However, it is unclear why genistein upregulates the levels of Nrf2 in the myocardium
In patients with elevated Liver enzymes / abnormal liver function and with or without Renal failure, think: acute tubular necrosis Rhabdomyolysis ischemic hepatitis alcoholic hepatic disease cyclopeptide-containing mushroom toxicity (eg Amanita Phalloides) viral hepatitis Wilson disease, other hepatic toxicities (eg, valproic acid, isoniazid [INH], statins, herbal medications, vinyl chloride, and polychlorinated biphenyls) Core questions [bg_faq_start] [1] Describe the metabolism of acetaminophen 4 pathways Glucuronidation (50% range 40-67%) Sulfation (30% range 20-46%) CYP (~10%) Direct Renal Clearance (~10%) Where it all goes bad for the body: N-acetyl-P-Aminophenol (aka Tylenol) gets oxidised via CYP2E1 to N-acetyl- p-benzoquinone imine NAPQI This is the TOXIC METABOLITE NAPQI usually combines with glutathione and gets excreted (renal) With toxic ingestion, this system gets over-run Glucuronidation & sulfation becomes saturated, glutathione stores deplete so NAPQI binds directly to hepatocytes = hepatocellular death (centrilobular cirrhosis or w/ massive OD entire parenchymal necrosis) Leads to cascade of MODS / SIRS / SHOCK / Cerebral Edema / ARDS / Death See Rosens figure 143.1 for acetaminophen metabolism and NAC mechanism of action [2] Describe the 4 stages of acetaminophen toxicity Stage 1 = Pre Injury ( 4 days) Death or recovery See Rosens Table 143.1 for time course and clinical stages of acetaminophen toxicity
Bottom line: Most side effects are gastrointestinal and can be managed by switching to a more bioavailable format like a liposomal liquid
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Here we summarize some of the most important achievements reached in this lively area of research
