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10.1136/bcr-2016-216870 http://scihub22266oqcxt.onion/10.1136/bcr-2016-216870 C5030594!5030594!27624449     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27624449&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27624449.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       BMJ+Case+Rep 2016 ; 2016 (ä): ä Nephropedia Template TP {{tp|p=27624449|t=2016. Familial hypomagnesaemia with secondary hypocalcaemia |pdf=|usr=}}{{27624449}} gab.com Text Familial hypomagnesaemia with secondary hypocalcaemia JO: BMJ Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=27624449 #FOAvip Magnesium is the second most abundant intracellular cation and plays an essential role in neuronal, skeletal and cardiac tissue. Hypomagnesaemia can cause hypocalcaemia by inhibiting parathyroid hormone release and inducing resistance at its receptor sites. Untreated hypomagnesaemia can lead to tetany, recurrent seizures, status epilepticus and life-threatening arrhythmias. Primary hypomagnesaemia with secondary hypocalcaemia (HSH) is a rare metabolic disorder of intestinal magnesium absorption. The condition typically presents in the neonatal period with neuromuscular excitability and seizures refractory to antiepileptic therapy. Early diagnosis and prompt magnesium replacement are essential to prevent death or long-term neurodevelopmental sequelae. Fewer than a hundred cases are reported in the literature. Recent advances have added significantly to our understanding of the genetic basis of HSH. We report the presentation and long-term follow-up of an affected female who was found to have a mutation in the transient receptor potential melastatin 6 (TRPM6) gene, encoding a transient receptor potential cation channel. Twit Text FOAVip Familial hypomagnesaemia with secondary hypocalcaemia ????BMJ Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=27624449 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27624449 #FOAvip English Wikipedia <ref>{{Cite pmid|27624449}}</ref> Familial hypomagnesaemia with secondary hypocalcaemia #MMPMID27624449 Patel S; Rayanagoudar G; Gelding S BMJ Case Rep 2016[]; 2016 (ä): ä PMID27624449show ga Magnesium is the second most abundant intracellular cation and plays an essential role in neuronal, skeletal and cardiac tissue. Hypomagnesaemia can cause hypocalcaemia by inhibiting parathyroid hormone release and inducing resistance at its receptor sites. Untreated hypomagnesaemia can lead to tetany, recurrent seizures, status epilepticus and life-threatening arrhythmias. Primary hypomagnesaemia with secondary hypocalcaemia (HSH) is a rare metabolic disorder of intestinal magnesium absorption. The condition typically presents in the neonatal period with neuromuscular excitability and seizures refractory to antiepileptic therapy. Early diagnosis and prompt magnesium replacement are essential to prevent death or long-term neurodevelopmental sequelae. Fewer than a hundred cases are reported in the literature. Recent advances have added significantly to our understanding of the genetic basis of HSH. We report the presentation and long-term follow-up of an affected female who was found to have a mutation in the transient receptor potential melastatin 6 (TRPM6) gene, encoding a transient receptor potential cation channel. äFamilial hypomagnesaemia with secondary hypocalcaemia (epmc).pdf DeepDyve Pubget Overpricing