Interleukin-1 antagonism in acute gout: Is targeting a single cytokine the answer?

摘要

Despite the existence of effective treatments, persons with gout continue to experience acute attacks. Among those who had an attack during the previous year, the risk of having at least 1 recurrent attack in the following year is 69% (1). Not surprisingly, persons with gout experience diminished quality of life and work disability (2), related not only to these recurrent flares, but also to the presence of painful and at times disfiguring tophi. Given that gout is a common crystal-induced inflammatory arthritis, with up to 6.1 million US adults having gout at some point in their lifetime (3), this disease presents a substantial public health burden.Management of gout consists of the following 3 strategies: treatment of acute attacks; lowering of serum uric acid levels in order to prevent acute flares and tissue deposition of uric acid crystals (tophi); and prophylaxis against flares, particularly during the initiation of urate-lowering therapy, and other strategies to prevent flares. Unfortunately, management of hyperuricemia in gout is suboptimal (4), and inappropriate treatment of acute attacks occurs frequently (1). The recommended options for management of acute attacks include agents that nonspecifically target inflammation, such as nonsteroi-dal antiinflammatory drugs (NSAIDs), colchicine, corti-costeroids, and possibly adrenocorticotropic hormone (ACTH) (5).