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It shares many adverse effects with other tyrosine\u2010kinase (<jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content>) inhibitors and antiangiogenic drugs. <jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content> inhibitors could have a direct toxicity on <jats:styled-content style=\"fixed-case\">CNS<\/jats:styled-content>, both by interfering with <jats:styled-content style=\"fixed-case\">TK<\/jats:styled-content>\u2010related pathways and by inhibiting angiogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aims<\/jats:title><jats:p>The aim of this study was to investigate whether sorafenib administration can be associated to metabolic encephalopathy in patients with cirrhosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We retrospectively reviewed medical records of all cirrhotic patients treated with sorafenib for <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content> afferent at our Department from January 2009 to December 2011.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Among 62 patients, we identified 10 patients with clinically significant cognitive impairment. Seven of these were clearly diagnosed with overt hepatic encephalopathy (<jats:styled-content style=\"fixed-case\">HE<\/jats:styled-content>), one with brain metastases and two with drug\u2010related toxic\u2010metabolic encephalopathy. These last two cases were characterized by severe cognitive impairment, mood alteration and memory deficit. Clinical exam, blood tests and brain <jats:styled-content style=\"fixed-case\">CT<\/jats:styled-content> excluded organic causes of encephalopathy and precipitating factors of <jats:styled-content style=\"fixed-case\">HE<\/jats:styled-content>. Sorafenib discontinuation was associated with complete reversal of the syndrome, which recurred on drug re\u2010administration in one case.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our study suggests that sorafenib may be a precipitating factor of metabolic encephalopathy in cirrhotic patients with advanced <jats:styled-content style=\"fixed-case\">HCC<\/jats:styled-content>. This neurological syndrome appears to be not responsive to the conventional treatment for <jats:styled-content style=\"fixed-case\">HE<\/jats:styled-content>, but it is fully reversible by drug discontinuation. It can be speculated that the potential direct neuronal action of sorafenib may represent a trigger for the onset of metabolic encephalopathy in a subset of cirrhotic patients.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12102","type":"journal-article","created":{"date-parts":[[2012,12,22]],"date-time":"2012-12-22T06:04:45Z","timestamp":1356156285000},"page":"488-493","source":"Crossref","is-referenced-by-count":14,"title":["Can the tyrosine kinase inhibitors trigger metabolic encephalopathy in cirrhotic patients?"],"prefix":"10.1111","volume":"33","author":[{"given":"Giovanni","family":"Brandi","sequence":"first","affiliation":[{"name":"Department of Experimental Diagnostic and Specialty Medicine University of Bologna Bologna Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Francesco","family":"de Rosa","sequence":"additional","affiliation":[{"name":"Department of Experimental Diagnostic and Specialty Medicine University of Bologna Bologna 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