A 42-year-old woman with increased hepatic aminotransferases is likely suffering from what after chronic alcohol use and high-dose acetaminophen intake?

The scenario presented describes a 42-year-old woman with increased hepatic aminotransferases who has a history of chronic alcohol use combined with high-dose acetaminophen intake. The combination of these factors strongly points toward an acetaminophen overdose as the likely cause of her hepatic condition.

In instances of acetaminophen overdose, especially when coupled with chronic alcohol consumption, the risk of liver damage escalates significantly. Chronic alcohol use induces certain liver enzymes, which can lead to the increased metabolism of acetaminophen into its toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI). This metabolite not only depletes glutathione reserves but also exacerbates liver injury due to its reactive nature, resulting in elevated liver enzymes, such as aminotransferases.

In this woman’s case, the history of high-dose acetaminophen use, in the context of her chronic alcohol intake, creates a perfect storm for acute liver injury consistent with acetaminophen toxicity, making it the most plausible diagnosis. The acute nature of her liver enzyme elevation following these exposures aligns well with the pathology seen in acetaminophen overdose.

In summary, due to the synergistic effect of alcohol on the metabolism of acetaminophen and the