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10.5217/ir.2015.13.3.227 http://scihub22266oqcxt.onion/10.5217/ir.2015.13.3.227 26130997!4479737!26130997     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26130997&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 Warning: Undefined variable $yww in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 538 Warning: Undefined variable $yww in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 538       Intest+Res 2015 ; 13 (3): 227-32 Nephropedia Template TP {{tp|p=26130997|t=2015. Lemonade Legs : Why do Some Patients Get Profound Hypomagnesaemia on Proton-Pump Inhibitors?|pdf=|usr=}}{{26130997}} gab.com Text Lemonade Legs : Why do Some Patients Get Profound Hypomagnesaemia on Proton-Pump Inhibitors JO: Intest Res http://www.kidney.de/pget.php?&tw=1&pmid=26130997 #FOAvip Proton pump inhibitors (PPIs) are widely used though an association with hypomagnesaemia and hypocalcaemia has only been described since 2006. Patients typically present after years of stable dosing with musculoskeletal, neurological or cardiac arrhythmic symptoms, but it is likely that many cases are under-recognised. Magnesium levels resolve rapidly on discontinuation of PPI therapy and hypomagnesaemia recurs rapidly on rechallenge with any agent in the class. The cellular mechanisms of magnesium homeostasis are increasingly being understood, including both passive paracellular absorption through claudins and active transcellular transporters, including the transient receptor potential channels (TRPM6) identified in the intestine and nephron. PPIs may alter luminal pH by modulating pancreatic secretions, affecting non-gastric H+K+ATPase secretion, altering transporter transcription or channel function. A small reduction in intestinal absorption appears pivotal in causing cumulative deficiency. Risk factors have been associated to help identify patients at risk of this effect but clinical vigilance remains necessary for diagnosis. Twit Text FOAVip Lemonade Legs : Why do Some Patients Get Profound Hypomagnesaemia on Proton-Pump Inhibitors ????Intest Res http://www.kidney.de/pget.php?&tw=1&pmid=26130997 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26130997 #FOAvip English Wikipedia <ref>{{Cite pmid|26130997}}</ref> Lemonade Legs : Why do Some Patients Get Profound Hypomagnesaemia on Proton-Pump Inhibitors? #MMPMID26130997 Atkinson NS; Reynolds DJ; Travis SP Intest Res 2015[Jul]; 13 (3): 227-32 PMID26130997show ga Proton pump inhibitors (PPIs) are widely used though an association with hypomagnesaemia and hypocalcaemia has only been described since 2006. Patients typically present after years of stable dosing with musculoskeletal, neurological or cardiac arrhythmic symptoms, but it is likely that many cases are under-recognised. Magnesium levels resolve rapidly on discontinuation of PPI therapy and hypomagnesaemia recurs rapidly on rechallenge with any agent in the class. The cellular mechanisms of magnesium homeostasis are increasingly being understood, including both passive paracellular absorption through claudins and active transcellular transporters, including the transient receptor potential channels (TRPM6) identified in the intestine and nephron. PPIs may alter luminal pH by modulating pancreatic secretions, affecting non-gastric H+K+ATPase secretion, altering transporter transcription or channel function. A small reduction in intestinal absorption appears pivotal in causing cumulative deficiency. Risk factors have been associated to help identify patients at risk of this effect but clinical vigilance remains necessary for diagnosis. ? Lemonade Legs : Why do Some Patients Get Profound Hypomagnesaemia on (epmc).pdf DeepDyve Pubget Overpricing