[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 64 of about 64
26. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


27. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Pheochromocytoma.
  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


28. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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


35. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Pheochromocytoma.
  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • MedlinePlus Health Information. consumer health - Pheochromocytoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


36. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Hazardous Substances Data Bank. CAPTOPRIL .
  • Hazardous Substances Data Bank. SODIUM CHLORIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


37. Beuschlein F, Reincke M: [Therapy-resistant hypertension--the endocrinological view]. MMW Fortschr Med; 2007 Mar 1;149(9):29-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Blood Pressure Medicines.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


41. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Adrenocortical Carcinoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):649-52 [11158024.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Sep;81(9):3173-6 [8784064.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Mar;84(4):485-92 [12732294.001]
  • [Cites] J Endocrinol. 2004 Jan;180(1):125-33 [14709151.001]
  • [Cites] J Mol Endocrinol. 2004 Jun;32(3):869-77 [15171718.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] J Clin Invest. 1977 Aug;60(2):455-64 [874104.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8948-52 [2848247.001]
  • [Cites] Lab Invest. 1990 Jul;63(1):132-6 [2374399.001]
  • [Cites] Cancer Res. 1990 Sep 1;50(17):5488-96 [2386954.001]
  • [Cites] Mol Endocrinol. 1993 Mar;7(3):423-33 [8387159.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Sep;77(3):731-7 [8396576.001]
  • [Cites] Mol Cell Endocrinol. 1994 Apr;100(1-2):45-50 [8056157.001]
  • [Cites] J Urol. 1995 Mar;153(3 Pt 2):1039-40 [7853554.001]
  • [Cites] Medicine (Baltimore). 1965 Jan;44:37-79 [14264352.001]
  • [Cites] Mol Cell Endocrinol. 2004 Dec 30;228(1-2):23-38 [15541570.001]
  • [Cites] Steroids. 2004 Dec;69(13-14):795-801 [15582534.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 May;95(1-5):35-9 [16024247.001]
  • [Cites] Pharmacol Rev. 2005 Sep;57(3):359-83 [16109840.001]
  • [Cites] J Endocrinol. 2006 Jan;188(1):59-68 [16394175.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Jun;91(6):2027-37 [16551738.001]
  • [Cites] J Steroid Biochem Mol Biol. 2006 Nov;101(4-5):254-62 [16979335.001]
  • [Cites] Arch Biochem Biophys. 2007 Aug 15;464(2):241-50 [17537398.001]
  • [Cites] J Endocrinol. 2007 Oct;195(1):39-48 [17911395.001]
  • [Cites] Hum Reprod. 2007 Nov;22(11):2981-91 [17848403.001]
  • [Cites] Eur J Endocrinol. 2003 Apr;148(4):457-61 [12656667.001]
  • (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
  •  go-up   go-down


42. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Endocrinol (Paris). 2000 Feb;61(1):52-60 [10790593.001]
  • [Cites] J Clin Endocrinol Metab. 2000 May;85(5):1863-7 [10843166.001]
  • [Cites] J Mol Endocrinol. 2009 Apr;42(4):319-30 [19158234.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1480-6 [18854423.001]
  • [Cites] Lancet. 2008 Jun 7;371(9628):1921-6 [18539224.001]
  • [Cites] Rev Esp Cardiol. 2008 Apr;61(4):418-21 [18405523.001]
  • [Cites] Endocr Rev. 2008 Apr;29(2):133-54 [18292466.001]
  • [Cites] J Hypertens. 2008 Apr;26(4):613-21 [18327065.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2203-8 [18250325.001]
  • [Cites] Mol Endocrinol. 2000 Jun;14(6):863-74 [10847588.001]
  • [Cites] Nat Rev Neurosci. 2001 Mar;2(3):175-84 [11256078.001]
  • [Cites] Mol Cell Endocrinol. 2001 Apr 25;175(1-2):157-71 [11325526.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Aug;281(2):C700-8 [11443069.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5426-32 [11733509.001]
  • [Cites] Mol Endocrinol. 2002 Mar;16(3):621-9 [11875121.001]
  • [Cites] Hypertension. 2003 Aug;42(2):161-5 [12796282.001]
  • [Cites] EMBO J. 2003 Oct 15;22(20):5403-11 [14532113.001]
  • [Cites] J Neurophysiol. 2003 Oct;90(4):2341-8 [12815014.001]
  • [Cites] Physiol Rev. 2004 Apr;84(2):489-539 [15044681.001]
  • [Cites] J Steroid Biochem. 1974 Aug;5(5):501-23 [4376199.001]
  • [Cites] Clin Sci Mol Med. 1975 Dec;49(6):527-34 [1204282.001]
  • [Cites] Steroids. 1978 Sep;32(2):257-67 [715820.001]
  • [Cites] Annu Rev Physiol. 1988;50:409-26 [3288099.001]
  • [Cites] Endocrinology. 1991 May;128(5):2534-9 [2019265.001]
  • [Cites] Endocrinology. 1993 Nov;133(5):2235-40 [8404675.001]
  • [Cites] Ann Intern Med. 1994 Dec 1;121(11):877-85 [7978702.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Feb;42(2):111-9 [7704954.001]
  • [Cites] Steroids. 1995 Jan;60(1):2-9 [7792810.001]
  • [Cites] Mol Cell Endocrinol. 1995 Dec 29;115(2):215-19 [8824897.001]
  • [Cites] J Steroid Biochem Mol Biol. 1996 Jul;58(4):417-24 [8903426.001]
  • [Cites] Endocrinology. 1997 Feb;138(2):835-8 [9003023.001]
  • [Cites] Steroids. 1997 Jan;62(1):10-20 [9029709.001]
  • [Cites] J Membr Biol. 1997 Apr 1;156(3):261-77 [9096067.001]
  • [Cites] Mol Endocrinol. 1997 May;11(5):638-49 [9139807.001]
  • [Cites] Endocrinology. 1997 Oct;138(10):4167-75 [9322926.001]
  • [Cites] Am J Physiol. 1999 May;276(5 Pt 2):F674-83 [10330049.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3422-7 [16492788.001]
  • [Cites] Mol Endocrinol. 2006 May;20(5):953-70 [16141358.001]
  • [Cites] Hypertension. 2006 Aug;48(2):232-8 [16801482.001]
  • [Cites] J Physiol. 2007 Jan 15;578(Pt 2):377-85 [17068099.001]
  • [Cites] Cell Biochem Biophys. 2007;47(2):209-56 [17652773.001]
  • [Cites] J Mol Endocrinol. 2007 Dec;39(6):365-74 [18055484.001]
  • [Cites] EMBO J. 2008 Jan 9;27(1):179-87 [18034154.001]
  • (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
  •  go-up   go-down


43. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


4
Advertisement
4. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Rhabdomyolysis.
  • Hazardous Substances Data Bank. SPIRONOLACTONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


45. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


46. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


47. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


48. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2003 May;88(5):2147-51 [12727968.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5308-19 [14500362.001]
  • [Cites] Proc Natl Acad Sci U S A. 1970 Sep;67(1):305-12 [4318781.001]
  • [Cites] Biochim Biophys Acta. 1975 Feb 19;377(2):271-81 [235302.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):890-3 [8077378.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1302-10 [15585558.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3531-6 [11061496.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):89-92 [10973256.001]
  • [Cites] Am J Hum Genet. 2002 Dec;71(6):1433-42 [12424709.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4324-9 [12213893.001]
  • [Cites] J Clin Endocrinol Metab. 2006 May;91(5):1943-9 [16464939.001]
  • [Cites] Clin Cancer Res. 2008 Jun 15;14(12):4016-24 [18559625.001]
  • [Cites] Eur J Hum Genet. 2008 Oct;16(10):1245-53 [18431404.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):794-800 [16767104.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Sep;91(9):3626-32 [16772351.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11571-5 [17178847.001]
  • [Cites] Curr Opin Endocrinol Diabetes Obes. 2007 Jun;14(3):219-25 [17940443.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2007 Nov;3(11):748-57 [17955016.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Feb;93(2):565-71 [18056771.001]
  • [Cites] N Engl J Med. 2008 Feb 14;358(7):750-2 [18272904.001]
  • [Cites] Horm Metab Res. 2008 May;40(5):347-53 [18491255.001]
  • [Cites] Endocr Dev. 2008;13:117-32 [18493137.001]
  • (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
  •  go-up   go-down


49. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Primary aldosteronism.
  • MedlinePlus Health Information. consumer health - Sodium.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


50. Aiba M, Fujibayashi M: Histopathological diagnosis and prognostic factors in adrenocortical carcinoma. Endocr Pathol; 2005;16(1):13-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Adrenocortical Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arch Surg. 2001 May;136(5):543-9 [11343545.001]
  • [Cites] J Biol Chem. 1991 Jun 15;266(17):10731-4 [2040591.001]
  • [Cites] Am J Surg Pathol. 2003 Jul;27(7):867-81 [12826878.001]
  • [Cites] Endocr Pathol. 2002 Summer;13(2):141-8 [12165663.001]
  • [Cites] Cancer. 2002 May 1;94(9):2333-43 [12015757.001]
  • [Cites] Surgery. 1992 Dec;112(6):981-6 [1360713.001]
  • [Cites] Med Pediatr Oncol. 1997 Mar;28(3):175-8 [9024511.001]
  • [Cites] Arch Surg. 1999 Feb;134(2):181-5 [10025460.001]
  • [Cites] Am J Surg Pathol. 1991 Oct;15(10 ):949-56 [1928551.001]
  • [Cites] Am J Clin Pathol. 1979 Sep;72(3):390-9 [474519.001]
  • [Cites] Endocr Pathol. 2003 Summer;14(2):107-16 [12858000.001]
  • [Cites] Pathol Int. 2004 Apr;54(4):273-8 [15028030.001]
  • [Cites] Mod Pathol. 2002 Sep;15(9):973-8 [12218215.001]
  • [Cites] Am J Pathol. 2003 Feb;162(2):521-31 [12547710.001]
  • [Cites] J Urol. 2003 Jan;169(1):5-11 [12478091.001]
  • [Cites] Acta Pathol Jpn. 1979 Mar;29(2):177-82 [552791.001]
  • [Cites] Am J Surg Pathol. 1989 Mar;13(3):202-6 [2919718.001]
  • [Cites] Am J Clin Pathol. 1991 Sep;96(3):334-40 [1652202.001]
  • [Cites] J Clin Endocrinol Metab. 2000 May;85(5):2048-56 [10843195.001]
  • [Cites] Mod Pathol. 2003 Aug;16(8):742-51 [12920217.001]
  • [Cites] Pathol Annu. 1992;27 Pt 1:1-53 [1736241.001]
  • [Cites] Am J Pathol. 1981 Jun;103(3):404-10 [7195152.001]
  • [Cites] Am J Pathol. 1986 Dec;125(3):431-5 [2432790.001]
  • [Cites] Cancer. 2001 Sep 15;92(6):1385-92 [11745214.001]
  • [Cites] Cancer. 1985 Feb 15;55(4):766-73 [3967172.001]
  • [Cites] Am J Surg Pathol. 1984 Mar;8(3):163-9 [6703192.001]
  • (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
  •  go-up   go-down


51. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Hyperaldosteronism.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


52. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Primary aldosteronism.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Surgery. 2004 Dec;136(6):1227-35 [15657580.001]
  • [Cites] Am Surg. 2007 Feb;73(2):174-80 [17305298.001]
  • [Cites] Expert Opin Pharmacother. 2006 Apr;7(5):563-73 [16553572.001]
  • [Cites] J Hypertens. 2007 Jan;25(1):177-86 [17143190.001]
  • [Cites] Surg Endosc. 2003 Feb;17(2):264-7 [12399875.001]
  • [Cites] Radiology. 2004 Apr;231(1):225-30 [14990812.001]
  • [Cites] Ann Pharmacother. 2002 Oct;36(10):1567-76 [12243608.001]
  • [Cites] J Hypertens. 2001 Mar;19(3):353-61 [11288803.001]
  • [Cites] Nephrol Dial Transplant. 2004 Apr;19(4):774-7 [15031328.001]
  • [Cites] J Am Coll Cardiol. 2005 Apr 19;45(8):1243-8 [15837256.001]
  • [Cites] Arq Bras Endocrinol Metabol. 2004 Oct;48(5):682-6 [15761539.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12 ):5814-7 [14671174.001]
  • [Cites] Curr Hypertens Rep. 2001 Oct;3(5):406-9 [11551375.001]
  • [Cites] J Hypertens. 2001 Jun;19(6):1161-5 [11403366.001]
  • [Cites] Ann Pharmacother. 2007 Jan;41(1):129-32 [17179189.001]
  • [Cites] World J Surg. 2005 Feb;29(2):155-9 [15650803.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2007 Mar;115(3):171-4 [17427105.001]
  • [Cites] Br J Clin Pharmacol. 1999 Nov;48(5):756-60 [10594479.001]
  • [Cites] Am J Hypertens. 2002 Aug;15(8):709-16 [12160194.001]
  • [Cites] Cancer. 2003 Feb 1;97(3):554-60 [12548596.001]
  • [Cites] Nat Clin Pract Nephrol. 2006 Apr;2(4):198-208; quiz, 1 p following 230 [16932426.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Mar;86(3):1083-90 [11238490.001]
  • [Cites] J Am Coll Cardiol. 2006 Dec 5;48(11):2293-300 [17161262.001]
  • [Cites] Ann Intern Med. 2001 Aug 21;135(4):258-61 [11511140.001]
  • [Cites] Endocrinology. 2003 Jun;144(6):2208-13 [12746276.001]
  • [Cites] World J Surg. 2006 May;30(5):879-85; discussion 886-7 [16680603.001]
  • [Cites] Hypertension. 2001 Jun;37(6):1440-3 [11408392.001]
  • [Cites] Hypertension. 2001 Sep;38(3 Pt 2):688-91 [11566957.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Nov;82(11):3570-3 [9360508.001]
  • (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
  •  go-up   go-down


53. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


54. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


55. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


56. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


57. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Primary aldosteronism.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


58. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Primary aldosteronism.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


59. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


60. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • University of Turin Instituional Repository AperTO. Full Text from .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


61. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Adrenal Hypertension.
  • Genetic Alliance. consumer health - Intracranial Hypertension.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


62. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


63. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


64. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - After Surgery.
  • MedlinePlus Health Information. consumer health - High Blood Pressure.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down






Advertisement