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10.1536/ihj.17-686 http://scihub22266oqcxt.onion/10.1536/ihj.17-686 30305584!ä!30305584 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+Heart+J 2018 ; 59 (6): 1466-1468 Nephropedia Template TP {{tp|p=30305584|t=2018. Persistent QT Prolongation in a Child with Gitelman Syndrome and SCN5A H558R Polymorphism |pdf=|usr=}}{{30305584}} gab.com Text Persistent QT Prolongation in a Child with Gitelman Syndrome and SCN5A H558R Polymorphism JO: Int Heart J http://www.kidney.de/pget.php?&tw=1&pmid=30305584 #FOAvip Gitelman syndrome (GS) is an inherited renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypomagnesemia, and low urinary calcium excretion. While it is considered a benign disease, severe ventricular arrhythmia and sudden cardiac death related to the prolongation of the QT interval have been reported in rare cases. Herein we report a 13-year-old girl with GS who presented with persistent prolongation of the QT interval, even after being treated for hypokalemia and hypomagnesemia. Genetic analysis identified SCN5A H558R polymorphism, which modulates the function of myocardial sodium channel, and SLC12A3 A588V mutation, which causes GS. The SCN5A polymorphism and GS-related electrolyte disturbance might have contributed to the persistent QT prolongation in this patient. Although no ventricular arrhythmias were recorded in this case, careful cardiac surveillance should be applied for avoiding life-threatening cardiac events. Twit Text FOAVip Persistent QT Prolongation in a Child with Gitelman Syndrome and SCN5A H558R Polymorphism ????Int Heart J http://www.kidney.de/pget.php?&tw=1&pmid=30305584 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30305584 #FOAvip English Wikipedia <ref>{{Cite pmid|30305584}}</ref> Persistent QT Prolongation in a Child with Gitelman Syndrome and SCN5A H558R Polymorphism #MMPMID30305584 Tsukakoshi T; Lin L; Murakami T; Shiono J; Izumi I; Horigome H Int Heart J 2018[Nov]; 59 (6): 1466-1468 PMID30305584show ga Gitelman syndrome (GS) is an inherited renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypomagnesemia, and low urinary calcium excretion. While it is considered a benign disease, severe ventricular arrhythmia and sudden cardiac death related to the prolongation of the QT interval have been reported in rare cases. Herein we report a 13-year-old girl with GS who presented with persistent prolongation of the QT interval, even after being treated for hypokalemia and hypomagnesemia. Genetic analysis identified SCN5A H558R polymorphism, which modulates the function of myocardial sodium channel, and SLC12A3 A588V mutation, which causes GS. The SCN5A polymorphism and GS-related electrolyte disturbance might have contributed to the persistent QT prolongation in this patient. Although no ventricular arrhythmias were recorded in this case, careful cardiac surveillance should be applied for avoiding life-threatening cardiac events. |*Polymorphism, Genetic[MESH] |Adolescent[MESH] |Female[MESH] |Genetic Markers[MESH] |Genetic Testing[MESH] |Gitelman Syndrome/complications/*diagnosis/genetics[MESH] |Humans[MESH] |Long QT Syndrome/complications/*diagnosis/genetics[MESH]Persistent QT Prolongation in a Child with Gitelman Syndrome and SCN5A(epmc).pdf DeepDyve Pubget Overpricing