Bartter syndrome medical therapy: Difference between revisions
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{{CMG}}{{AE}}{{TAM}} | {{CMG}}{{AE}}{{TAM}} | ||
==Overview== | ==Overview== | ||
[[Prostaglandin]] synthetase inhibitors suppress the production of [[prostaglandin]]. [[Potassium chloride]] supplements are given for [[hypokalemia]]. [[Spironolactone]], Amiloride, [[Triamterene]], [[ ACEI|Angiotensin-converting enzyme (ACE) inhibitors]], [[NSAIDS|Nonsteroidal drug anti-inflammatory drugs]] (NSAID) are given to patients for the treatment of [[Bartter syndrome]]. [[Growth hormone]] (GH) is given for growth retardation. [[Calcium]] or [[magnesium]] supplements are given for [[muscle spasm]] and [[tetany]]. | |||
==Medical Therapy== | ==Medical Therapy== | ||
*Prostaglandin synthetase inhibitors suppress the production of [[prostaglandin]]. This corrects all the chemical features of the syndrome except the urinary loss of [[potassium]].<ref name="pmid820194">{{cite journal| author=Gill JR, Frölich JC, Bowden RE, Taylor AA, Keiser HR, Seyberth HW | display-authors=etal| title=Bartter's syndrome: a disorder characterized by high urinary prostaglandins and dependence of hyperreninemia on prostaglandin synthesis. | journal=Am J Med | year= 1976 | volume= 61 | issue= 1 | pages= 43-51 | pmid=820194 | doi=10.1016/0002-9343(76)90029-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=820194 }} </ref> | *Prostaglandin synthetase inhibitors suppress the production of [[prostaglandin]]. This corrects all the chemical features of the syndrome except the urinary loss of [[potassium]].<ref name="pmid820194">{{cite journal| author=Gill JR, Frölich JC, Bowden RE, Taylor AA, Keiser HR, Seyberth HW | display-authors=etal| title=Bartter's syndrome: a disorder characterized by high urinary prostaglandins and dependence of hyperreninemia on prostaglandin synthesis. | journal=Am J Med | year= 1976 | volume= 61 | issue= 1 | pages= 43-51 | pmid=820194 | doi=10.1016/0002-9343(76)90029-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=820194 }} </ref> | ||
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*[[Angiotensin-converting enzyme (ACE) inhibitors]], such as [[captopril]], [[enalapril]] and [[lisinopril]]. | *[[Angiotensin-converting enzyme (ACE) inhibitors]], such as [[captopril]], [[enalapril]] and [[lisinopril]]. | ||
*Nonsteroidal drug anti-inflammatory drugs (NSAID) such as [[indomethacin]] and [[naproxen]] which decrease the activity of the enzyme [[cyclo-oxygenase]] (COX) which increases [[prostaglandin]] synthesis. | *Nonsteroidal drug anti-inflammatory drugs (NSAID) such as [[indomethacin]] and [[naproxen]] which decrease the activity of the enzyme [[cyclo-oxygenase]] (COX) which increases [[prostaglandin]] synthesis. | ||
*[[Growth hormone]] (GH) for growth retardation. | *[[Growth hormone]] (GH) for [[growth retardation]]. | ||
*Calcium or magnesium supplements in the presence of muscle spasm and tetany.<ref name="pmid26140272">{{cite journal| author=Al Shibli A, Narchi H| title=Bartter and Gitelman syndromes: Spectrum of clinical manifestations caused by different mutations. | journal=World J Methodol | year= 2015 | volume= 5 | issue= 2 | pages= 55-61 | pmid=26140272 | doi=10.5662/wjm.v5.i2.55 | pmc=4482822 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26140272 }} </ref> | *[[Calcium]] or [[magnesium]] supplements in the presence of [[muscle spasm]] and [[tetany]].<ref name="pmid26140272">{{cite journal| author=Al Shibli A, Narchi H| title=Bartter and Gitelman syndromes: Spectrum of clinical manifestations caused by different mutations. | journal=World J Methodol | year= 2015 | volume= 5 | issue= 2 | pages= 55-61 | pmid=26140272 | doi=10.5662/wjm.v5.i2.55 | pmc=4482822 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26140272 }} </ref> | ||
==References== | ==References== | ||
Latest revision as of 20:57, 5 August 2020
Main article: Bartter syndrome
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Tayyaba Ali, M.D.[2]
Overview
Prostaglandin synthetase inhibitors suppress the production of prostaglandin. Potassium chloride supplements are given for hypokalemia. Spironolactone, Amiloride, Triamterene, Angiotensin-converting enzyme (ACE) inhibitors, Nonsteroidal drug anti-inflammatory drugs (NSAID) are given to patients for the treatment of Bartter syndrome. Growth hormone (GH) is given for growth retardation. Calcium or magnesium supplements are given for muscle spasm and tetany.
Medical Therapy
- Prostaglandin synthetase inhibitors suppress the production of prostaglandin. This corrects all the chemical features of the syndrome except the urinary loss of potassium.[1]
- Hypokalemia should be treated. Potassium chloride supplements are preferred salt because of the coexisting chloride deficiencies in these patients.
- Spironolactone, aldosterone antagonist.
- Amiloride reduces potassium and hydrogen excretion, by inhibiting epithelial sodium channels (ENaC).
- Triamterene decreases calcium excretion and increases magnesium loss.
- Angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril and lisinopril.
- Nonsteroidal drug anti-inflammatory drugs (NSAID) such as indomethacin and naproxen which decrease the activity of the enzyme cyclo-oxygenase (COX) which increases prostaglandin synthesis.
- Growth hormone (GH) for growth retardation.
- Calcium or magnesium supplements in the presence of muscle spasm and tetany.[2]
References
- ↑ Gill JR, Frölich JC, Bowden RE, Taylor AA, Keiser HR, Seyberth HW; et al. (1976). "Bartter's syndrome: a disorder characterized by high urinary prostaglandins and dependence of hyperreninemia on prostaglandin synthesis". Am J Med. 61 (1): 43–51. doi:10.1016/0002-9343(76)90029-2. PMID 820194.
- ↑ Al Shibli A, Narchi H (2015). "Bartter and Gitelman syndromes: Spectrum of clinical manifestations caused by different mutations". World J Methodol. 5 (2): 55–61. doi:10.5662/wjm.v5.i2.55. PMC 4482822. PMID 26140272.