Genetic Forms of Primary Aldosteronism
Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldo...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Stowasser, Michael [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Anmerkung: |
© Adis Data Information BV 2007 |
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| Übergeordnetes Werk: |
Enthalten in: High blood pressure & cardiovascular prevention - [S.l.] : Springer International, 2003, 14(2007), 2 vom: Juni, Seite 75-81 |
|---|---|
| Übergeordnetes Werk: |
volume:14 ; year:2007 ; number:2 ; month:06 ; pages:75-81 |
| Links: |
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| DOI / URN: |
10.2165/00151642-200714020-00004 |
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| Katalog-ID: |
SPR037103180 |
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| 245 | 1 | 0 | |a Genetic Forms of Primary Aldosteronism |
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| 520 | |a Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. | ||
| 700 | 1 | |a Fallo, Francesco |4 aut | |
| 700 | 1 | |a So, Albertina |4 aut | |
| 700 | 1 | |a Jeske, Yvette |4 aut | |
| 700 | 1 | |a Kelemen, Livia |4 aut | |
| 700 | 1 | |a Pilon, Catia |4 aut | |
| 700 | 1 | |a Gordon, Richard |4 aut | |
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| 952 | |d 14 |j 2007 |e 2 |c 06 |h 75-81 | ||
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10.2165/00151642-200714020-00004 doi (DE-627)SPR037103180 (SPR)00151642-200714020-00004-e DE-627 ger DE-627 rakwb eng Stowasser, Michael verfasserin aut Genetic Forms of Primary Aldosteronism 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2007 Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. Fallo, Francesco aut So, Albertina aut Jeske, Yvette aut Kelemen, Livia aut Pilon, Catia aut Gordon, Richard aut Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 14(2007), 2 vom: Juni, Seite 75-81 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:14 year:2007 number:2 month:06 pages:75-81 https://dx.doi.org/10.2165/00151642-200714020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 14 2007 2 06 75-81 |
| spelling |
10.2165/00151642-200714020-00004 doi (DE-627)SPR037103180 (SPR)00151642-200714020-00004-e DE-627 ger DE-627 rakwb eng Stowasser, Michael verfasserin aut Genetic Forms of Primary Aldosteronism 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2007 Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. Fallo, Francesco aut So, Albertina aut Jeske, Yvette aut Kelemen, Livia aut Pilon, Catia aut Gordon, Richard aut Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 14(2007), 2 vom: Juni, Seite 75-81 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:14 year:2007 number:2 month:06 pages:75-81 https://dx.doi.org/10.2165/00151642-200714020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 14 2007 2 06 75-81 |
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10.2165/00151642-200714020-00004 doi (DE-627)SPR037103180 (SPR)00151642-200714020-00004-e DE-627 ger DE-627 rakwb eng Stowasser, Michael verfasserin aut Genetic Forms of Primary Aldosteronism 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2007 Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. Fallo, Francesco aut So, Albertina aut Jeske, Yvette aut Kelemen, Livia aut Pilon, Catia aut Gordon, Richard aut Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 14(2007), 2 vom: Juni, Seite 75-81 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:14 year:2007 number:2 month:06 pages:75-81 https://dx.doi.org/10.2165/00151642-200714020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 14 2007 2 06 75-81 |
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10.2165/00151642-200714020-00004 doi (DE-627)SPR037103180 (SPR)00151642-200714020-00004-e DE-627 ger DE-627 rakwb eng Stowasser, Michael verfasserin aut Genetic Forms of Primary Aldosteronism 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2007 Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. Fallo, Francesco aut So, Albertina aut Jeske, Yvette aut Kelemen, Livia aut Pilon, Catia aut Gordon, Richard aut Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 14(2007), 2 vom: Juni, Seite 75-81 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:14 year:2007 number:2 month:06 pages:75-81 https://dx.doi.org/10.2165/00151642-200714020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 14 2007 2 06 75-81 |
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10.2165/00151642-200714020-00004 doi (DE-627)SPR037103180 (SPR)00151642-200714020-00004-e DE-627 ger DE-627 rakwb eng Stowasser, Michael verfasserin aut Genetic Forms of Primary Aldosteronism 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2007 Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. Fallo, Francesco aut So, Albertina aut Jeske, Yvette aut Kelemen, Livia aut Pilon, Catia aut Gordon, Richard aut Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 14(2007), 2 vom: Juni, Seite 75-81 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:14 year:2007 number:2 month:06 pages:75-81 https://dx.doi.org/10.2165/00151642-200714020-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 14 2007 2 06 75-81 |
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Stowasser, Michael @@aut@@ Fallo, Francesco @@aut@@ So, Albertina @@aut@@ Jeske, Yvette @@aut@@ Kelemen, Livia @@aut@@ Pilon, Catia @@aut@@ Gordon, Richard @@aut@@ |
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Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. 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Stowasser, Michael Genetic Forms of Primary Aldosteronism |
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genetic forms of primary aldosteronism |
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Genetic Forms of Primary Aldosteronism |
| abstract |
Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. © Adis Data Information BV 2007 |
| abstractGer |
Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. © Adis Data Information BV 2007 |
| abstract_unstemmed |
Abstract Numerous recent reports suggest that primary aldosteronism (PAL) is much more common than previously thought, accounting for 5–10% of hypertensive patients with most being normokalaemic. A recent Framingham study analysis has revealed the aldosterone/renin ratio, a marker of autonomous aldosterone production, to be an independent predictor of blood pressure progression and hypertension development. The description of two familial forms and Framingham results showing significant heritability of the aldosterone/renin ratio suggests a genetic basis for PAL. One rare, glucocorticoid-remediable, familial form (familial hyperaldosteronism type I [FH-I]), is caused by an adrenocorticotropic hormone-regulated, hybrid CYP11B1/CYP11B2 gene mutation and is associated with a wide spectrum of phenotypic expression from normotension to severe hypertension, which may cause early death from stroke, but is readily controlled by giving low-dose glucocorticoids. Identification of the underlying mutation has permitted development of genetic tests, greatly facilitating diagnosis. Familial hyperaldosteronism type II (FH-II), which is not glucocorticoid-remediable and not associated with the hybrid gene mutation, is at least five times more common than FH-I. Linkage studies have implicated a locus at chromosome 7p22 in three of five families with FH-II so far studied, and candidate genes within the linked locus are currently being closely examined. Since FH-II is clinically indistinguishable from apparently non-familial PAL, mutations causing FH-II are likely to be operative in the wider PAL population. As has occurred with FH-I, the search for its genetic basis brings with it the hope of new, more streamlined genetic methods of detection and a better understanding of its pathophysiology. © Adis Data Information BV 2007 |
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Genetic Forms of Primary Aldosteronism |
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Fallo, Francesco So, Albertina Jeske, Yvette Kelemen, Livia Pilon, Catia Gordon, Richard |
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2024-07-03T21:08:40.802Z |
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| score |
7.398694 |