https://www.selleckchem.com/products/grl0617.html
Animal models have suggested that in acetaminophen toxicity, encephalopathy may be secondary to an alternative mechanism other than hyperammonemia which may explain the lack of correlation between initial hyperammonemia and encephalopathy in this cohort. Additionally, a lack of empiric treatment for hyperammonemia did not appear to alter the course of any of the patients. None of these patients developed encephalopathy. In cases of acetaminophen-induced hepatotoxicity, ammonia concentrations do not correlate with encephalopathy and empi
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