Gout is a common and painful inflammatory arthritis caused by monosodium urate crystal deposition into joints in the setting of hyperuricemia. Recent reports indicate an increase in prevalence and incidence of gout worldwide. While genetics, dietary habits, and lifestyle play a significant role in the development of gout, risk factors also include diabetes, hypertension, obesity, chronic kidney disease, and metabolic disease among others. As such, accompanying comorbidities must also be considered when choosing therapeutic agents for urate-lowering therapy (ULT) and gout flares. This article will focus on reviewing gout pathophysiology and discussion of currently available pharmacological and nonpharmacological options for chronic gout management, gout flare therapy, and prophylactic measures. Despite an increase in prevalence, optimal gout management remains elusive and challenging with only a third to half of patients receiving definitive treatment and fewer than half of patients remaining adherent to treatment. Current strategies for optimal chronic gout management include the “treat to target” method, which focuses on targeting serum urate level of 5–6 mg/dL or lower. Additional approaches for chronic gout management include starting ULTs with 3–6 months of prophylaxis to reduce the risk of precipitating gout flares during initiation. Both improvement of the recognition and diagnosis of gout and more widespread provider adherence to international rheumatology society recommendations for gout management remain barriers to optimal gout management worldwide. This article will also serve as a review of current urate-lowering pharmacological options including xanthine oxidase inhibitors, uricosurics, and uricase therapy as well as burgeoning new medications on the horizon including novel potent xanthine oxidase inhibitors (including tigulixostat), sodium-glucose transporter-2 inhibitors, and selective URAT1 inhibitors. Additionally, this article will review pharmacological approaches to treating gout flares (including nonsteroidal anti-inflammatory drugs, glucocorticoids, and colchicine) and discuss the role of patient comorbidities in selection of optimal therapy. The present review will also discuss the role and limitations of novel interleukin-1 (IL-1) antagonists (including anakinra and canakinumab) in the treatment of gout flares. Lastly, this article will also discuss nonpharmacological intervention for gout management and discuss novel therapies for chronic gout management, gout flare, and prophylaxis on the horizon.
McCarty et al. (Fri,) studied this question.