Acetaminophen, caffeine, and magnesium salicylate and Liver disease

Acetaminophen is primarily metabolized in the liver to inactive forms. However, small quantities are converted by minor pathways to metabolites that can cause hepatotoxicity or methemoglobinemia. Patients with hepatic impairment may be at increased risk of toxicity due to increased minor metabolic pathway activity. Likewise, chronic or overuse of acetaminophen can saturate the primary hepatic enzymes and lead to increased metabolism by minor pathways. Severe liver injury, including cases of acute liver failure resulting in liver transplant and death, has been reported in patients using acetaminophen. Therapy with acetaminophen should be administered cautiously in patients with hepatic insufficiency. Clinical monitoring of hepatic function is recommended. Instruct patients to avoid drinking alcohol while taking acetaminophen-containing medications. Patients should be warned not to exceed the maximum recommended total daily dosage of acetaminophen (4 g/day in adults and children 12 years of age or older), and to read all prescription and over-the-counter medication labels to ensure they are not taking multiple acetaminophen-containing products, or check with a healthcare professional if they are unsure.

In general, CNS stimulants are extensively metabolized by the liver. Their plasma clearance may be decreased and their half-life prolonged in patients with impaired hepatic function. Therapy with CNS stimulants should be administered cautiously in patients with moderate to severe liver disease, and the dosage should be adjusted accordingly. Additionally, postmarketing reports have shown that atomoxetine can cause severe liver injury. Laboratory testing should be done at the first sign or symptom of liver dysfunction (jaundice, dark urine, upper quadrant tenderness) and treatment should be discontinued in patients with evidence of liver injury.