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Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL?
Postgrad Med. 2016 Sep; 128(7):706-15.PM

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+Show Affiliations

a Department of Family Practice , Michigan State University , Kalamazoo , MI , USA.b Department of Medicine , University of Florida , Gainesville , FL , USA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

27558643

Citation

Ruoff, Gary, and N Lawrence Edwards. "Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 Mg/dL?" Postgraduate Medicine, vol. 128, no. 7, 2016, pp. 706-15.
Ruoff G, Edwards NL. Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL? Postgrad Med. 2016;128(7):706-15.
Ruoff, G., & Edwards, N. L. (2016). Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL? Postgraduate Medicine, 128(7), 706-15. https://doi.org/10.1080/00325481.2016.1221732
Ruoff G, Edwards NL. Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 Mg/dL. Postgrad Med. 2016;128(7):706-15. PubMed PMID: 27558643.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL? AU - Ruoff,Gary, AU - Edwards,N Lawrence, Y1 - 2016/08/25/ PY - 2016/8/26/entrez PY - 2016/8/26/pubmed PY - 2017/1/26/medline KW - Gout KW - MSU crystals KW - hyperuricemia KW - inflammatory arthritis KW - joint damage KW - joint erosion KW - monosodium urate KW - serum uric acid KW - tophi KW - treatment guidelines SP - 706 EP - 15 JF - Postgraduate medicine JO - Postgrad Med VL - 128 IS - 7 N2 - 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. SN - 1941-9260 UR - https://www.unboundmedicine.com/medline/citation/27558643/Overview_of_Serum_Uric_Acid_Treatment_Targets_in_Gout:_Why_Less_Than_6_mg/dL DB - PRIME DP - Unbound Medicine ER -