Recent developments in the understanding of NSAID-induced liver fibrosis: linking fundamental mechanisms to specific therapy ideas

Abstract

One of the most often prescribed medicine class worldwide is that of non-steroidal anti-inflammatory drugs. NSAIDs exhibit the action of a common mechanism consisting of cyclooxygenase inhibition, the enzymes in charge of producing prostanoids. NSAIDs are primarily weak organic acids and have been connected to liver disease for multiple decades. Interstitial collagens are produced in excess and deposited in the liver's extracellular matrix, resulting in hepatic fibrosis. Only a few NSAIDs exhibit inherent dose-dependent toxicity. Dietary changes, alcohol abstinence, and antiviral drugs are examples of current therapy. Nevertheless, such etiology-driven treatment is typically inadequate in patients with late-stage fibrosis or cirrhosis. The development of practice guidelines by multidisciplinary panels of experts includes suggestions of helpful remedy options for the particular reason of liver injury, stage of fibrosis, or occurrence of co-morbidities linked to a continuing loss of liver function. We listed the causes of hepatic injuries, including NSAIDs, and the prevailing theories behind anti-fibrotic treatments.