Gout is a metabolic disorder characterized by hyperuricemia. Asymptomatic hyperuricemia ought not to be treated until arthritis; renal calculi or tophi become evident. The cornerstone of therapy of acute attack is often nonsteroidal anti-inflammatory drugs (NSAIDs), barring specific situations wherein colchicine and corticosteroids do have a role. Usually NSAIDs with stronger anti-inflammatory action are used in high and quickly repeated doses and have a slower response response as compared to colchicine, they are better tolerated. Colchicine has a unique mechanism action. Intra-articular corticosteroids provide relief in acute attack and are given in patients having inability to tolerate NSAIDs and colchicine. Chronic gout requires treatments with drugs that either promote excretion (e.g., probenecid, lesinurad) or prevent its synthesis through inhibition of enzyme xanthine oxidase (allopurinol, febuxostat, etc.). Pegloticase and rasburicase, being a recombinant uricase enzyme, oxidize uric acid to highly soluble allantoin excreted in urine. In spite of these effective treatment modalities, question arises on their safety profile. Newer treatment options are being extensively studied especially interleukin-1 (IL-1) inhibitors but their approval is still pending. The quest for an optimally designed drug with desirable efficacy and acceptable safety profile is still on.
Part of the book: Recent Advances in Gout