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Primary hyperaldosteronism : evaluation of procedures for diagnosis and localization
We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all...
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Published in: | Quarterly journal of medicine 1993-06, Vol.86 (6), p.383-392 |
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container_title | Quarterly journal of medicine |
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creator | HAMBLING, C JUNG, R. T BROWNING, M. C. K GUNN, A ANDERSON, J. M |
description | We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-seleno-methyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients. |
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T ; BROWNING, M. C. K ; GUNN, A ; ANDERSON, J. M</creator><creatorcontrib>HAMBLING, C ; JUNG, R. T ; BROWNING, M. C. K ; GUNN, A ; ANDERSON, J. M</creatorcontrib><description>We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-seleno-methyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients.</description><identifier>ISSN: 0033-5622</identifier><identifier>EISSN: 2058-1130</identifier><identifier>PMID: 8171186</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adenoma - complications ; Adenoma - diagnosis ; Adrenal Gland Neoplasms - complications ; Adrenal Gland Neoplasms - diagnosis ; Adrenal Glands - blood supply ; Adrenal Glands - pathology ; Adrenals. Adrenal axis. Renin-angiotensin system (diseases) ; Adult ; Aged ; Aldosterone - blood ; Aldosterone - urine ; Biological and medical sciences ; Endocrinopathies ; Female ; Humans ; Hyperaldosteronism - diagnosis ; Hyperaldosteronism - diagnostic imaging ; Hyperaldosteronism - etiology ; Hyperplasia ; Male ; Medical sciences ; Middle Aged ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Radiography ; Renin - blood ; Veins</subject><ispartof>Quarterly journal of medicine, 1993-06, Vol.86 (6), p.383-392</ispartof><rights>1993 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4800849$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8171186$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HAMBLING, C</creatorcontrib><creatorcontrib>JUNG, R. T</creatorcontrib><creatorcontrib>BROWNING, M. C. K</creatorcontrib><creatorcontrib>GUNN, A</creatorcontrib><creatorcontrib>ANDERSON, J. M</creatorcontrib><title>Primary hyperaldosteronism : evaluation of procedures for diagnosis and localization</title><title>Quarterly journal of medicine</title><addtitle>Q J Med</addtitle><description>We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-seleno-methyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients.</description><subject>Adenoma - complications</subject><subject>Adenoma - diagnosis</subject><subject>Adrenal Gland Neoplasms - complications</subject><subject>Adrenal Gland Neoplasms - diagnosis</subject><subject>Adrenal Glands - blood supply</subject><subject>Adrenal Glands - pathology</subject><subject>Adrenals. Adrenal axis. Renin-angiotensin system (diseases)</subject><subject>Adult</subject><subject>Aged</subject><subject>Aldosterone - blood</subject><subject>Aldosterone - urine</subject><subject>Biological and medical sciences</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperaldosteronism - diagnosis</subject><subject>Hyperaldosteronism - diagnostic imaging</subject><subject>Hyperaldosteronism - etiology</subject><subject>Hyperplasia</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Radiography</subject><subject>Renin - blood</subject><subject>Veins</subject><issn>0033-5622</issn><issn>2058-1130</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><recordid>eNo9kE1LxDAYhIMo67r6E4QcxFshH5s09SaLrsKCHtZzeZu81Ujb1KQV1l9vcYunOczDMDMnZCmYMhnnkp2SJWNSZkoLcU4uUvpkTChViAVZGJ5zbvSS7F-jbyEe6MehxwiNC2nAGDqfWnpH8RuaEQYfOhpq2sdg0Y0RE61DpM7DexeSTxQ6R5tgofE_f_AlOauhSXg164q8PT7sN0_Z7mX7vLnfZT3X-ZAhcxzRoLaVEFCBq2pu1iY3opAKK1YUwthaWeGc0MYwLWWhhEMLkGvHUK7I7TF3avY1YhrK1ieLTQMdhjGVuRYmZ-tiAq9ncKxadGV_HF3ON0z-zexDmmbUETrr0z-2NoyZKeYXMHtokA</recordid><startdate>19930601</startdate><enddate>19930601</enddate><creator>HAMBLING, C</creator><creator>JUNG, R. T</creator><creator>BROWNING, M. C. K</creator><creator>GUNN, A</creator><creator>ANDERSON, J. M</creator><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19930601</creationdate><title>Primary hyperaldosteronism : evaluation of procedures for diagnosis and localization</title><author>HAMBLING, C ; JUNG, R. T ; BROWNING, M. C. K ; GUNN, A ; ANDERSON, J. M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p167t-e0d1ee8e6cb22abadbf1848782935eb09928cf5c2dd26880633952decaa76d0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adenoma - complications</topic><topic>Adenoma - diagnosis</topic><topic>Adrenal Gland Neoplasms - complications</topic><topic>Adrenal Gland Neoplasms - diagnosis</topic><topic>Adrenal Glands - blood supply</topic><topic>Adrenal Glands - pathology</topic><topic>Adrenals. Adrenal axis. Renin-angiotensin system (diseases)</topic><topic>Adult</topic><topic>Aged</topic><topic>Aldosterone - blood</topic><topic>Aldosterone - urine</topic><topic>Biological and medical sciences</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperaldosteronism - diagnosis</topic><topic>Hyperaldosteronism - diagnostic imaging</topic><topic>Hyperaldosteronism - etiology</topic><topic>Hyperplasia</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Radiography</topic><topic>Renin - blood</topic><topic>Veins</topic><toplevel>online_resources</toplevel><creatorcontrib>HAMBLING, C</creatorcontrib><creatorcontrib>JUNG, R. T</creatorcontrib><creatorcontrib>BROWNING, M. C. K</creatorcontrib><creatorcontrib>GUNN, A</creatorcontrib><creatorcontrib>ANDERSON, J. 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M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Primary hyperaldosteronism : evaluation of procedures for diagnosis and localization</atitle><jtitle>Quarterly journal of medicine</jtitle><addtitle>Q J Med</addtitle><date>1993-06-01</date><risdate>1993</risdate><volume>86</volume><issue>6</issue><spage>383</spage><epage>392</epage><pages>383-392</pages><issn>0033-5622</issn><eissn>2058-1130</eissn><abstract>We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-seleno-methyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>8171186</pmid><tpages>10</tpages></addata></record> |
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subjects | Adenoma - complications Adenoma - diagnosis Adrenal Gland Neoplasms - complications Adrenal Gland Neoplasms - diagnosis Adrenal Glands - blood supply Adrenal Glands - pathology Adrenals. Adrenal axis. Renin-angiotensin system (diseases) Adult Aged Aldosterone - blood Aldosterone - urine Biological and medical sciences Endocrinopathies Female Humans Hyperaldosteronism - diagnosis Hyperaldosteronism - diagnostic imaging Hyperaldosteronism - etiology Hyperplasia Male Medical sciences Middle Aged Non tumoral diseases. Target tissue resistance. Benign neoplasms Radiography Renin - blood Veins |
title | Primary hyperaldosteronism : evaluation of procedures for diagnosis and localization |
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