Hepatotoxicity

An herb that resolves one health problem while creating another is not a net benefit and should be reconsidered. Most herbs are beneficial for the liver, particularly bitter herbs, but a specific set of six herbs carries hepatotoxic risk for certain populations or under certain conditions. Pretomanid-containing clinical trials reported liver enzyme elevations leading to withdrawal or treatment interruption. Once glutathione is depleted, the toxic acetaminophen metabolite kills hepatocytes through necrosis. When liver enzymes are saturated by excess acetaminophen, a third metabolic pathway activates and produces a reactive toxic metabolite. The exact mechanism of hepatotoxicity from bedaquiline, delamanid, and pretomanid is not fully characterized. Drug-induced phospholipidosis is proposed as a broader hepatotoxicity mechanism for all three drugs. Female patients may have elevated hepatotoxicity signals because lipophilic drugs can be stored in adipose tissue and sustain higher plasma concentrations. Which part of a plant is used — root, stem, or leaf — can determine whether the herb is safe or hepatotoxic. Routine liver function testing is recommended for all patients receiving be…