Hepatorenal Effects of Ibuprofen Compared with other NSAIDs and Paracetamol

Liver reactions have long been known with many NSAIDs (e.g. aspirin, diclofenac, piroxicam) as well as ibuprofen and paracetamol (acetaminophen). In this chapter the occurrence and actions of known hepatotoxic drugs affecting liver functions and the factors that can contribute to liver toxicity of NSAIDs. Elevation of liver enzymes is the most frequent of the liver reactions attributed to NSAIDs and paracetamol. More serious reactions include jaundice and fulminant liver failure. Overall, the evidence for serious liver reactions from ibuprofen and other NSAIDs suggests that these reactions are infrequent. Many case reports are inadequate in providing sufficient information to attribute causality to this or other drugs taken concomitantly or the existence of prior or concurrent conditions that are known to affect liver functions or cause liver toxicity. The kidney is also a site of toxicity of NSAIDs linked to high concentrations of drugs that are excreted via this organ. The pathology of renal conditions from NSAIDs analgesics varies from acute to chronic effects depending on dose and duration in intake. Much of the kidney effects are due to direct toxic effects on the renal tubular and glomerular systems. Inhibition of prostaglandin production is a major factor accounting for physiological changes and renal tubular actions of NSAIDs. Ibuprofen at OTC doses has relative low toxicity to both hepatic and renal systems, but can be more toxic at prescription or higher doses, but still is among the lowest toxicity of all NSAIDs and coxibs.