldosteronoma for the regulation of aldosterone secretion by aberrant hormone receptors.
  • RESULTS: Renin-independent stimulation of aldosterone secretion was observed in vivo after a mixed meal, oral glucose, or administration of glucose-dependent insulinotropic peptide (GIP), vasopressin, and tegaserod.
  • The mixed meal-mediated stimulation of aldosterone was not present in five other cases of aldosteronoma.
  • A smaller response of aldosterone after GIP infusion was observed in a normal subject.
  • Aldosterone secretion was stimulated by GIP in primary cultures of this patient's aldosteronoma.
  • The GIP receptor protein was also found at lower levels in zona glomerulosa cells of the normal adjacent adrenal gland.
  • [MeSH-major] Adrenal Cortex Neoplasms / secretion. Adrenocortical Adenoma / secretion. Aldosterone / secretion. Receptors, Gastrointestinal Hormone / physiology

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  • (PMID = 19066304.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Corticotropin; 0 / Receptors, Gastrointestinal Hormone; 0 / Receptors, Vasopressin; 0 / gastric inhibitory polypeptide receptor; 158165-40-3 / Receptors, Serotonin, 5-HT4; 4964P6T9RB / Aldosterone; 59392-49-3 / Gastric Inhibitory Polypeptide; 9002-60-2 / Adrenocorticotropic Hormone
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36. Willenberg HS, Späth M, Maser-Gluth C, Engers R, Anlauf M, Dekomien G, Schott M, Schinner S, Cupisti K, Scherbaum WA: Sporadic solitary aldosterone- and cortisol-co-secreting adenomas: endocrine, histological and genetic findings in a subtype of primary aldosteronism. Hypertens Res; 2010 May;33(5):467-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sporadic solitary aldosterone- and cortisol-co-secreting adenomas: endocrine, histological and genetic findings in a subtype of primary aldosteronism.
  • Adrenal adenomas producing both aldosterone and cortisol (A/CPAs) have been described in only a few cases.
  • Aldosterone, 18-hydroxycorticosterone (18-OH-B) and 18-hydroxycortisol (18-OH-F) were not suppressible with fludrocortisone in either patient and were partly suppressible with dexamethasone in one of the patients.
  • Adrenal insufficiency developed in both patients after operation and lasted for more than 6 months.
  • Aldosterone and hybrid corticosteroids returned to normal 8 weeks after adrenalectomy.
  • The most common germline mutations in the aldosterone synthase gene and the aldosterone synthase/11beta-hydroxylase hybrid gene were absent.
  • [MeSH-major] Adrenal Cortex Neoplasms / secretion. Adrenocortical Adenoma / secretion. Aldosterone / secretion. Hydrocortisone / secretion. Hyperaldosteronism / physiopathology

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  • (PMID = 20186151.001).
  • [ISSN] 1348-4214
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase; WI4X0X7BPJ / Hydrocortisone
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37. Dierks A, Lichtenauer UD, Sackmann S, Spyroglou A, Shapiro I, Geyer M, Manonopoulou J, Reincke M, Hantel C, Beuschlein F: Identification of adrenal genes regulated in a potassium-dependent manner. J Mol Endocrinol; 2010 Oct;45(4):193-206
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  • [Title] Identification of adrenal genes regulated in a potassium-dependent manner.
  • Potassium and angiotensin II are the main stimulators of aldosterone secretion from the adrenal cortex.
  • As potassium-induced in vivo gene regulation in the adrenal cortex has not been studied in detail, we applied a stepwise screening approach: first, we investigated the effects of chronic potassium substitution in mice.
  • Microarray analysis of adrenal glands revealed a set of genes (set A) that were counter-regulated in a high potassium (HP) and low potassium substitution group, while others (set B) were highly upregulated in the HP intake group.
  • Finally, to provide indirect evidence for the potential relevance of the detected changes for autonomous aldosterone secretion, expression analysis of aldosterone-producing adenomas was compared with normal adrenal glands.
  • Similarly, in Conn's adenomas, mostly genes from set B displayed changes in expression pattern in comparison to normal adrenal glands, while genes from set A were mostly unchanged.
  • Thus, while in vivo models can help in identifying genes potentially involved in potassium-dependent aldosterone secretion, these findings also underline the necessity to interpret potassium-induced gene regulation on the basis of the experimental setting.
  • [MeSH-major] Adrenal Glands / drug effects. Adrenal Glands / metabolism. Gene Expression Regulation / drug effects. Potassium / pharmacology
  • [MeSH-minor] Adenoma / blood. Adenoma / genetics. Adenoma / secretion. Aldosterone / blood. Aldosterone / secretion. Animals. Cytochrome P-450 CYP11B2 / genetics. Cytochrome P-450 CYP11B2 / metabolism. Gene Expression Regulation, Neoplastic / drug effects. Mice. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic / genetics. Time Factors. Up-Regulation / drug effects

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  • (PMID = 20647392.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; RWP5GA015D / Potassium
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38. Weng SW, Yang CH, Huang WT, Chen MC, Wang PW: Malignant hypertension secondary to cortisol-secreting adrenal tumour. N Z Med J; 2005 Jun 3;118(1216):U1498
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  • [Title] Malignant hypertension secondary to cortisol-secreting adrenal tumour.
  • Adrenal cortical tumour-induced malignant hypertension is rare, except for some documented aldosterone-producing adenomas.
  • This case in Taiwan is only the second reported case with malignant hypertension secondary to a cortisol-secreting adrenal tumour.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / secretion. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / secretion. Hydrocortisone / secretion. Hypertension, Malignant / etiology

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  • (PMID = 15937532.001).
  • [ISSN] 1175-8716
  • [Journal-full-title] The New Zealand medical journal
  • [ISO-abbreviation] N. Z. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antihypertensive Agents; WI4X0X7BPJ / Hydrocortisone
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39. Hahner S, Fassnacht M, Hammer F, Schammann M, Weismann D, Hansen IA, Allolio B: Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis. Eur J Endocrinol; 2005 Jan;152(1):143-53

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  • [Title] Evidence against a role of human airway trypsin-like protease--the human analogue of the growth-promoting rat adrenal secretory protease--in adrenal tumourigenesis.
  • OBJECTIVE: A serine protease from rat adrenal cortex was recently characterized and named adrenal secretory protease (AsP).
  • AsP is expressed in the adrenal cortex and is capable of cleaving pro-gamma-melanocyte-stimulating hormone (1-76 N-terminus of pro-opiomelanocortin) into fragments that act as adrenal mitogens.
  • AsP may therefore play a crucial role in adrenal growth and tumourigenesis.
  • The aim of this study was to further characterize the human homologue of AsP and its possible role in adrenal tumourigenesis.
  • While high expression of HAT mRNA was found in the trachea and in the gastrointestinal tract, expression in the adrenal was only very weak.
  • We further investigated HAT expression in five normal adrenal glands, 15 adrenocortical adenomas (five hormonally inactive adenomas, five aldosterone-producing adenomas and five cortisol-producing adenomas), nine adrenocortical carcinomas, five phaeochromocytomas and two adrenal hyperplasias.
  • Weak HAT expression was detectable in only two out of five normal adrenal glands, in one out of twenty-four adrenocortical tumours and four out of five phaeochromocytomas.
  • However, the expression in the adrenal tissue was several orders of magnitude lower than in the trachea.
  • In addition, we could not detect any HAT transcripts in a sample of fetal adrenal.
  • CONCLUSION: Gene structure and tissue distribution of HAT, the human homologue of the rat adrenal secretory protease AsP, reveal major interspecies differences.
  • The observation of very low expression levels in normal adrenal tissue and adrenocortical tumours casts doubt about a role for HAT in the physiological and pathological growth of adrenocortical cells.

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  • (PMID = 15762198.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / RNA, Neoplasm; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / human airway trypsin-like protease
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40. Yen RF, Wu VC, Liu KL, Cheng MF, Wu YW, Chueh SC, Lin WC, Wu KD, Tzen KY, Lu CC, TAIPAI Study Group: 131I-6beta-iodomethyl-19-norcholesterol SPECT/CT for primary aldosteronism patients with inconclusive adrenal venous sampling and CT results. J Nucl Med; 2009 Oct;50(10):1631-7
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  • [Title] 131I-6beta-iodomethyl-19-norcholesterol SPECT/CT for primary aldosteronism patients with inconclusive adrenal venous sampling and CT results.
  • The 2 main causes of primary aldosteronism (PA) are aldosterone-producing adenoma (APA) and idiopathic adrenal hyperplasia (IAH).
  • Dexamethasone-suppression (131)I-6beta-iodomethyl-19-norcholesterol (NP-59) adrenal scintigraphy can assess the functioning of the adrenal cortex.
  • This study evaluated the diagnostic usefulness of NP-59 SPECT/CT in differentiating APA from IAH and in predicting postadrenalectomy clinical outcome for PA patients who had inconclusive adrenal venous sampling (AVS) and CT results.
  • METHODS: We retrospectively reviewed the 31 adrenal lesions of 27 patients (age range, 33-71 y; mean age +/- SD, 50.4 +/- 10.9 y) who had been clinically confirmed (by saline infusion and captopril tests) to have PA, had inconclusive CT and AVS test results, and had undergone NP-59 imaging before adrenalectomy.
  • The NP-59 results were negative for 7 of the 23 patients with unilateral adrenal lesions, and none of these 7 patients had shown postsurgical clinical improvement.
  • [MeSH-major] 19-Iodocholesterol / analogs & derivatives. Adrenal Glands / blood supply. Hyperaldosteronism / diagnosis. Hyperaldosteronism / physiopathology. Veins
  • [MeSH-minor] Adenoma / complications. Adenoma / radiography. Adenoma / radionuclide imaging. Adrenalectomy. Adult. Aged. Diagnosis, Differential. Female. Humans. Hyperplasia / complications. Hyperplasia / radiography. Hyperplasia / radionuclide imaging. Male. Middle Aged. Retrospective Studies. Sensitivity and Specificity. Tomography, Emission-Computed, Single-Photon. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19759122.001).
  • [ISSN] 1535-5667
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 30461-91-7 / 19-Iodocholesterol; 68232-36-0 / 6-iodomethylcholesterol
  • [Investigator] Wu VC; Lin YH; Ho YL; Chang HW; Lin LY; Hu FC; Liu KL; Wang SM; Huang KH; Chen YM; Kuo CC; Chueh SC; Lu CC; Chang FC; Liao SC; Yen RF; Lin WC; Hsieh BS; Wu KD
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41. Moreau F, Mittre H, Benhaim A, Bois C, Bertherat J, Carreau S, Reznik Y: Aromatase expression in the normal human adult adrenal and in adrenocortical tumors: biochemical, immunohistochemical, and molecular studies. Eur J Endocrinol; 2009 Jan;160(1):93-9
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  • [Title] Aromatase expression in the normal human adult adrenal and in adrenocortical tumors: biochemical, immunohistochemical, and molecular studies.
  • Its expression in the adrenal is poorly studied except for the rare estrogen-producing adrenocortical tumors.
  • In order to further characterize aromatase expression in the adrenal, we evaluated the aromatase enzyme activity, Cyp19a1 gene expression level, and promoter utilization in normal adrenal tissues and in adrenocortical secreting tumors.
  • DESIGN AND METHODS: Six normal adult adrenals (NA), 2 feminizing adrenal tumors (FT), 10 cortisol-producing adenomas with overt (CS, n=4) or sub-clinical Cushing syndrome (SCS, n=6) and 3 aldosterone-producing adenomas (APA) were studied.
  • Promoter regions PII and PI.4-derived transcripts were also studied in NA, FT, and other steroid-producing tumors by a semi-quantitative comparative RT-PCR.
  • Immunofluorescence analysis was performed in normal human adrenal tissues.
  • CONCLUSION: Aromatase is expressed at similar levels in normal adrenal and in adrenocortical tumors, but at variably high levels in FT.

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  • (PMID = 18974231.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.14.14.1 / Aromatase
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42. Hsiao HP, Kirschner LS, Bourdeau I, Keil MF, Boikos SA, Verma S, Robinson-White AJ, Nesterova M, Lacroix A, Stratakis CA: Clinical and genetic heterogeneity, overlap with other tumor syndromes, and atypical glucocorticoid hormone secretion in adrenocorticotropin-independent macronodular adrenal hyperplasia compared with other adrenocortical tumors. J Clin Endocrinol Metab; 2009 Aug;94(8):2930-7
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  • [Title] Clinical and genetic heterogeneity, overlap with other tumor syndromes, and atypical glucocorticoid hormone secretion in adrenocorticotropin-independent macronodular adrenal hyperplasia compared with other adrenocortical tumors.
  • OBJECTIVE: ACTH-independent macronodular adrenal hyperplasia (AIMAH) is often associated with subclinical cortisol secretion or atypical Cushing's syndrome (CS).
  • 2) adrenocortical cortisol-producing adenoma with CS (n = 15);.
  • 3) aldosterone-producing adenoma (n = 19); and 4) single adenomas with clinically nonsignificant cortisol secretion (n = 32).
  • One patient had a GNAS mutation in adrenal nodules only.

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  • (PMID = 19509103.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Other-IDs] NLM/ PMC2730864
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43. Rossi GP, Bernini G, Caliumi C, Desideri G, Fabris B, Ferri C, Ganzaroli C, Giacchetti G, Letizia C, Maccario M, Mallamaci F, Mannelli M, Mattarello MJ, Moretti A, Palumbo G, Parenti G, Porteri E, Semplicini A, Rizzoni D, Rossi E, Boscaro M, Pessina AC, Mantero F, PAPY Study Investigators: A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J Am Coll Cardiol; 2006 Dec 5;48(11):2293-300
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  • METHODS: Consecutive hypertensive patients referred to 14 hypertension centers underwent a diagnostic protocol composed of measurement of Na+ and K+ in serum and 24-h urine, sitting plasma renin activity, and aldosterone at baseline and after 50 mg captopril.
  • The patients with an aldosterone/renin ratio >40 at baseline, and/or >30 after captopril, and/or a probability of PA (by a logistic discriminant function) > or =50% underwent imaging tests and adrenal vein sampling (AVS) or adrenocortical scintigraphy to identify the underlying adrenal pathology.
  • An aldosterone-producing adenoma (APA) was diagnosed in patients who in addition to excess autonomous aldosterone secretion showed:.
  • 1) lateralized aldosterone secretion at AVS or adrenocortical scintigraphy, 2) adenoma at surgery and pathology, and 3) a blood pressure decrease after adrenalectomy.
  • Evidence of excess autonomous aldosterone secretion without such criteria led to a diagnosis of idiopathic hyperaldosteronism (IHA).
  • [MeSH-minor] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / diagnosis. Adrenal Glands / blood supply. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / diagnosis. Adult. Aldosterone / blood. Blood Specimen Collection. Female. Humans. Male. Middle Aged. Prevalence. Prospective Studies. Radionuclide Imaging. Veins

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  • (PMID = 17161262.001).
  • [ISSN] 1558-3597
  • [Journal-full-title] Journal of the American College of Cardiology
  • [ISO-abbreviation] J. Am. Coll. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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44. Oki K, Yamane K, Sakashita Y, Kamei N, Watanabe H, Toyota N, Shigeta M, Sasano H, Kohno N: Primary aldosteronism and hypercortisolism due to bilateral functioning adrenocortical adenomas. Clin Exp Nephrol; 2008 Oct;12(5):382-7
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  • A 50-year-old male patient with a 15-year history of hypertension was referred to our hospital for evaluation of bilateral adrenal tumors.
  • Computed tomographic scan showed 10-mm masses in each adrenal gland.
  • Preoperative endocrinological examinations revealed autonomous cortisol and aldosterone secretion in this patient.
  • The results of a subsequent adrenal venous catheterization study were consistent with the presence of a left cortisol-producing tumor and a right aldosterone-producing tumor.
  • A left partial adrenalectomy was performed initially, but cortisol and aldosterone over-secretion persisted.
  • Pathological examination of the resected specimens, including immunohistochemical analysis, demonstrated that both adenomas possibly produced cortisol and aldosterone.
  • This is an extremely rare case of bilateral adrenal tumors, in which the left adrenocortical tumor produced and secreted cortisol or both cortisol and aldosterone and the right one produced and secreted both aldosterone and cortisol, as confirmed by clinical findings and pathological studies using immunohistochemical analysis.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Cushing Syndrome / etiology. Hyperaldosteronism / etiology
  • [MeSH-minor] Aldosterone / metabolism. Diagnosis, Differential. Humans. Hydrocortisone / metabolism. Male. Middle Aged

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  • (PMID = 18543063.001).
  • [ISSN] 1342-1751
  • [Journal-full-title] Clinical and experimental nephrology
  • [ISO-abbreviation] Clin. Exp. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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45. Gomez-Sanchez CE, Rossi GP, Fallo F, Mannelli M: Progress in primary aldosteronism: present challenges and perspectives. Horm Metab Res; 2010 Jun;42(6):374-81
Genetic Alliance. consumer health - Primary aldosteronism.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary Aldosteronism (PA) is a disorder of the adrenal zona glomerulosa (ZG) in which aldosterone secretion is increased and is relatively autonomous of normal regulatory mechanisms.
  • A recent conference in Munich organized by Prof. Reincke addressed advances and challenges related to the screening, diagnosis, and identification of uni- and bilateral involvement of the diseased adrenal of PA.
  • This implies that one or several yet unidentified stimuli can drive aldosterone overproduction, as well as the proliferation of aldosterone-producing cells.
  • Current diagnostic procedures allow to determine whether inappropriate aldosterone production is driven by one or both adrenal glands and thus to establish optimal treatment.
  • [MeSH-minor] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / diagnosis. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / diagnosis. Adrenocortical Adenoma / metabolism. Aldosterone / blood. Diagnosis, Differential. Goiter, Nodular / diagnosis. Goiter, Nodular / metabolism. Humans. Renin / blood

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  • [Copyright] Georg Thieme Verlag KG Stuttgart-New York.
  • (PMID = 20091458.001).
  • [ISSN] 1439-4286
  • [Journal-full-title] Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
  • [ISO-abbreviation] Horm. Metab. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL027255
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone; EC 3.4.23.15 / Renin
  • [Number-of-references] 104
  • [Other-IDs] NLM/ NIHMS773220; NLM/ PMC4823770
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46. Leitolf H, Dixit KC, Higham CE, Brabant G: Licorice - or more? Exp Clin Endocrinol Diabetes; 2010 Apr;118(4):250-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Morning ambulant aldosterone was slightly increased at 801 pmol/L and renin activity was undetectable.
  • Urinary 24 h aldosterone excretion was significantly increased at 162 ng/24 h with normal cortisol and catecholamine excretion.
  • Morning plasma aldosterone increased to 1 449 pmol/ml, renin activity remained undetectable but 24 h urine aldosterone excretion increased to 434 ng/24 h with a reduction in urinary cortisol excretion.
  • Abdominal imaging with US and MRI showed a 2.7 cmx2.2 cmx1.7 cm left adrenal mass.
  • He underwent laparoscopic left adrenalectomy and histology confirmed aldosterone producing adrenal adenoma.
  • Post-operatively his aldosterone and serum potassium levels normalized and he became normotensive without any antihypertensive medication.
  • [MeSH-major] Adrenal Cortex Neoplasms / ultrasonography. Adrenocortical Adenoma / ultrasonography. Aldosterone / blood. Glycyrrhiza / adverse effects. Hypokalemia / etiology

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  • [Copyright] (c) J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart. New York.
  • (PMID = 20213599.001).
  • [ISSN] 1439-3646
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Potassium, Dietary; 4964P6T9RB / Aldosterone
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47. Bassett MH, Mayhew B, Rehman K, White PC, Mantero F, Arnaldi G, Stewart PM, Bujalska I, Rainey WE: Expression profiles for steroidogenic enzymes in adrenocortical disease. J Clin Endocrinol Metab; 2005 Sep;90(9):5446-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Excess production of aldosterone or cortisol has profound effects on cardiovascular function and impacts other major organ systems.
  • The mechanisms leading to the autonomous hypersecretion of aldosterone or cortisol in aldosterone-producing adenoma (APA) or cortisol-producing adenoma (CPA) are unknown.
  • OBJECTIVE: The objective of this study was to compare the expression profiles of several steroid-metabolizing enzymes and transcription factors from normal adrenal (NA), APAs, and CPAs.
  • RESULTS: A microarray indicated a greater than 3-fold increase in the expression of CYP11B2 (aldosterone synthase) in APA, whereas 11beta-hydroxysteroid dehydrogenase type 2 (HSD11B2) and HSD17B1 had greater than 3-fold increases in expression in CPA compared with NA.
  • Real-time RT-PCR showed that APAs produced higher levels of HSD3B2, CYP21 (21-hydroxylase), and CYP11B2 mRNA, whereas CPAs produced higher levels of CYP11A (cholesterol side-chain cleavage), CYP17 (17alpha-hydroxylase/17-20 lyase), HSD3B2, and CYP11B1 (11beta-hydroxylase) mRNA compared with normal adrenal.
  • Steroidogenic factor-1, DAX-1 (dosage-sensitive sex reversal, adrenal hypoplasia congenita, critical region on the X chromosome gene 1), and GATA-6 were expressed at higher levels in APAs and CPAs, whereas NURR1 was expressed at higher levels in APAs than in CPAs or NAs.
  • CONCLUSION: Elevated production of aldosterone in APAs and of cortisol in CPAs is associated with increased expression of enzymes needed for corticosteroid production along with alterations in transcription factors that enhance the expression of steroid-metabolizing enzymes.
  • [MeSH-major] Adenoma / enzymology. Adrenal Cortex Hormones / biosynthesis. Adrenal Cortex Neoplasms / enzymology. Aldosterone / metabolism. Gene Expression Regulation, Enzymologic. Hydrocortisone / metabolism

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  • (PMID = 15985477.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-069950; United States / NIDDK NIH HHS / DK / DK-43140; United States / NICHD NIH HHS / HD / HD-11149
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Enzymes; 0 / NR5A1 protein, human; 0 / RNA, Messenger; 0 / Steroidogenic Factor 1; 0 / Transcription Factors; 4964P6T9RB / Aldosterone; WI4X0X7BPJ / Hydrocortisone
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48. Szücs N, Gláz E, Varga I, Tóth M, Kiss R, Patócs A, Jakab C, Perner F, Járay J, Horányi J, Dabasi G, Molnár F, Major L, Füto L, Rácz K, Tulassay Z: [Diagnosis and treatment outcome in primary aldosteronism based on a retrospective analysis of 187 cases]. Orv Hetil; 2006 Jan 15;147(2):51-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Aldosterone-producing adenoma was detected in more than two thirds of patients (n = 135), whereas idiopathic hyperaldosteronism was found in 46 patients.
  • For the diagnosis of familial hyperaldosteronism type I, molecular biological studies of the aldosterone-synthase/11beta-hydroxylase gene chimera were carried out in 30 patients but none of them showed the presence of the chimeric gene.
  • When comparing the clinical parameters of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism, no significant differences were found in the time period between the diagnosis of hypertension and the diagnosis of primary aldosteronism, or in the systolic and diastolic blood pressure values.
  • The mean of the lowest documented serum potassium concentration was slightly lower in patients with aldosterone-producing adenoma (2.8 +/- 0.1 mmol/l) compared to those with idiopathic hyperaldosteronism (3.1 +/- 0.2 mmol/l), but the difference was not significant.
  • The ratio of plasma aldosterone concentration (ng/dl) to plasma renin activity (ng/ml/h) was above 20 in all patients with aldosterone-producing adenoma and in all but 5 cases with idiopathic hyperaldosteronism.
  • When cases showing an elevation of plasma cortisol level during the test were excluded, this test differentiated patients with aldosterone-producing adenoma from those with idiopathic hyperaldosteronism with a sensitivity of 69% and a specificity of 92%.
  • In cases of adrenocortical adenomas not or not clearly detectable by radiological imaging techniques, as well as in cases with bilateral adrenocortical adenomas, selective adrenal vein sampling was performed (n = 55).
  • All but 4 patients with aldosterone-producing adenoma underwent adrenalectomy.
  • CONCLUSIONS: These observations are in contrast with the results of international studies which showed a high frequency of normokalemic primary aldosteronism and a more frequent occurrence of idiopathic hyperaldosteronism well treatable with aldosterone-antagonists.
  • [MeSH-major] Adenoma / surgery. Adrenal Cortex Neoplasms / surgery. Aldosterone / secretion. Hyperaldosteronism / diagnosis. Hyperaldosteronism / therapy. Mineralocorticoid Receptor Antagonists / therapeutic use

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  • (PMID = 16509213.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists; 0 / Mutant Chimeric Proteins; 4964P6T9RB / Aldosterone; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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49. Urbanet R, Pilon C, Calcagno A, Peschechera A, Hubert EL, Giacchetti G, Gomez-Sanchez C, Mulatero P, Toffanin M, Sonino N, Zennaro MC, Giorgino F, Vettor R, Fallo F: Analysis of insulin sensitivity in adipose tissue of patients with primary aldosteronism. J Clin Endocrinol Metab; 2010 Aug;95(8):4037-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The objective of the study was to assess the effect of high aldosterone levels on insulin sensitivity of adipose tissue in humans.
  • METHODS: Visceral adipose tissue (VAT) was obtained from patients with aldosterone-producing adenoma (APA; n=14) and, as controls, nonfunctioning adenoma (NFA; n=14) undergoing laparoscopic adrenalectomy.
  • The effect of increasing aldosterone concentrations on 2-deoxy-[3H]d-glucose uptake was tested in human sc abdominal adipocytes.
  • In cultured adipocytes, basal and insulin-stimulated glucose uptake were unaffected by 1-100 nM (normal/hyperaldosteronism) and impaired only by much higher, up to 10 microM, aldosterone concentrations.
  • CONCLUSIONS: Gene expression of insulin signaling/inflammatory molecules was similar in VAT of APA and NFA patients, not supporting an effect of aldosterone excess on insulin sensitivity of adipose tissues.
  • Only at pharmacological concentrations and through GR activation, aldosterone reduced glucose uptake in adipocytes.
  • [MeSH-minor] Adiponectin / genetics. Adiponectin / metabolism. Adrenal Cortex Neoplasms / genetics. Adrenal Cortex Neoplasms / metabolism. Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. Adrenocorticotropic Hormone / blood. Aldosterone / blood. Analysis of Variance. Blotting, Western. Female. Humans. Hydrocortisone / blood. Immunohistochemistry. Male. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Mineralocorticoid / genetics. Receptors, Mineralocorticoid / metabolism. Renin / blood. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20484481.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Insulin; 0 / RNA, Messenger; 0 / Receptors, Mineralocorticoid; 4964P6T9RB / Aldosterone; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.23.15 / Renin; WI4X0X7BPJ / Hydrocortisone
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50. Beuschlein F, Reincke M: [Therapy-resistant hypertension--the endocrinological view]. MMW Fortschr Med; 2007 Mar 1;149(9):29-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This includes primary hyperaldosteronism due to an aldosterone-producing adenoma, or a bilateral adrenal hyperplasia, hypercortisolism caused by a tumor of the adrenals, or an ACTH-dependent form of Cushing's syndrome, as also excessive catecholamines caused by a pheochromocytoma or a paraganglioma.
  • In addition to surgical treatment, specific pharmacotherapeutic measures for the prevention or follow-up treatment of excess adrenal hormones are available.
  • [MeSH-minor] Adrenal Cortex Neoplasms / complications. Adrenal Cortex Neoplasms / diagnosis. Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms / diagnosis. Adrenocortical Adenoma / complications. Adrenocortical Adenoma / diagnosis. Diagnosis, Differential. Drug Resistance. Humans. Pheochromocytoma / complications. Pheochromocytoma / diagnosis

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  • [CommentIn] MMW Fortschr Med. 2007 Jun 14;149(24):8 [17668740.001]
  • (PMID = 17612246.001).
  • [ISSN] 1438-3276
  • [Journal-full-title] MMW Fortschritte der Medizin
  • [ISO-abbreviation] MMW Fortschr Med
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Catecholamines
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51. Nishikawa T, Matsuzawa Y, Saito J, Omura M: Is it Possible to Extirpate Cardiovascular Events in Primary Aldosteronism After Surgical Treatment. Jpn Clin Med; 2010;1:21-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is well known that primary aldosteronism (PA) due to aldosterone-producing adenoma (APA) is a surgically curable secondary hypertension.
  • Adrenal venous sampling (AVS) can diagnose the laterality of hypersecretion of aldosterone in those patients, while it is still impossible to differentiate bilateral hypersecretion of bilateral aldosterone-producing adenomas (Blt-APAs) from that of bilateral hyperplasia of IHA.
  • To solve the problem, we try to develop a new method of supper-selective ACTH-stimulated adrenal venous sampling (SS-ACTH-AVS).
  • Adrenal effluents were sampled super-selectively at the central veins and at one or two tributaries of adrenal veins in each gland.
  • We would like to emphasize that SS-ACTH-AVS can precisely analyze the situation of hyperfunction of steroidogenesis in each side of adrenals as well as in some tiny lesions inside the adrenal cortex which are not visible in the CT images.
  • Thus, we should perform SS-ACTH-AVS especially in the case demonstrating the existence of bilateral adrenal lesions such as unilateral and bilateral tumors, or even no tumor in both sides in the patients with PA.

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  • (PMID = 23946677.001).
  • [Journal-full-title] Japanese clinical medicine
  • [ISO-abbreviation] Jpn Clin Med
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3738501
  • [Keywords] NOTNLM ; adrenal adenoma / adrenal hyperplasia / adrenal vein sampling / hypertension
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52. Saldutti L, Romano GG, Romano F: Open adrenalectomy surgery: an obsolete technique? About a case of Conn's syndrome. Ann Ital Chir; 2008 Jan-Feb;79(1):47-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The authors report a case of an adenoma of Conn brought to their attention and treated by them in open surgery.
  • 1) to the adenoma producing aldosterone, responsive to the ACTH, which represents the most common form (60-70%), responsive to surgery and with full recovery (70%) of cases.
  • 2) to the bilateral hyperplasia, responsive to the angiotensine II, 25-30% of the cases, susceptible to medical therapy with receptorial antagonists of aldosterone.
  • Comparative studies have shown that laparoscopic surgery adopted by experienced surgeons can treat the adrenal pathology in a mininvasive way, with good results for effectiveness and safety, and for these reasons the laparoscopic treatment is considered the gold standard for this pathology.
  • But adrenal pathology is rare, 4% in people suffering hypertension, and from 0.35 to 4.4% in tumours.
  • For this reason the authors believe that "open" surgery in adrenal pathology is not obsolete and that surgical teams which have experience in retroperitoneal pathology must intervene adopting a laparotomic approach, with the aim to operate the sick person, who totally confides himself to the surgeon, in an appropriate way.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy / methods. Adrenocortical Adenoma / surgery

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  • (PMID = 18572739.001).
  • [ISSN] 0003-469X
  • [Journal-full-title] Annali italiani di chirurgia
  • [ISO-abbreviation] Ann Ital Chir
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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53. Young WF: Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol (Oxf); 2007 May;66(5):607-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Great strides have been made in our understanding of the pathophysiology of primary aldosteronism syndrome since Conn's description of the clinical presentation of a patient with an aldosterone-producing adenoma (APA) more than 50 years ago.
  • Using the plasma aldosterone to plasma renin activity ratio as a case-finding test, followed by aldosterone suppression confirmatory testing, has resulted in much higher prevalence estimates of 5-13% of all patients with hypertension.
  • In addition, there has been a new recognition of the aldosterone-specific cardiovascular morbidity and mortality associated with aldosterone excess.
  • Patients with hypertension and hypokalaemia (regardless of presumed cause), treatment-resistant hypertension (three antihypertensive drugs and poor control), severe hypertension (>or= 160 mmHg systolic or >or= 100 mmHg diastolic), hypertension and an incidental adrenal mass, onset of hypertension at a young age or patients being evaluated for other forms of secondary hypertension should undergo screening for primary aldosteronism.
  • In patients with suspected primary aldosteronism, screening can be accomplished by measuring a morning (preferably between 0800 and 1000 h) ambulatory paired random plasma aldosterone concentration (PAC) and plasma renin activity (PRA).
  • An increased PAC:PRA ratio is not diagnostic by itself, and primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion.
  • Aldosterone suppression testing can be performed with orally administered sodium chloride and measurement of urinary aldosterone or with intravenous sodium chloride loading and measurement of PAC.
  • Unilateral adrenalectomy in patients with APA or unilateral adrenal hyperplasia results in normalization of hypokalaemia in all these patients; hypertension is improved in all and is cured in approximately 30-60% of them.
  • In bilateral adrenal forms of primary aldosteronism, unilateral or bilateral adrenalectomy seldom corrects the hypertension and they should be treated medically with a mineralocorticoid receptor antagonist.
  • [MeSH-minor] Adrenal Cortex Neoplasms / complications. Adrenalectomy. Adrenocortical Adenoma / complications. Diagnosis, Differential. Humans. Hypertension / etiology. Hypokalemia / etiology. Mineralocorticoid Receptor Antagonists / therapeutic use


54. Bruno RM, Ghiadoni L, Mazzi V, Taddei S: [Resistant hypertension: a case report]. Recenti Prog Med; 2010 Jan;101(1):35-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 72-years-old man, having 230-210/110-90 mmHg with a 5-drugs antihypertensive regimen, was diagnosed with an aldosterone-producing adenoma.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Hyperaldosteronism / etiology. Hypertension / etiology

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  • (PMID = 20391685.001).
  • [ISSN] 0034-1193
  • [Journal-full-title] Recenti progressi in medicina
  • [ISO-abbreviation] Recenti Prog Med
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antihypertensive Agents
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55. Pang TC, Bambach C, Monaghan JC, Sidhu SB, Bune A, Delbridge LW, Sywak MS: Outcomes of laparoscopic adrenalectomy for hyperaldosteronism. ANZ J Surg; 2007 Sep;77(9):768-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Primary hyperaldosteronism is a frequent cause of resistant hypertension and is amenable to surgical intervention when caused by a unilateral aldosterone-producing adenoma.
  • Blood pressure (BP), serum aldosterone levels, plasma renin activity, serum potassium and antihypertensive requirement were measured before and after adrenalectomy.
  • Serum aldosterone levels were significantly lower (698 (confidence interval 534-862) pg/mL vs 181 (confidence interval 139-225) pg/mL, P < 0.0001).
  • Larger adrenal gland size and older age at time of surgery are predictors of persisting hypertension.
  • [MeSH-major] Adrenal Cortex Diseases / surgery. Adrenal Cortex Neoplasms / surgery. Adrenal Glands / pathology. Adrenalectomy. Adrenocortical Adenoma / surgery. Hyperaldosteronism / surgery

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  • (PMID = 17685956.001).
  • [ISSN] 1445-1433
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Australia
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56. Aiba M, Fujibayashi M: Histopathological diagnosis and prognostic factors in adrenocortical carcinoma. Endocr Pathol; 2005;16(1):13-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • These special type tumors include pediatric adrenocortical tumors, oncocytomas, and aldosterone-producing tumors of pure zona glomerulosa type.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis
  • [MeSH-minor] Adenoma, Oxyphilic. Adult. Aged. Aged, 80 and over. Aldosterone / metabolism. Biomarkers, Tumor / metabolism. Cell Nucleus / pathology. Female. Humans. Immunohistochemistry. Infant. Insulin-Like Growth Factor II / metabolism. Male. Neoplasm Staging. Prognosis

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  • (PMID = 16000842.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 4964P6T9RB / Aldosterone; 67763-97-7 / Insulin-Like Growth Factor II
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57. Moo TA, Zarnegar R, Duh QY: Prediction of successful outcome in patients with primary aldosteronism. Curr Treat Options Oncol; 2007 Aug;8(4):314-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary aldosteronism is characterized by hypertension with or without hypokalemia and a high plasma aldosterone concentration (PAC) with a concurrent low plasma renin activity (PRA).
  • The most common subtypes of primary aldosteronism are aldosterone-producing adenoma (42%) and bilateral idiopathic hyperaldosteronism (58%).
  • Bilateral idiopathic hyperaldosteronism is best managed pharmacologically and improves with the use of aldosterone receptor antagonists.
  • Aldosterone producing adenoma and unilateral adrenal hyperplasia are appropriately treated with laparoscopic adrenalectomy.
  • Now, with accumulating evidence of the detrimental effects of aldosterone to the myocardium, vascular endothelium and kidneys, treatment also focuses on normalizing aldosterone levels or blocking aldosterone action at the receptor level.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Hyperaldosteronism / therapy. Mineralocorticoid Receptor Antagonists / therapeutic use

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  • (PMID = 18058076.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mineralocorticoid Receptor Antagonists
  • [Number-of-references] 29
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58. Zhang GX, Wang BJ, Ouyang JZ, Deng XY, Ma X, Li HZ, Wu Z, Liu SL, Xu H, Zhang X: Polymorphisms in CYP11B2 and CYP11B1 genes associated with primary hyperaldosteronism. Hypertens Res; 2010 May;33(5):478-84

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Several frequent polymorphisms in the CYP11B2 gene are suggested to be associated with essential hypertension and aldosterone secretion.
  • The rs6410 allelic frequencies in patients with aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were significantly different from those in controls at P=1.09 x 10(-5) and 0.015, respectively.
  • [MeSH-major] Adrenal Cortex Neoplasms / genetics. Adrenocortical Adenoma / genetics. Cytochrome P-450 CYP11B2 / genetics. Hyperaldosteronism / genetics. Steroid 11-beta-Hydroxylase / genetics

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  • (PMID = 20339375.001).
  • [ISSN] 1348-4214
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase
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59. Bimpaki EI, Nesterova M, Stratakis CA: Abnormalities of cAMP signaling are present in adrenocortical lesions associated with ACTH-independent Cushing syndrome despite the absence of mutations in known genes. Eur J Endocrinol; 2009 Jul;161(1):153-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Bilateral adrenal hyperplasias (BAHs) may be caused by mutations of genes that code for molecules that participate in cAMP signaling.
  • Little is known about cAMP signaling in adrenal lesions associated with ACTH-independent Cushing syndrome (AICS) that do not harbor mutations in known genes.
  • DESIGN: Samples from 27 patients (ages 5-60 years) were studied and compared with normal adrenocortical tissue (n=4) and aldosterone-producing adenomas (APA, n=5).
  • RESULTS: Cortisol-producing adenomas (CPAs) and other lesions that were GNAS, PRKAR1A, PDE11A, and PDE8B gene mutation-negative were compared with PRKAR1A mutation-positive lesions, normal tissue, and APAs; abnormalities of the cAMP-signaling pathway were found in both BAHs and CPAs.
  • CONCLUSION: Lesions of the adrenal associated with AICS, independently of their GNAS, PRKAR1A, PDE11A, and PDE8B mutation status, have functional abnormalities of cAMP signaling.

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  • (PMID = 19429701.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 9002-60-2 / Adrenocorticotropic Hormone; E0399OZS9N / Cyclic AMP; EC 2.3.1.48 / CREB-Binding Protein; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / PDE8B protein, human; EC 3.1.4.35 / PDE11A protein, human; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; WI4X0X7BPJ / Hydrocortisone
  • [Other-IDs] NLM/ NIHMS305405; NLM/ PMC3136809
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60. Nicol MR, Papacleovoulou G, Evans DB, Penning TM, Strachan MW, Advani A, Johnson SJ, Quinton R, Mason JI: Estrogen biosynthesis in human H295 adrenocortical carcinoma cells. Mol Cell Endocrinol; 2009 Mar 5;300(1-2):115-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Adrenocortical carcinoma is an uncommon malignancy and feminizing symptoms secondary to adrenal estrogen-secretion are extremely rare.
  • Western immunoblotting of an estrogen-secreting adrenal carcinoma revealed notable levels of both aromatase and AKR1C3 expression while an aldosterone-producing adrenal adenoma lacked aromatase expression and showed a reduced level of AKR1C3 expression.
  • Immunohistochemistry of the carcinoma-bearing adrenal revealed localization of AKR1C3 not only in the tumor but also principally in the zona reticularis of the normal adrenal tissue.
  • Adrenal aromatase and AKR1C3 expression therefore appear to be features of adrenocortical malignancies that are associated with biosynthesis of active estrogen.

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  • (PMID = 19026713.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090744-07; United States / NCI NIH HHS / CA / R01 CA090744; United States / NCI NIH HHS / CA / R01 CA090744-07; United States / NCI NIH HHS / CA / R01-CA90744
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Estrogens; 1F7A44V6OU / Colforsin; 37221-79-7 / Vasoactive Intestinal Peptide; EC 1.1.- / 17-Hydroxysteroid Dehydrogenases; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C3 protein, human; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.14.1 / Aromatase; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
  • [Other-IDs] NLM/ NIHMS99072; NLM/ PMC2673546
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61. Zarnegar R, Young WF Jr, Lee J, Sweet MP, Kebebew E, Farley DR, Thompson GB, Grant CS, Clark OH, Duh QY: The aldosteronoma resolution score: predicting complete resolution of hypertension after adrenalectomy for aldosteronoma. Ann Surg; 2008 Mar;247(3):511-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To develop a prediction model using information readily available, at clinical presentation, which could determine whether patients with aldosterone-producing adenomas would have complete resolution of hypertension after adrenalectomy.
  • [MeSH-major] Adrenal Cortex Neoplasms / surgery. Adrenalectomy. Adrenocortical Adenoma / surgery. Hypertension / therapy

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  • (PMID = 18376197.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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62. Chitalia N, Weeg N, Antonios TF: Aldosterone-producing adrenal adenoma and idiopathic intracranial hypertension--a pathogenetic link for aldosterone? QJM; 2010 Sep;103(9):699-702
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aldosterone-producing adrenal adenoma and idiopathic intracranial hypertension--a pathogenetic link for aldosterone?
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenocortical Adenoma / complications. Aldosterone / secretion. Hyperaldosteronism / complications. Pseudotumor Cerebri / etiology

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  • (PMID = 20179082.001).
  • [ISSN] 1460-2393
  • [Journal-full-title] QJM : monthly journal of the Association of Physicians
  • [ISO-abbreviation] QJM
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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63. Gomez-Sanchez CE, Gomez-Sanchez EP: Aldosterone-producing adenomas: mining for genes. Hypertension; 2010 Jun;55(6):1306-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aldosterone-producing adenomas: mining for genes.

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  • (PMID = 20385966.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL027255-26A1; United States / NHLBI NIH HHS / HL / R01 HL027255; United States / NHLBI NIH HHS / HL / HL27255; United States / NHLBI NIH HHS / HL / R01 HL027255-26A1
  • [Publication-type] Comment; Editorial; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
  • [Other-IDs] NLM/ NIHMS198695; NLM/ PMC2878664
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64. Ohta Y, Sakata S, Miyata E, Iguchi A, Momosaki S, Tsuchihashi T: Case report: Coexistence of pheochromocytoma and bilateral aldosterone-producing adenomas in a 36-year-old woman. J Hum Hypertens; 2010 Aug;24(8):555-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case report: Coexistence of pheochromocytoma and bilateral aldosterone-producing adenomas in a 36-year-old woman.
  • [MeSH-major] Adrenal Cortex Neoplasms / complications. Adrenal Gland Neoplasms / complications. Adrenocortical Adenoma / complications. Aldosterone / secretion. Pheochromocytoma / complications

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  • (PMID = 20410920.001).
  • [ISSN] 1476-5527
  • [Journal-full-title] Journal of human hypertension
  • [ISO-abbreviation] J Hum Hypertens
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 4964P6T9RB / Aldosterone
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