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.

10.4254/wjh.v7.i29.2859 http://scihub22266oqcxt.onion/10.4254/wjh.v7.i29.2859 C4678372!4678372!26692151     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26692151&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       World+J+Hepatol 2015 ; 7 (29): 2859-70 Nephropedia Template TP {{tp|p=26692151|t=2015. Wilson?s disease: A review of what we have learned |pdf=|usr=}}{{26692151}} gab.com Text Wilson s disease: A review of what we have learned JO: World J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26692151 #FOAvip Wilson?s disease (WD), which results from the defective ATP7B protein product, is characterized by impaired copper metabolism and its clinical consequences vary from an asymptomatic state to fulminant hepatic failure, chronic liver disease with or without cirrhosis, neurological, and psychiatric manifestations. A high grade of suspicion is warranted to not miss cases of WD, especially less florid cases with only mild elevation of transaminases, or isolated neuropsychiatric involvement. Screening in first and second relatives of index cases is mandatory, and treatment must commence upon establishment of diagnosis. Treatment strategies include chelators such as D-penicillamine and trientine, while zinc salts act as inductors of methallothioneins, which favor a negative copper balance and a reduction of free plasmatic copper. As an orphan disease, research is lacking in this field, especially regarding therapeutic strategies which are associated with better patient compliance and which could eventually also reverse established injury. Twit Text FOAVip Wilson s disease: A review of what we have learned ????World J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26692151 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26692151 #FOAvip English Wikipedia <ref>{{Cite pmid|26692151}}</ref> Wilson?s disease: A review of what we have learned #MMPMID26692151 Rodriguez-Castro KI; Hevia-Urrutia FJ; Sturniolo GC World J Hepatol 2015[Dec]; 7 (29): 2859-70 PMID26692151show ga Wilson?s disease (WD), which results from the defective ATP7B protein product, is characterized by impaired copper metabolism and its clinical consequences vary from an asymptomatic state to fulminant hepatic failure, chronic liver disease with or without cirrhosis, neurological, and psychiatric manifestations. A high grade of suspicion is warranted to not miss cases of WD, especially less florid cases with only mild elevation of transaminases, or isolated neuropsychiatric involvement. Screening in first and second relatives of index cases is mandatory, and treatment must commence upon establishment of diagnosis. Treatment strategies include chelators such as D-penicillamine and trientine, while zinc salts act as inductors of methallothioneins, which favor a negative copper balance and a reduction of free plasmatic copper. As an orphan disease, research is lacking in this field, especially regarding therapeutic strategies which are associated with better patient compliance and which could eventually also reverse established injury. äWilson?s disease: A review of what we have learned (epmc).pdf DeepDyve Pubget Overpricing