Bartter syndrome historical perspective: Difference between revisions
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==Overview== | ==Overview== | ||
==Historical Perspective== | ==Historical Perspective== | ||
* Bartter | * [[Bartter syndrome]] was first discovered by Bartter et al.and introduced in a seminal paper in the December issue of the American Journal of Medicine in 1962. | ||
*Authors in the paper reported two pediatric patients with growth and developmental delay associated with hypokalemic alkalosis and normal blood pressure despite high aldosterone production. | *Authors in the paper reported two pediatric patients with growth and developmental delay associated with [[metabolic alkalosis|hypokalemic alkalosis]] and normal [[blood pressure]] despite high [[aldosterone]] production. | ||
*The syndrome named after Bartter. This disease was observed in children as well as in adults, females as well as males.<ref name="pmid16773399">{{cite journal| author=Proesmans W| title=Threading through the mizmaze of Bartter syndrome. | journal=Pediatr Nephrol | year= 2006 | volume= 21 | issue= 7 | pages= 896-902 | pmid=16773399 | doi=10.1007/s00467-006-0113-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16773399 }} </ref> | *The syndrome named after [[Bartter]]. This disease was observed in children as well as in adults, females as well as males.<ref name="pmid16773399">{{cite journal| author=Proesmans W| title=Threading through the mizmaze of Bartter syndrome. | journal=Pediatr Nephrol | year= 2006 | volume= 21 | issue= 7 | pages= 896-902 | pmid=16773399 | doi=10.1007/s00467-006-0113-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16773399 }} </ref> | ||
*Authors described in the paper that this disease is characterized by hypokalemia, metabolic alkalosis, hyperreninemia, secondary hyperaldosteronism, and normal blood pressure. | *Authors described in the paper that this disease is characterized by [[hypokalemia]], [[metabolic alkalosis]], hyperreninemia, [[secondary hyperaldosteronism]], and normal [[blood pressure]]. | ||
*Hyperrinemia on histopathological examination is characterized by hyperplasia of juxtaglomerular complex.<ref name="pmid13969763">{{cite journal| author=BARTTER FC, PRONOVE P, GILL JR, MACCARDLE RC| title=Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome. | journal=Am J Med | year= 1962 | volume= 33 | issue= | pages= 811-28 | pmid=13969763 | doi=10.1016/0002-9343(62)90214-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13969763 }} </ref> | *Hyperrinemia on histopathological examination is characterized by hyperplasia of [[juxtaglomerular apparatus|juxtaglomerular complex]].<ref name="pmid13969763">{{cite journal| author=BARTTER FC, PRONOVE P, GILL JR, MACCARDLE RC| title=Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome. | journal=Am J Med | year= 1962 | volume= 33 | issue= | pages= 811-28 | pmid=13969763 | doi=10.1016/0002-9343(62)90214-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13969763 }} </ref> | ||
*Fichman <ref name="pmid798488">{{cite journal| author=Fichman MP, Telfer N, Zia P, Speckart P, Golub M, Rude R| title=Role of prostaglandins in the pathogenesis of Bartter's syndrome. | journal=Am J Med | year= 1976 | volume= 60 | issue= 6 | pages= 785-97 | pmid=798488 | doi=10.1016/0002-9343(76)90892-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=798488 }} </ref> , Verberckmoes <ref name="urlwww.kidney-international.org">{{cite web |url=https://www.kidney-international.org/article/S0085-2538(15)31580-5/pdf |title=www.kidney-international.org |format= |work= |accessdate=}}</ref>, and Gill <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 a 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> in 1976 explained that the production of prostaglandin E2 increases in urine in patients with Bartter syndrome. Later, only the urinary metabolite 6 keto, PGF1, has been measured. Further investigation disclosed that the potent vasodilator PGI2 increases in the blood vessels in Bartter syndrome.<ref name="pmid90861">{{cite journal| author=Güllner HG, Cerletti C, Bartter FC, Smith JB, Gill JR| title=Prostacyclin overproduction in Bartter's syndrome. | journal=Lancet | year= 1979 | volume= 2 | issue= 8146 | pages= 767-9 | pmid=90861 | doi=10.1016/s0140-6736(79)92116-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=90861 }} </ref> | *Fichman <ref name="pmid798488">{{cite journal| author=Fichman MP, Telfer N, Zia P, Speckart P, Golub M, Rude R| title=Role of prostaglandins in the pathogenesis of Bartter's syndrome. | journal=Am J Med | year= 1976 | volume= 60 | issue= 6 | pages= 785-97 | pmid=798488 | doi=10.1016/0002-9343(76)90892-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=798488 }} </ref> , Verberckmoes <ref name="urlwww.kidney-international.org">{{cite web |url=https://www.kidney-international.org/article/S0085-2538(15)31580-5/pdf |title=www.kidney-international.org |format= |work= |accessdate=}}</ref>, and Gill <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 a 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> in 1976 explained that the production of prostaglandin E2 increases in urine in patients with Bartter syndrome. Later, only the urinary metabolite 6 keto, PGF1, has been measured. Further investigation disclosed that the potent vasodilator PGI2 increases in the blood vessels in Bartter syndrome.<ref name="pmid90861">{{cite journal| author=Güllner HG, Cerletti C, Bartter FC, Smith JB, Gill JR| title=Prostacyclin overproduction in Bartter's syndrome. | journal=Lancet | year= 1979 | volume= 2 | issue= 8146 | pages= 767-9 | pmid=90861 | doi=10.1016/s0140-6736(79)92116-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=90861 }} </ref> | ||
*Earlier, physicians misdiagnosed cystic fibrosis as having Bartter syndrome. In cystic fibrosis, patients lose excessive quantities of sodium, potassium, and chloride in sweat. Excessive loss of electrolytes occurs in urine in a similar pattern in Bartter syndrome.<ref name="pmid6356778">{{cite journal| author=Davison AG, Snodgrass GJ| title=Cystic fibrosis mimicking Bartter's syndrome. | journal=Acta Paediatr Scand | year= 1983 | volume= 72 | issue= 5 | pages= 781-3 | pmid=6356778 | doi=10.1111/j.1651-2227.1983.tb09814.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6356778 }} </ref> | *Earlier, physicians misdiagnosed [[cystic fibrosis]] as having [[Bartter syndrome]]. In [[cystic fibrosis]], patients lose excessive quantities of [[sodium]], [[potassium]], and [[chloride]] in sweat. Excessive loss of [[electrolytes]] occurs in urine in a similar pattern in [[Bartter syndrome]].<ref name="pmid6356778">{{cite journal| author=Davison AG, Snodgrass GJ| title=Cystic fibrosis mimicking Bartter's syndrome. | journal=Acta Paediatr Scand | year= 1983 | volume= 72 | issue= 5 | pages= 781-3 | pmid=6356778 | doi=10.1111/j.1651-2227.1983.tb09814.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6356778 }} </ref> | ||
==References== | ==References== | ||
Revision as of 18:20, 5 August 2020
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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
Historical Perspective
- Bartter syndrome was first discovered by Bartter et al.and introduced in a seminal paper in the December issue of the American Journal of Medicine in 1962.
- Authors in the paper reported two pediatric patients with growth and developmental delay associated with hypokalemic alkalosis and normal blood pressure despite high aldosterone production.
- The syndrome named after Bartter. This disease was observed in children as well as in adults, females as well as males.[1]
- Authors described in the paper that this disease is characterized by hypokalemia, metabolic alkalosis, hyperreninemia, secondary hyperaldosteronism, and normal blood pressure.
- Hyperrinemia on histopathological examination is characterized by hyperplasia of juxtaglomerular complex.[2]
- Fichman [3] , Verberckmoes [4], and Gill [5] in 1976 explained that the production of prostaglandin E2 increases in urine in patients with Bartter syndrome. Later, only the urinary metabolite 6 keto, PGF1, has been measured. Further investigation disclosed that the potent vasodilator PGI2 increases in the blood vessels in Bartter syndrome.[6]
- Earlier, physicians misdiagnosed cystic fibrosis as having Bartter syndrome. In cystic fibrosis, patients lose excessive quantities of sodium, potassium, and chloride in sweat. Excessive loss of electrolytes occurs in urine in a similar pattern in Bartter syndrome.[7]
References
- ↑ Proesmans W (2006). "Threading through the mizmaze of Bartter syndrome". Pediatr Nephrol. 21 (7): 896–902. doi:10.1007/s00467-006-0113-7. PMID 16773399.
- ↑ BARTTER FC, PRONOVE P, GILL JR, MACCARDLE RC (1962). "Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome". Am J Med. 33: 811–28. doi:10.1016/0002-9343(62)90214-0. PMID 13969763.
- ↑ Fichman MP, Telfer N, Zia P, Speckart P, Golub M, Rude R (1976). "Role of prostaglandins in the pathogenesis of Bartter's syndrome". Am J Med. 60 (6): 785–97. doi:10.1016/0002-9343(76)90892-5. PMID 798488.
- ↑ "www.kidney-international.org".
- ↑ 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 a dependence of hyperreninemia on prostaglandin synthesis". Am J Med. 61 (1): 43–51. doi:10.1016/0002-9343(76)90029-2. PMID 820194.
- ↑ Güllner HG, Cerletti C, Bartter FC, Smith JB, Gill JR (1979). "Prostacyclin overproduction in Bartter's syndrome". Lancet. 2 (8146): 767–9. doi:10.1016/s0140-6736(79)92116-0. PMID 90861.
- ↑ Davison AG, Snodgrass GJ (1983). "Cystic fibrosis mimicking Bartter's syndrome". Acta Paediatr Scand. 72 (5): 781–3. doi:10.1111/j.1651-2227.1983.tb09814.x. PMID 6356778.