Keep in mind that these measurable liver enzymes are elevated as a result of acute liver parenchymal inflammation and leak out of the the hepatic functional units with an insult (drugs, acute viral hepatitis, acute and chronic  ETOH hepatitis, tylenol overdose, shock liver from decreased forward blood flow seen in shock states or successful resusitation from cardiac arrest with ALT/AST levels in the 1,000-10,000's, passive congestion from right heart failure just to name a few). Cirrhotics have the opposite. They can't systhesize. Severely depressed levels of the coagulation factors and albumin sysnthesis leading to bleeding tendancies and 3rd spacing of fluid (peripheral edema, ascites), an inabitity to conjugate bilirubin (leading to jaundice), and depressed levels of AST/ALT < LLN.

Question. Is the poison also the tonic? The primary liver inflammation supposedly caused by APB actually ameliorated by secondarily?