Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

http://scihub22266oqcxt.onion/ 22876566!ä!22876566 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Pediatr+Endocrinol+Metab 2012 ; 25 (5-6): 599-602 Nephropedia Template TP {{tp|p=22876566|t=2012. Primary familial hypomagnesemia syndrome: a new approach in treatment |pdf=|usr=}}{{22876566}} gab.com Text Primary familial hypomagnesemia syndrome: a new approach in treatment JO: J Pediatr Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=22876566 #FOAvip Primary familial hypomagnesemia is a rare genetically determined disorder characterized by a selective defect in magnesium (Mg) absorption. Mutations of the transient receptor potential melastatin 6 (TRPM6) gene, which codes for TRPM6, the basic channel for intestinal Mg absorption and a new member of the transient receptor potential (TRP) family of cation channels, result in primary hypomagnesemia. Here we present a 14-year-old Turkish girl whose first symptoms manifested as neonatal tetany at 17 days old. During her follow-up, she was mainly taking high-dose oral Mg therapy. However, intravenous Mg and calcium (Ca) therapies were given during symptomatic attacks. When her requirements for Ca and Mg were increased during the pubertal growth period, which overlapped with increased loss of Mg during the summer, oral Ca and active vitamin D (calcitriol, Rocaltrol) were added. Calcitriol is needed because hypomagnesemia results in decreased production and resistance to the actions of active vitamin D, which leads to the disturbance of intracellular signal transmission. Although high-dose oral Mg is reported as a sufficient therapy in most of the patients with primary familial hypomagnesemia, addition of active vitamin D to the usual oral Mg and Ca therapy seems very useful, as in this patient. Twit Text FOAVip Primary familial hypomagnesemia syndrome: a new approach in treatment ????J Pediatr Endocrinol Metab http://www.kidney.de/pget.php?&tw=1&pmid=22876566 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22876566 #FOAvip English Wikipedia <ref>{{Cite pmid|22876566}}</ref> Primary familial hypomagnesemia syndrome: a new approach in treatment #MMPMID22876566 Nesibe A; Sinasi O J Pediatr Endocrinol Metab 2012[]; 25 (5-6): 599-602 PMID22876566show ga Primary familial hypomagnesemia is a rare genetically determined disorder characterized by a selective defect in magnesium (Mg) absorption. Mutations of the transient receptor potential melastatin 6 (TRPM6) gene, which codes for TRPM6, the basic channel for intestinal Mg absorption and a new member of the transient receptor potential (TRP) family of cation channels, result in primary hypomagnesemia. Here we present a 14-year-old Turkish girl whose first symptoms manifested as neonatal tetany at 17 days old. During her follow-up, she was mainly taking high-dose oral Mg therapy. However, intravenous Mg and calcium (Ca) therapies were given during symptomatic attacks. When her requirements for Ca and Mg were increased during the pubertal growth period, which overlapped with increased loss of Mg during the summer, oral Ca and active vitamin D (calcitriol, Rocaltrol) were added. Calcitriol is needed because hypomagnesemia results in decreased production and resistance to the actions of active vitamin D, which leads to the disturbance of intracellular signal transmission. Although high-dose oral Mg is reported as a sufficient therapy in most of the patients with primary familial hypomagnesemia, addition of active vitamin D to the usual oral Mg and Ca therapy seems very useful, as in this patient. |Adolescent[MESH] |Calcitriol/*administration & dosage[MESH] |Calcium/*administration & dosage[MESH] |Drug Therapy, Combination[MESH] |Female[MESH] |Humans[MESH] |Hypercalciuria/*drug therapy/genetics[MESH] |Magnesium/*administration & dosage[MESH] |Nephrocalcinosis/*drug therapy/genetics[MESH] |Renal Tubular Transport, Inborn Errors/*drug therapy/genetics[MESH] |TRPM Cation Channels/genetics[MESH]Primary familial hypomagnesemia syndrome: a new approach in treatment (epmc).pdf DeepDyve Pubget Overpricing