Treatment of gout and hyperuricemia, an update

Acute gouty arthritis (gouty attack) is an acute inflammation of a joint or joints. Since the pain is often severe, though transient, it decreases QOL (quality of life) of the patient very much. Therefore, the aim of the treatment of acute gouty attack is to improve QOL by relieving the pain of the patient. Gout is a very old disease whose description goes back to 5 B.C. by Hippocrates in ancient Greece. Surprisingly, he described the effectiveness of colchicine from a plant Colchicum autumnale as a therapeutic agent. Colchicine blocks the formation of microtubules in neutrophils and inhibits the migration of the cells to inflammatory lesions. Although the effectiveness of colchicine for acute gouty arthritis has long been obvious, evidence from a controlled study for colchicine is not sufficient. Typically oral colchicine given at a dose of, at most, 1.8 mg/d, is used in the early stage of an acute gouty attack or even before the initiation of the pain. Experienced gout patients can often predict the arthritis by some local feeling (aura). However, the administration of colchicine every hour until adverse events occur, such as diarrhea, is no longer recommended. Either NSAID or corticosteroid is used when a small dose of colchicine is not sufficiently Purpose: To update the treatment of gout and hyperuricemia based on papers from various countries. Findings: Treatment of gout and hyperuricemia is composed of three segments (a) treatment of acute gouty attack, (b) treatment of hyperuricemia, and (c) treatment of associated disorders. For the treatment of hyperuricemia, in addition to allopurinol, a xanthine oxidase/dehydrogenase inhibitor, febuxostat is now used. Stevens-Johnson’s syndrome and toxic epidermal necrolysis caused by allopurinol is strongly associated with HLA-B*5801 present at rather high frequencies in some Asian populations. Many transporters in microtubules of the kidney have been identified by molecular biology and GWAS (genome-wide association study). Uricosuric drugs inhibit the function of SLC22A12 and other transporters, and decrease the reabsorption of urate into blood. For tumor lysis syndrome, rasburicase and pegloticase are used, while the latter is also used for chronic gout refractory to other treatments. Although serum urate concentration is positively associated with cardiovascular death, it is controversial as to whether urate is directly associated with the disorder or only a marker. Guidelines for the management of gout have been published from Europe and US, while guidelines for the management of hyperuricemia and gout have been released from Japan. Conclusion: Patients with gout and hyperuricemia should be managed or treated by the methods suited to individual patients and to their conditions.