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'''Pseudohyperaldosteronism''' (also '''pseudoaldosteronism''') is a medical condition which mimics the effects of elevated aldosterone ( |
'''Pseudohyperaldosteronism''' (also '''pseudoaldosteronism''') is a medical condition which mimics the effects of [[hyperaldosteronism|elevated aldosterone (hyperaldosteronism)]] by presenting with [[high blood pressure]], [[hypokalemia|low blood potassium levels (hypokalemia)]], [[metabolic alkalosis]], and low levels of [[plasma renin activity]] (PRA).<ref name=":25">{{Cite journal|last1=Raina|first1=Rupesh|last2=Krishnappa|first2=Vinod|last3=Das|first3=Abhijit|last4=Amin|first4=Harshesh|last5=Radhakrishnan|first5=Yeshwanter|last6=Nair|first6=Nikhil R.|last7=Kusumi|first7=Kirsten|date=2019-07-01|title=Overview of Monogenic or Mendelian Forms of Hypertension|journal=Frontiers in Pediatrics|volume=7|page=263|doi=10.3389/fped.2019.00263|issn=2296-2360|pmc=6613461|pmid=31312622|doi-access=free }}</ref><ref name=":35">{{Citation|last1=Mubarik|first1=Ateeq|title=Liddle Syndrome|date=2020|url=http://www.ncbi.nlm.nih.gov/books/NBK536911/|work=StatPearls|place=Treasure Island (FL)|publisher=StatPearls Publishing|pmid=30725596|access-date=2020-10-21|last2=Anastasopoulou|first2=Catherine|last3=Riahi|first3=Shayan|last4=Aeddula|first4=Narothama R.}}</ref> However, unlike hyperaldosteronism, this conditions exhibits low or normal levels of [[aldosterone]] in the blood.<ref name=":25"/><ref name=":35"/> Causes include genetic disorders (e.g. [[apparent mineralocorticoid excess syndrome]], [[Liddle's syndrome]], and types of [[congenital adrenal hyperplasia]]), acquired conditions (e.g. [[Cushing's syndrome]] and [[mineralocorticoid]]-producing [[adrenal tumor]]s), metabolic disorders, and dietary imbalances including excessive consumption of [[liquorice|licorice]].<ref name=":25"/><ref name=":03">{{Cite journal|last1=Sabbadin|first1=Chiara|last2=Bordin|first2=Luciana|last3=Donà|first3=Gabriella|last4=Manso|first4=Jacopo|last5=Avruscio|first5=Giampiero|last6=Armanini|first6=Decio|date=2019|title=Licorice: From Pseudohyperaldosteronism to Therapeutic Uses|journal=Frontiers in Endocrinology|volume=10|pages=484|doi=10.3389/fendo.2019.00484|issn=1664-2392|pmc=6657287|pmid=31379750|doi-access=free }}</ref><ref name=":15">{{Cite journal|last1=Tetti|first1=Martina|last2=Monticone|first2=Silvia|last3=Burrello|first3=Jacopo|last4=Matarazzo|first4=Patrizia|last5=Veglio|first5=Franco|last6=Pasini|first6=Barbara|last7=Jeunemaitre|first7=Xavier|last8=Mulatero|first8=Paolo|date=2018-03-11|title=Liddle Syndrome: Review of the Literature and Description of a New Case|journal=International Journal of Molecular Sciences|volume=19|issue=3|page=812|doi=10.3390/ijms19030812|issn=1422-0067|pmc=5877673|pmid=29534496|doi-access=free }}</ref> Confirmatory diagnosis depends on the specific cause and may involve blood tests, urine tests, or [[genetic testing]]; however, all forms of this condition exhibit abnormally low concentrations of both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) which differentiates this group of conditions from other forms of [[secondary hypertension]].<ref name=":25"/><ref name=":35"/> Treatment is tailored to the specific cause and focuses on symptom control, blood pressure management, and avoidance of triggers.<ref name=":25"/> |
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==Presentation== |
==Presentation== |
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The presentation of pseudohyperaldosteronism varies depending on the cause. The genetic conditions such as Liddle's syndrome and |
The presentation of pseudohyperaldosteronism varies depending on the cause. The genetic conditions such as [[Liddle's syndrome]] and [[congenital adrenal hyperplasia]] present in childhood or earlier in life than the acquired causes which can present at any age.<ref name=":25"/><ref name=":15"/><ref name=":35"/> Adult patients present with clinical history of [[resistant hypertension]] despite typical medical therapy and lifestyle changes.<ref name=":25"/><ref name=":15"/> [[Hypertension]] itself is most often [[asymptomatic]].<ref name=":15"/> Symptoms of [[hypokalemia]] include fatigue, muscular weakness, and increased urine production.<ref name=":15"/><ref name=":35"/> |
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==Causes== |
==Causes== |
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=== Genetic forms === |
=== Genetic forms === |
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Genetic disorders that lead to this condition include Liddle's syndrome, |
Genetic disorders that lead to this condition include [[Liddle's syndrome]], [[apparent mineralocorticoid excess]] (AME), and two types of [[congenital adrenal hyperplasia]] (CAH).<ref name=":25"/><ref name=":35"/> |
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* '''Liddle's syndrome''' is [[autosomal dominant]] disorder affecting epithelial sodium channels ([[Epithelial sodium channel|ENaC]]) in the distal tubules of the kidneys. In this disorder, a gain of function mutation decreases ENaC degradation leading to increased renal absorption of sodium and water.<ref name=":15"/><ref name=":35"/> |
* '''Liddle's syndrome''' is [[autosomal dominant]] disorder affecting epithelial sodium channels ([[Epithelial sodium channel|ENaC]]) in the distal tubules of the kidneys. In this disorder, a gain of function mutation decreases ENaC degradation leading to increased renal absorption of sodium and water.<ref name=":15"/><ref name=":35"/> |
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* '''Apparent mineralocorticoid excess''' genetic forms include [[Autosomal Recessive|autosomal recessive]] disorders with mutations lowering the activity of the enzyme [[Corticosteroid 11-beta-dehydrogenase isozyme 2|11-beta-hydroxysteroid dehydrogenase type 2]] (11-β-HSD2).<ref name=":25"/> These mutations limit the ability of 11-β-HSD2 to transform active cortisol to the less active [[cortisone]].<ref name=":35"/> Excess cortisol is then able to bind and activate mineralocorticoid receptors due to receptor cross-reactivity leading to aldosterone-like effects.<ref name=":25"/> |
* '''Apparent mineralocorticoid excess''' genetic forms include [[Autosomal Recessive|autosomal recessive]] disorders with mutations lowering the activity of the enzyme [[Corticosteroid 11-beta-dehydrogenase isozyme 2|11-beta-hydroxysteroid dehydrogenase type 2]] (11-β-HSD2).<ref name=":25"/> These mutations limit the ability of 11-β-HSD2 to transform active cortisol to the less active [[cortisone]].<ref name=":35"/> Excess cortisol is then able to bind and activate mineralocorticoid receptors due to receptor cross-reactivity leading to aldosterone-like effects.<ref name=":25"/> |
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* '''Congenital |
* '''Congenital adrenal hyperplasia''' is an autosomal recessive disorder with multiple types, two of which lead to pseudohyperaldosteronism.<ref name=":25"/> Deficiency of [[Congenital adrenal hyperplasia due to 11β-hydroxylase deficiency|11-beta-hydroxylase]] blocks the conversion of [[11-Deoxycorticosterone|11-deoxycorticosterone]] (DOC) to [[corticosterone]] leading to an excess of DOC which acts as a mineralocorticoid similar to aldosterone. Deficiency of 17-alpha-hydroxylase blocks the conversion of [[pregnenolone]] and [[progesterone]] to their 17-a-hydroxy forms leading to increased mineralocorticoid production.<ref name=":25"/> |
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=== Acquired forms === |
=== Acquired forms === |
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Some causes of pseudohyperaldosteronism can be acquired throughout life with examples including [[adrenal tumor]]s and [[ |
Some causes of pseudohyperaldosteronism can be acquired throughout life with examples including [[adrenal tumor]]s and [[ectopic ACTH syndrome]].<ref name=":5">{{Cite journal|last=Choi|first=Kyu Bok|date=June 2007|title=Hypertensive Hypokalemic Disorders|journal=Electrolytes & Blood Pressure |volume=5|issue=1|pages=34–41|doi=10.5049/EBP.2007.5.1.34|issn=1738-5997|pmc=3894504|pmid=24459498}}</ref> |
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* '''Adrenal tumor''' subtypes include adrenal adenomas that produce 11-deoxycorticosterone (DOC) leading to increased mineralocorticoid activity without elevated aldosterone.<ref>{{Cite journal|last1=Wada|first1=N.|last2=Kubo|first2=M.|last3=Kijima|first3=H.|last4=Yamane|first4=Y.|last5=Nishikawa|first5=T.|last6=Sasano|first6=H.|last7=Koike|first7=T.|date=October 1995|title=A case of deoxycorticosterone-producing adrenal adenoma|journal=Endocrine Journal|volume=42|issue=5|pages=637–642|doi=10.1507/endocrj.42.637|issn=0918-8959|pmid=8574286|doi-access=free}}</ref> |
* '''Adrenal tumor''' subtypes include adrenal adenomas that produce 11-deoxycorticosterone (DOC) leading to increased mineralocorticoid activity without elevated aldosterone.<ref>{{Cite journal|last1=Wada|first1=N.|last2=Kubo|first2=M.|last3=Kijima|first3=H.|last4=Yamane|first4=Y.|last5=Nishikawa|first5=T.|last6=Sasano|first6=H.|last7=Koike|first7=T.|date=October 1995|title=A case of deoxycorticosterone-producing adrenal adenoma|journal=Endocrine Journal|volume=42|issue=5|pages=637–642|doi=10.1507/endocrj.42.637|issn=0918-8959|pmid=8574286|doi-access=free}}</ref> |
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* '''Ectopic ACTH syndrome''' describes conditions leading to excess production of [[adrenocorticotropic hormone]] (ACTH) subsequently leading to mineralocorticoid production.<ref name=":5" /> This can arise in ectopic forms of Cushing's syndrome associated with [[Small-cell carcinoma|small-cell lung cancers]] and other ACTH-producing tumors.<ref name=":5" /> The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects.<ref name=":5" /> |
* '''Ectopic ACTH syndrome''' describes conditions leading to excess production of [[adrenocorticotropic hormone]] (ACTH) subsequently leading to mineralocorticoid production.<ref name=":5" /> This can arise in ectopic forms of [[Cushing's syndrome]] associated with [[Small-cell carcinoma|small-cell lung cancers]] and other ACTH-producing tumors.<ref name=":5" /> The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects.<ref name=":5" /> |
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=== Metabolic and dietary forms === |
=== Metabolic and dietary forms === |
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[[File:2013.02-402-022aP Liquorice products tue05feb2013.jpg|thumb|right|200px|Various edible products containing [[liquorice]]. Excessive consumption of |
[[File:2013.02-402-022aP Liquorice products tue05feb2013.jpg|thumb|right|200px|Various edible products containing [[liquorice|licorice]]. Excessive consumption of licorice can lead to pseudohyperaldosteronism due to the plant's high concentrations of [[Enoxolone|Glycyrrhetinic acid]].<ref>{{Cite journal |last=Sontia |first=Bruno |last2=Mooney |first2=Jan |last3=Gaudet |first3=Lise |last4=Touyz |first4=Rhian M. |date=2008-02-14 |title=Pseudohyperaldosteronism, Liquorice, and Hypertension |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8109973/ |journal=The Journal of Clinical Hypertension |volume=10 |issue=2 |pages=153–157 |doi=10.1111/j.1751-7176.2008.07470.x |issn=1524-6175 |pmc=8109973 |pmid=18256580}}</ref>]] |
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Metabolic causes include conditions of [[glucocorticoid]] resistance<ref>{{Cite journal|last1=Martinez-Aguayo|first1=Alejandro|last2=Fardella|first2=Carlos|date=2009|title=Genetics of hypertensive syndrome|journal=Hormone Research|volume=71|issue=5|pages=253–259|doi=10.1159/000208798|issn=1423-0046|pmid=19339789|s2cid=11267816|doi-access=free}}</ref> and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy.<ref name=":25"/> Dietary causes include overconsumption of licorice-containing products.<ref name=":03"/><ref name=":4">{{Cite journal|last=Makino|first=Toshiaki|date=2014|title=3-Monoglucuronyl glycyrrhretinic acid is a possible marker compound related to licorice-induced pseudoaldosteronism|journal=Biological & Pharmaceutical Bulletin|volume=37|issue=6|pages=898–902|doi=10.1248/bpb.b13-00997|issn=1347-5215|pmid=24882402|doi-access=free}}</ref> [[Enoxolone|Glycyrrhetinic acid]] in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the [[mineralocorticoid receptor]] by cortisol leading to aldosterone-like effects.<ref name=":03"/><ref name=":4" /> |
Metabolic causes include conditions of [[glucocorticoid]] resistance<ref>{{Cite journal|last1=Martinez-Aguayo|first1=Alejandro|last2=Fardella|first2=Carlos|date=2009|title=Genetics of hypertensive syndrome|journal=Hormone Research|volume=71|issue=5|pages=253–259|doi=10.1159/000208798|issn=1423-0046|pmid=19339789|s2cid=11267816|doi-access=free}}</ref> and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy.<ref name=":25"/> Dietary causes include overconsumption of [[liquorice|licorice]]-containing products.<ref name=":03"/><ref name=":4">{{Cite journal|last=Makino|first=Toshiaki|date=2014|title=3-Monoglucuronyl glycyrrhretinic acid is a possible marker compound related to licorice-induced pseudoaldosteronism|journal=Biological & Pharmaceutical Bulletin|volume=37|issue=6|pages=898–902|doi=10.1248/bpb.b13-00997|issn=1347-5215|pmid=24882402|doi-access=free}}</ref> [[Enoxolone|Glycyrrhetinic acid]] in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the [[mineralocorticoid receptor]] by cortisol leading to aldosterone-like effects.<ref name=":03"/><ref name=":4" /> |
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==Diagnosis== |
==Diagnosis== |
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==Treatment== |
==Treatment== |
||
Specific treatment of pseudohyperaldosteronism depends on the inciting cause. General management focuses on countering the effects of excess mineralocorticoid activity to achieve adequate blood pressure control and avoid end-organ damage and cardiovascular mortality.<ref name=":25"/> In some cases, specific antihypertensive medications may be recommended. In Liddle's syndrome, ENaC-binding potassium-sparing diuretics (e.g. [[amiloride]] or [[triamterene]]) are used to counter the excess ENaC activity.<ref name=":15"/><ref>{{Cite journal|last1=Hanukoglu|first1=Israel|last2=Hanukoglu|first2=Aaron|date=2016-04-01|title=Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases|journal=Gene|volume=579|issue=2|pages=95–132|doi=10.1016/j.gene.2015.12.061|issn=0378-1119|pmc=4756657|pmid=26772908}}</ref><ref name=":35"/> In AME, the mineralocorticoid receptor-binding potassium-sparing |
Specific treatment of pseudohyperaldosteronism depends on the inciting cause. General management focuses on countering the effects of excess mineralocorticoid activity to achieve adequate [[blood pressure]] control and avoid end-organ damage and [[cardiovascular]] mortality.<ref name=":25"/> In some cases, specific antihypertensive medications may be recommended. In Liddle's syndrome, ENaC-binding potassium-sparing diuretics (e.g. [[amiloride]] or [[triamterene]]) are used to counter the excess ENaC activity.<ref name=":15"/><ref>{{Cite journal|last1=Hanukoglu|first1=Israel|last2=Hanukoglu|first2=Aaron|date=2016-04-01|title=Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases|journal=Gene|volume=579|issue=2|pages=95–132|doi=10.1016/j.gene.2015.12.061|issn=0378-1119|pmc=4756657|pmid=26772908}}</ref><ref name=":35"/> In AME, the mineralocorticoid receptor-binding [[potassium-sparing diuretic]]s (e.g. [[spironolactone]] or [[eplerenone]]) are used to [[Mineralocorticoid receptor antagonist|limit aldosterone receptor activity]].<ref name=":25" /> Other medications such as [[glucocorticoids]] are added in AME and CAH to inhibit ACTH and further cortisol production.<ref name=":25" /> Lifestyle changes such as a [[low sodium diet]] are also used for managing [[hypertension]],<ref name=":25" /><ref name=":35" /> and cessation of [[licorice]] intake is recommended in cases of licorice overconsumption.<ref name=":25" /><ref name=":03"/> |
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==See also== |
==See also== |
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* [[Apparent mineralocorticoid excess syndrome]] |
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* [[Primary aldosteronism]] |
* [[Primary aldosteronism]] |
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* [[Secondary hypertension]] |
* [[Secondary hypertension]] |
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Revision as of 13:58, 29 May 2024
| Pseudohyperaldosteronism | |
|---|---|
| Other names | Pseudoaldosteronism |
Pseudohyperaldosteronism (also pseudoaldosteronism) is a medical condition which mimics the effects of elevated aldosterone (hyperaldosteronism) by presenting with high blood pressure, low blood potassium levels (hypokalemia), metabolic alkalosis, and low levels of plasma renin activity (PRA).[1][2] However, unlike hyperaldosteronism, this conditions exhibits low or normal levels of aldosterone in the blood.[1][2] Causes include genetic disorders (e.g. apparent mineralocorticoid excess syndrome, Liddle's syndrome, and types of congenital adrenal hyperplasia), acquired conditions (e.g. Cushing's syndrome and mineralocorticoid-producing adrenal tumors), metabolic disorders, and dietary imbalances including excessive consumption of licorice.[1][3][4] Confirmatory diagnosis depends on the specific cause and may involve blood tests, urine tests, or genetic testing; however, all forms of this condition exhibit abnormally low concentrations of both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) which differentiates this group of conditions from other forms of secondary hypertension.[1][2] Treatment is tailored to the specific cause and focuses on symptom control, blood pressure management, and avoidance of triggers.[1]
Presentation
The presentation of pseudohyperaldosteronism varies depending on the cause. The genetic conditions such as Liddle's syndrome and congenital adrenal hyperplasia present in childhood or earlier in life than the acquired causes which can present at any age.[1][4][2] Adult patients present with clinical history of resistant hypertension despite typical medical therapy and lifestyle changes.[1][4] Hypertension itself is most often asymptomatic.[4] Symptoms of hypokalemia include fatigue, muscular weakness, and increased urine production.[4][2]
Causes
This condition has several known causes including genetic disorders, acquired conditions, metabolic derangements, and dietary imbalances. All causes mimic the effects of elevated aldosterone without raising aldosterone levels but achieve this through varying mechanisms.[1]
Genetic forms
Genetic disorders that lead to this condition include Liddle's syndrome, apparent mineralocorticoid excess (AME), and two types of congenital adrenal hyperplasia (CAH).[1][2]
- Liddle's syndrome is autosomal dominant disorder affecting epithelial sodium channels (ENaC) in the distal tubules of the kidneys. In this disorder, a gain of function mutation decreases ENaC degradation leading to increased renal absorption of sodium and water.[4][2]
- Apparent mineralocorticoid excess genetic forms include autosomal recessive disorders with mutations lowering the activity of the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (11-β-HSD2).[1] These mutations limit the ability of 11-β-HSD2 to transform active cortisol to the less active cortisone.[2] Excess cortisol is then able to bind and activate mineralocorticoid receptors due to receptor cross-reactivity leading to aldosterone-like effects.[1]
- Congenital adrenal hyperplasia is an autosomal recessive disorder with multiple types, two of which lead to pseudohyperaldosteronism.[1] Deficiency of 11-beta-hydroxylase blocks the conversion of 11-deoxycorticosterone (DOC) to corticosterone leading to an excess of DOC which acts as a mineralocorticoid similar to aldosterone. Deficiency of 17-alpha-hydroxylase blocks the conversion of pregnenolone and progesterone to their 17-a-hydroxy forms leading to increased mineralocorticoid production.[1]
Acquired forms
Some causes of pseudohyperaldosteronism can be acquired throughout life with examples including adrenal tumors and ectopic ACTH syndrome.[5]
- Adrenal tumor subtypes include adrenal adenomas that produce 11-deoxycorticosterone (DOC) leading to increased mineralocorticoid activity without elevated aldosterone.[6]
- Ectopic ACTH syndrome describes conditions leading to excess production of adrenocorticotropic hormone (ACTH) subsequently leading to mineralocorticoid production.[5] This can arise in ectopic forms of Cushing's syndrome associated with small-cell lung cancers and other ACTH-producing tumors.[5] The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects.[5]
Metabolic and dietary forms
Metabolic causes include conditions of glucocorticoid resistance[8] and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy.[1] Dietary causes include overconsumption of licorice-containing products.[3][9] Glycyrrhetinic acid in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the mineralocorticoid receptor by cortisol leading to aldosterone-like effects.[3][9]
Diagnosis
In patients with hypertension, diagnostic clues pointing to pseudohyperaldosteronism can be found on routine labwork. These include low serum potassium (hypokalemia), elevated serum sodium (hypernatremia), and elevated serum bicarbonate (metabolic alkalosis).[1] Urine studies may show elevated urine potassium (kaliuresis). To further differentiate between hyperaldosteronism and pseudohyperaldosteronism, studies including plasma renin activity (PRA) and plasma aldosterone concentration (PAC) can be obtained.[1][2] Pseudohyperaldosteronism will exhibit low levels of both PRA and PAC while hyperaldosteronism will demonstrate elevated PAC.[1] Confirmatory tests to diagnose the specific forms of pseudohyperaldosteronism vary depending on the cause. The genetic conditions such as Liddle's syndrome and CAH can be confirmed with genetic tests for the affected genes.[1][4] CAH can also be confirmed by analyzing enzyme levels following ACTH stimulation testing.[1] AME can be diagnosed with a 24 hour urine collection exhibiting an increased ratio of urinary cortisol to urinary cortisone.[1]
Treatment
Specific treatment of pseudohyperaldosteronism depends on the inciting cause. General management focuses on countering the effects of excess mineralocorticoid activity to achieve adequate blood pressure control and avoid end-organ damage and cardiovascular mortality.[1] In some cases, specific antihypertensive medications may be recommended. In Liddle's syndrome, ENaC-binding potassium-sparing diuretics (e.g. amiloride or triamterene) are used to counter the excess ENaC activity.[4][10][2] In AME, the mineralocorticoid receptor-binding potassium-sparing diuretics (e.g. spironolactone or eplerenone) are used to limit aldosterone receptor activity.[1] Other medications such as glucocorticoids are added in AME and CAH to inhibit ACTH and further cortisol production.[1] Lifestyle changes such as a low sodium diet are also used for managing hypertension,[1][2] and cessation of licorice intake is recommended in cases of licorice overconsumption.[1][3]
See also
References
- ^ a b c d e f g h i j k l m n o p q r s t u v w x y Raina, Rupesh; Krishnappa, Vinod; Das, Abhijit; Amin, Harshesh; Radhakrishnan, Yeshwanter; Nair, Nikhil R.; Kusumi, Kirsten (2019-07-01). "Overview of Monogenic or Mendelian Forms of Hypertension". Frontiers in Pediatrics. 7: 263. doi:10.3389/fped.2019.00263. ISSN 2296-2360. PMC 6613461. PMID 31312622.
- ^ a b c d e f g h i j k Mubarik, Ateeq; Anastasopoulou, Catherine; Riahi, Shayan; Aeddula, Narothama R. (2020), "Liddle Syndrome", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 30725596, retrieved 2020-10-21
- ^ a b c d Sabbadin, Chiara; Bordin, Luciana; Donà, Gabriella; Manso, Jacopo; Avruscio, Giampiero; Armanini, Decio (2019). "Licorice: From Pseudohyperaldosteronism to Therapeutic Uses". Frontiers in Endocrinology. 10: 484. doi:10.3389/fendo.2019.00484. ISSN 1664-2392. PMC 6657287. PMID 31379750.
- ^ a b c d e f g h Tetti, Martina; Monticone, Silvia; Burrello, Jacopo; Matarazzo, Patrizia; Veglio, Franco; Pasini, Barbara; Jeunemaitre, Xavier; Mulatero, Paolo (2018-03-11). "Liddle Syndrome: Review of the Literature and Description of a New Case". International Journal of Molecular Sciences. 19 (3): 812. doi:10.3390/ijms19030812. ISSN 1422-0067. PMC 5877673. PMID 29534496.
- ^ a b c d Choi, Kyu Bok (June 2007). "Hypertensive Hypokalemic Disorders". Electrolytes & Blood Pressure. 5 (1): 34–41. doi:10.5049/EBP.2007.5.1.34. ISSN 1738-5997. PMC 3894504. PMID 24459498.
- ^ Wada, N.; Kubo, M.; Kijima, H.; Yamane, Y.; Nishikawa, T.; Sasano, H.; Koike, T. (October 1995). "A case of deoxycorticosterone-producing adrenal adenoma". Endocrine Journal. 42 (5): 637–642. doi:10.1507/endocrj.42.637. ISSN 0918-8959. PMID 8574286.
- ^ Sontia, Bruno; Mooney, Jan; Gaudet, Lise; Touyz, Rhian M. (2008-02-14). "Pseudohyperaldosteronism, Liquorice, and Hypertension". The Journal of Clinical Hypertension. 10 (2): 153–157. doi:10.1111/j.1751-7176.2008.07470.x. ISSN 1524-6175. PMC 8109973. PMID 18256580.
- ^ Martinez-Aguayo, Alejandro; Fardella, Carlos (2009). "Genetics of hypertensive syndrome". Hormone Research. 71 (5): 253–259. doi:10.1159/000208798. ISSN 1423-0046. PMID 19339789. S2CID 11267816.
- ^ a b Makino, Toshiaki (2014). "3-Monoglucuronyl glycyrrhretinic acid is a possible marker compound related to licorice-induced pseudoaldosteronism". Biological & Pharmaceutical Bulletin. 37 (6): 898–902. doi:10.1248/bpb.b13-00997. ISSN 1347-5215. PMID 24882402.
- ^ Hanukoglu, Israel; Hanukoglu, Aaron (2016-04-01). "Epithelial sodium channel (ENaC) family: Phylogeny, structure-function, tissue distribution, and associated inherited diseases". Gene. 579 (2): 95–132. doi:10.1016/j.gene.2015.12.061. ISSN 0378-1119. PMC 4756657. PMID 26772908.