Acetaminophen can be hepatotoxic. In most cases, acetaminophen hepatotoxicity occurs as a result of an acute overdose, however, moderately excessive doses, if taken chronically, can also produce hepatotoxicity. Regular use of acetaminophen for periods of 5-39 months produced hepatotoxicity in 11 patients. Elevated hepatic enzymes and hypoprothrombinemia are seen. GI bleeding can occur secondary to low prothrombin levels.
Hepatic necrosis is the major adverse reaction of acetaminophen.
In addition, poisoning can lead to mental changes, characterized by initial CNS stimulation and subsequent CNS depression. Young children appear to be at less risk of developing hepatotoxicity, possibly because of an age-related difference in the metabolism of the drug. It has also been suggested that recent fasting is associated with hepatotoxicity in patients taking higher than recommended doses. The risk of renal complications appears to be higher in alcoholic patients. Recently, acetaminophen has been implicated as a contributing factor in the decline of renal function in patients with underlying renal disease, including diabetic nephropathy.