title: Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL?
abstract: Gout is a progressive, painful, debilitating form of inflammatory arthritis. It is caused by factors that elevate the concentration of serum uric acid (sUA), leading to hyperuricemia (sUA >6.8 mg/dL). Continued elevated sUA can result in monosodium urate (MSU) crystal deposition in joints and soft tissues, and can cause acute and chronic inflammation. The prevalence of hyperuricemia and gout has increased over the last few decades, likely due to an aging population, changes in lifestyles and diet, and an increase in gout-associated comorbidities. Untreated or improperly treated gout can lead to chronic manifestation of the disease, including persistent inflammation, increased number of flares, development of tophi, and structural joint damage. Data show that even when patients are asymptomatic, ongoing inflammation and subsequent damage occurs locally at the joint and systemically. The aim of long-term treatment of gout is to reduce sUA levels to <6 mg/dL, which is below the saturation point of MSU (6.8 mg/dL), to inhibit formation of new crystals and to promote dissolution of existing crystals. Gout treatment should improve disease outcomes by eliminating gout flares, inducing long-term resolution of tophi, and more effectively managing comorbidities, many of which are associated with hyperuricemia. A number of studies have demonstrated that treating to the target of <6 mg/dL, by using effective therapies to lower sUA, results in reduction in the incidence of gout flares as well as shrinkage and eventual disappearance of tophi. Gout is often poorly managed due to a number of factors including lack of physician and patient adherence to treatment guidelines. Patients need to be educated about their diagnosis and management of the disease, such as the influence of diet and the importance of compliance with long-term treatment. With treatment, regular sUA monitoring, and patient adherence, gout is a curable disease.
authors: a Department of Family Practice , Michigan State University , Kalamazoo , MI , USA.
authors: Gary
authors: G
authors: Ruoff
authors: b Department of Medicine , University of Florida , Gainesville , FL , USA.
authors: N Lawrence
authors: NL
authors: Edwards
mesh_terms: D019468:Disease Management; D006073:Gout / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006074:Gout Suppressants / Q000494:pharmacology*; D006801:Humans; D033461:Hyperuricemia / Q000378:metabolism / Q000517:prevention & control / Q000523:psychology; D010349:Patient Compliance; D014527:Uric Acid / Q000032:analysis / Q000378:metabolism
chemical_list: D006074:Gout Suppressants; D014527:Uric Acid
keywords: Gout; MSU crystals; hyperuricemia; inflammatory arthritis; joint damage; joint erosion; monosodium urate; serum uric acid; tophi; treatment guidelines