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10.1111/bcp.12885 http://scihub22266oqcxt.onion/10.1111/bcp.12885 C4876174!4876174 !26773235     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26773235 &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       Br+J+Clin+Pharmacol 2016 ; 81 (6 ): 1030-6 Nephropedia Template TP {{tp|p=26773235 |t=2016. Mechanism of isoniazid-induced hepatotoxicity: then and now |pdf=|usr=}}{{26773235 }} gab.com Text Mechanism of isoniazid-induced hepatotoxicity: then and now JO: Br J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=26773235 #FOAvip Isoniazid (INH) remains a mainstay for the treatment of tuberculosis despite the fact that it can cause liver failure. Previous mechanistic hypotheses have classified this type of drug-induced liver injury (DILI) as 'metabolic idiosyncrasy' which was thought not to involve an immune response and was mainly due to the bioactivation of the acetylhydrazine metabolite. However, more recent studies support an alternative hypothesis, specifically, that INH itself is directly bioactivated to a reactive metabolite, which in some patients leads to an immune response and liver injury. Furthermore, there appear to be two phenotypes of INH-induced liver injury. Most cases involve mild liver injury, which resolves with immune tolerance, while other cases appear to have a more severe phenotype that is associated with the production of anti-drug/anti-CYP P450 antibodies and can progress to liver failure. Twit Text FOAVip Mechanism of isoniazid-induced hepatotoxicity: then and now ????Br J Clin Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=26773235 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26773235 #FOAvip English Wikipedia <ref>{{Cite pmid|26773235 }}</ref> Mechanism of isoniazid-induced hepatotoxicity: then and now #MMPMID26773235 Metushi I ; Uetrecht J ; Phillips E Br J Clin Pharmacol 2016[Jun]; 81 (6 ): 1030-6 PMID26773235 show ga Isoniazid (INH) remains a mainstay for the treatment of tuberculosis despite the fact that it can cause liver failure. Previous mechanistic hypotheses have classified this type of drug-induced liver injury (DILI) as 'metabolic idiosyncrasy' which was thought not to involve an immune response and was mainly due to the bioactivation of the acetylhydrazine metabolite. However, more recent studies support an alternative hypothesis, specifically, that INH itself is directly bioactivated to a reactive metabolite, which in some patients leads to an immune response and liver injury. Furthermore, there appear to be two phenotypes of INH-induced liver injury. Most cases involve mild liver injury, which resolves with immune tolerance, while other cases appear to have a more severe phenotype that is associated with the production of anti-drug/anti-CYP P450 antibodies and can progress to liver failure. |*Chemical and Drug Induced Liver Injury [MESH] |Antitubercular Agents/adverse effects/pharmacokinetics [MESH] |Biotransformation [MESH] |Humans [MESH]Mechanism of isoniazid-induced hepatotoxicity: then and now (epmc).pdf DeepDyve Pubget Overpricing